---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '18445'
abstract:
- lang: eng
text: Acquisition of specialized cellular features is controlled by the ordered
expression of transcription factors (TFs) along differentiation trajectories.
Here, we find a member of the Onecut TF family, ONECUT3, expressed in postmitotic
neurons that leave their Ascl1+/Onecut1/2+ proliferative domain in the vertebrate
hypothalamus to instruct neuronal differentiation. We combined single-cell RNA-seq
and gain-of-function experiments for gene network reconstruction to show that
ONECUT3 affects the polarization and morphogenesis of both hypothalamic GABA-derived
dopamine and thyrotropin-releasing hormone (TRH)+ glutamate neurons through neuron
navigator-2 (NAV2). In vivo, siRNA-mediated knockdown of ONECUT3 in neonatal mice
reduced NAV2 mRNA, as well as neurite complexity in Onecut3-containing neurons,
while genetic deletion of Onecut3/ceh-48 in C. elegans impaired neurocircuit wiring,
and sensory discrimination-based behaviors. Thus, ONECUT3, conserved across neuronal
subtypes and many species, underpins the polarization and morphological plasticity
of phenotypically distinct neurons that descend from a common pool of Ascl1+ progenitors
in the hypothalamus.
acknowledgement: "The authors thank Z. Máté, G. Szabó, and F. Erdélyi for the custom
generation of transgenic mouse lines, C. Fekete for Trh transgenic tissues (all
from the Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest,
Hungary), A. Goudmaeker for IVF recovery of a frozen mouse line (SSS animal facility,
Université catholique de Louvain), and Y. Yanagawa (Department of Genetic and Behavioral
Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan) for
providing GAD67gfp/+ mice. We also thank S. Cloer, D. Preininger, and A. Weissenbacher
(Tiergarten Schönbrunn, Vienna, Austria) for providing naked mole rats, Seba’s fruit
bats, and Indian flying foxes, as well as F. Aujard (CNRS, UMR 7179 ‘Adaptive mechanisms
and evolution’, France) for Microcebus tissues. I. Milenkovic and G.G. Kovács (Clinical
Institute of Neurology, Medical University of Vienna, Vienna, Austria) are acknowledged
for providing post-mortem human brain samples. We are indebted to S. Rehman (Medical
University of Vienna), M. Kalusa (University of Leipzig, Leipzig, Germany), and
W. Reimann (Paul Flechsig Institute for Brain Research, Leipzig, Germany) for their
technical assistance. C. elegans strains were provided by the National Bioresource
Project for the nematode, Japan, and the CGC, with the latter being funded by the
NIH Office of Research Infrastructure Programs (P40 OD010440). This work was supported
by the Austrian Science Fund (FWF, P 34121-B; to E.K.), the Swedish Research Council
(2023-03058, T.Ha; 2020-01688, T.Hö.), the Swedish Brain Foundation (Hjärnfonden,
FO2022-0300, to T.Ha.), the Novo Nordisk Foundation (NNF23OC0084476, to T.Ha.),
the European Research Council (FOODFORLIFE, ERC-2020-AdG-101021016; to T.Ha.), the
Université Catholique de Louvain (‘Fonds spéciaux de recherche’-FSR, to F.C.), and
Fonds de la Recherche Scientifique F.R.S.-FNRS (‘Project de recherche (PDR)’ #T.0039.21,
to F.C.). S.J.E. is supported by the Simons Foundation #543069. I.L. is supported
by a post-doctoral fellowship from the Human Frontiers Science Program (LT000335/2020-L).
E.R. holds a PhD grant from the FRIA (F.R.S.-FNRS, Belgium). F.C. is a Research
Director of the F.R.S.-FNRS (Belgium).\r\nOpen access funding provided by Karolinska
Institute."
article_number: '8631'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Maja
full_name: Zupančič, Maja
last_name: Zupančič
- first_name: Erik
full_name: Keimpema, Erik
last_name: Keimpema
- first_name: Evgenii O.
full_name: Tretiakov, Evgenii O.
last_name: Tretiakov
- first_name: Stephanie J.
full_name: Eder, Stephanie J.
last_name: Eder
- first_name: Itamar
full_name: Lev, Itamar
last_name: Lev
- first_name: Lukas
full_name: Englmaier, Lukas
last_name: Englmaier
- first_name: Pradeep
full_name: Bhandari, Pradeep
id: 45EDD1BC-F248-11E8-B48F-1D18A9856A87
last_name: Bhandari
orcid: 0000-0003-0863-4481
- first_name: Simone A.
full_name: Fietz, Simone A.
last_name: Fietz
- first_name: Wolfgang
full_name: Härtig, Wolfgang
last_name: Härtig
- first_name: Estelle
full_name: Renaux, Estelle
last_name: Renaux
- first_name: Andreas
full_name: Villunger, Andreas
last_name: Villunger
- first_name: Tomas
full_name: Hökfelt, Tomas
last_name: Hökfelt
- first_name: Manuel
full_name: Zimmer, Manuel
last_name: Zimmer
- first_name: Frédéric
full_name: Clotman, Frédéric
last_name: Clotman
- first_name: Tibor
full_name: Harkany, Tibor
last_name: Harkany
citation:
ama: Zupančič M, Keimpema E, Tretiakov EO, et al. Concerted transcriptional regulation
of the morphogenesis of hypothalamic neurons by ONECUT3. Nature Communications.
2024;15. doi:10.1038/s41467-024-52762-z
apa: Zupančič, M., Keimpema, E., Tretiakov, E. O., Eder, S. J., Lev, I., Englmaier,
L., … Harkany, T. (2024). Concerted transcriptional regulation of the morphogenesis
of hypothalamic neurons by ONECUT3. Nature Communications. Springer Nature.
https://doi.org/10.1038/s41467-024-52762-z
chicago: Zupančič, Maja, Erik Keimpema, Evgenii O. Tretiakov, Stephanie J. Eder,
Itamar Lev, Lukas Englmaier, Pradeep Bhandari, et al. “Concerted Transcriptional
Regulation of the Morphogenesis of Hypothalamic Neurons by ONECUT3.” Nature
Communications. Springer Nature, 2024. https://doi.org/10.1038/s41467-024-52762-z.
ieee: M. Zupančič et al., “Concerted transcriptional regulation of the morphogenesis
of hypothalamic neurons by ONECUT3,” Nature Communications, vol. 15. Springer
Nature, 2024.
ista: Zupančič M, Keimpema E, Tretiakov EO, Eder SJ, Lev I, Englmaier L, Bhandari
P, Fietz SA, Härtig W, Renaux E, Villunger A, Hökfelt T, Zimmer M, Clotman F,
Harkany T. 2024. Concerted transcriptional regulation of the morphogenesis of
hypothalamic neurons by ONECUT3. Nature Communications. 15, 8631.
mla: Zupančič, Maja, et al. “Concerted Transcriptional Regulation of the Morphogenesis
of Hypothalamic Neurons by ONECUT3.” Nature Communications, vol. 15, 8631,
Springer Nature, 2024, doi:10.1038/s41467-024-52762-z.
short: M. Zupančič, E. Keimpema, E.O. Tretiakov, S.J. Eder, I. Lev, L. Englmaier,
P. Bhandari, S.A. Fietz, W. Härtig, E. Renaux, A. Villunger, T. Hökfelt, M. Zimmer,
F. Clotman, T. Harkany, Nature Communications 15 (2024).
date_created: 2024-10-20T22:02:05Z
date_published: 2024-10-05T00:00:00Z
date_updated: 2025-09-08T14:25:06Z
day: '05'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1038/s41467-024-52762-z
external_id:
isi:
- '001409493300014'
pmid:
- '39366958'
file:
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creator: dernst
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month: '10'
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oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Concerted transcriptional regulation of the morphogenesis of hypothalamic neurons
by ONECUT3
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 15
year: '2024'
...
---
_id: '15385'
abstract:
- lang: eng
text: "Relevant information about the data can be found in the 'Readme_Data.txt'
file. \r\nA previous version of the publication can be found on BioRxiv: https://www.biorxiv.org/content/10.1101/2022.10.11.511691v4\r\nand
published in Plos Biology (2024)"
acknowledged_ssus:
- _id: PreCl
- _id: M-Shop
- _id: LifeSc
- _id: Bio
acknowledgement: 'We thank Armel Nicolas, Bella Bruszel and Ewelina Dutkiewicz from
the ISTA Mass Spectrometry Service (Lab Services Facilities) for all Proteomics
work, including samples preparation, LC/MS data acquisition, searches and data evaluation.
We thank Prof. Peter Jonas for his suggestion on the involvement of potassium channels
and members of the Neuroethology group for their comments on the manuscript. Katalin
Szigeti and Julie Murmann for experimental help. This research was supported by
the Scientific Service Units of ISTA through resources provided by the Lab Support
Facility, the Imaging and Optics Facility, the Machine Shop Unit and the Preclinical
Facility, especially Freyja Langer and Michael Schunn. '
article_processing_charge: No
author:
- first_name: Laura
full_name: Burnett, Laura
id: 3B717F68-F248-11E8-B48F-1D18A9856A87
last_name: Burnett
orcid: 0000-0002-8937-410X
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: Olga
full_name: Symonova, Olga
id: 3C0C7BC6-F248-11E8-B48F-1D18A9856A87
last_name: Symonova
orcid: 0000-0003-2012-9947
- first_name: Tomas
full_name: Masson, Tomas
id: 93ac43e8-8599-11eb-9b86-f6efb0a4c207
last_name: Masson
orcid: 0000-0002-2634-6283
- first_name: Tomas A
full_name: Vega Zuniga, Tomas A
id: 2E7C4E78-F248-11E8-B48F-1D18A9856A87
last_name: Vega Zuniga
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
- first_name: Maximilian A
full_name: Jösch, Maximilian A
id: 2BD278E6-F248-11E8-B48F-1D18A9856A87
last_name: Jösch
orcid: 0000-0002-3937-1330
citation:
ama: Burnett L, Koppensteiner P, Symonova O, et al. Shared behavioural impairments
in visual perception and place avoidance across different autism models are driven
by periaqueductal grey hypoexcitability in Setd5 haploinsufficient mice. 2024.
doi:10.15479/AT:ISTA:15385
apa: Burnett, L., Koppensteiner, P., Symonova, O., Masson, T., Vega Zuniga, T. A.,
Contreras, X., … Jösch, M. A. (2024). Shared behavioural impairments in visual
perception and place avoidance across different autism models are driven by periaqueductal
grey hypoexcitability in Setd5 haploinsufficient mice. Institute of Science and
Technology Austria. https://doi.org/10.15479/AT:ISTA:15385
chicago: Burnett, Laura, Peter Koppensteiner, Olga Symonova, Tomas Masson, Tomas
A Vega Zuniga, Ximena Contreras, Thomas Rülicke, Ryuichi Shigemoto, Gaia Novarino,
and Maximilian A Jösch. “Shared Behavioural Impairments in Visual Perception and
Place Avoidance across Different Autism Models Are Driven by Periaqueductal Grey
Hypoexcitability in Setd5 Haploinsufficient Mice.” Institute of Science and Technology
Austria, 2024. https://doi.org/10.15479/AT:ISTA:15385.
ieee: L. Burnett et al., “Shared behavioural impairments in visual perception
and place avoidance across different autism models are driven by periaqueductal
grey hypoexcitability in Setd5 haploinsufficient mice.” Institute of Science and
Technology Austria, 2024.
ista: Burnett L, Koppensteiner P, Symonova O, Masson T, Vega Zuniga TA, Contreras
X, Rülicke T, Shigemoto R, Novarino G, Jösch MA. 2024. Shared behavioural impairments
in visual perception and place avoidance across different autism models are driven
by periaqueductal grey hypoexcitability in Setd5 haploinsufficient mice, Institute
of Science and Technology Austria, 10.15479/AT:ISTA:15385.
mla: Burnett, Laura, et al. Shared Behavioural Impairments in Visual Perception
and Place Avoidance across Different Autism Models Are Driven by Periaqueductal
Grey Hypoexcitability in Setd5 Haploinsufficient Mice. Institute of Science
and Technology Austria, 2024, doi:10.15479/AT:ISTA:15385.
short: L. Burnett, P. Koppensteiner, O. Symonova, T. Masson, T.A. Vega Zuniga, X.
Contreras, T. Rülicke, R. Shigemoto, G. Novarino, M.A. Jösch, (2024).
corr_author: '1'
date_created: 2024-05-13T15:04:04Z
date_published: 2024-05-15T00:00:00Z
date_updated: 2025-09-08T07:57:11Z
day: '15'
ddc:
- '570'
department:
- _id: MaJö
- _id: PreCl
- _id: SiHi
- _id: RySh
- _id: GaNo
doi: 10.15479/AT:ISTA:15385
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has_accepted_license: '1'
keyword:
- ASD
- periaqueductal gray
- perception
- behavior
- potassium channels
month: '05'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '17142'
relation: used_in_publication
status: public
status: public
title: Shared behavioural impairments in visual perception and place avoidance across
different autism models are driven by periaqueductal grey hypoexcitability in Setd5
haploinsufficient mice
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: research_data
user_id: 68b8ca59-c5b3-11ee-8790-cd641c68093d
year: '2024'
...
---
APC_amount: 6081,83 EUR
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '17142'
abstract:
- lang: eng
text: Despite the diverse genetic origins of autism spectrum disorders (ASDs), affected
individuals share strikingly similar and correlated behavioural traits that include
perceptual and sensory processing challenges. Notably, the severity of these sensory
symptoms is often predictive of the expression of other autistic traits. However,
the origin of these perceptual deficits remains largely elusive. Here, we show
a recurrent impairment in visual threat perception that is similarly impaired
in 3 independent mouse models of ASD with different molecular aetiologies. Interestingly,
this deficit is associated with reduced avoidance of threatening environments—a
nonperceptual trait. Focusing on a common cause of ASDs, the Setd5 gene mutation,
we define the molecular mechanism. We show that the perceptual impairment is caused
by a potassium channel (Kv1)-mediated hypoexcitability in a subcortical node essential
for the initiation of escape responses, the dorsal periaqueductal grey (dPAG).
Targeted pharmacological Kv1 blockade rescued both perceptual and place avoidance
deficits, causally linking seemingly unrelated trait deficits to the dPAG. Furthermore,
we show that different molecular mechanisms converge on similar behavioural phenotypes
by demonstrating that the autism models Cul3 and Ptchd1, despite having similar
behavioural phenotypes, differ in their functional and molecular alteration. Our
findings reveal a link between rapid perception controlled by subcortical pathways
and appropriate learned interactions with the environment and define a nondevelopmental
source of such deficits in ASD.
acknowledgement: 'This work was supported by a European Research Council Starting
Grant 756502 (MJ). '
article_number: e3002668
article_processing_charge: Yes
article_type: original
author:
- first_name: Laura
full_name: Burnett, Laura
id: 3B717F68-F248-11E8-B48F-1D18A9856A87
last_name: Burnett
orcid: 0000-0002-8937-410X
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: Olga
full_name: Symonova, Olga
id: 3C0C7BC6-F248-11E8-B48F-1D18A9856A87
last_name: Symonova
orcid: 0000-0003-2012-9947
- first_name: Tomas
full_name: Masson, Tomas
id: 93ac43e8-8599-11eb-9b86-f6efb0a4c207
last_name: Masson
orcid: 0000-0002-2634-6283
- first_name: Tomas A
full_name: Vega Zuniga, Tomas A
id: 2E7C4E78-F248-11E8-B48F-1D18A9856A87
last_name: Vega Zuniga
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
- first_name: Maximilian A
full_name: Jösch, Maximilian A
id: 2BD278E6-F248-11E8-B48F-1D18A9856A87
last_name: Jösch
orcid: 0000-0002-3937-1330
citation:
ama: Burnett L, Koppensteiner P, Symonova O, et al. Shared behavioural impairments
in visual perception and place avoidance across different autism models are driven
by periaqueductal grey hypoexcitability in Setd5 haploinsufficient mice. PLoS
Biology. 2024;22. doi:10.1371/journal.pbio.3002668
apa: Burnett, L., Koppensteiner, P., Symonova, O., Masson, T., Vega Zuniga, T. A.,
Contreras, X., … Jösch, M. A. (2024). Shared behavioural impairments in visual
perception and place avoidance across different autism models are driven by periaqueductal
grey hypoexcitability in Setd5 haploinsufficient mice. PLoS Biology. Public
Library of Science. https://doi.org/10.1371/journal.pbio.3002668
chicago: Burnett, Laura, Peter Koppensteiner, Olga Symonova, Tomas Masson, Tomas
A Vega Zuniga, Ximena Contreras, Thomas Rülicke, Ryuichi Shigemoto, Gaia Novarino,
and Maximilian A Jösch. “Shared Behavioural Impairments in Visual Perception and
Place Avoidance across Different Autism Models Are Driven by Periaqueductal Grey
Hypoexcitability in Setd5 Haploinsufficient Mice.” PLoS Biology. Public
Library of Science, 2024. https://doi.org/10.1371/journal.pbio.3002668.
ieee: L. Burnett et al., “Shared behavioural impairments in visual perception
and place avoidance across different autism models are driven by periaqueductal
grey hypoexcitability in Setd5 haploinsufficient mice,” PLoS Biology, vol.
22. Public Library of Science, 2024.
ista: Burnett L, Koppensteiner P, Symonova O, Masson T, Vega Zuniga TA, Contreras
X, Rülicke T, Shigemoto R, Novarino G, Jösch MA. 2024. Shared behavioural impairments
in visual perception and place avoidance across different autism models are driven
by periaqueductal grey hypoexcitability in Setd5 haploinsufficient mice. PLoS
Biology. 22, e3002668.
mla: Burnett, Laura, et al. “Shared Behavioural Impairments in Visual Perception
and Place Avoidance across Different Autism Models Are Driven by Periaqueductal
Grey Hypoexcitability in Setd5 Haploinsufficient Mice.” PLoS Biology, vol.
22, e3002668, Public Library of Science, 2024, doi:10.1371/journal.pbio.3002668.
short: L. Burnett, P. Koppensteiner, O. Symonova, T. Masson, T.A. Vega Zuniga, X.
Contreras, T. Rülicke, R. Shigemoto, G. Novarino, M.A. Jösch, PLoS Biology 22
(2024).
corr_author: '1'
date_created: 2024-06-16T22:01:05Z
date_published: 2024-06-10T00:00:00Z
date_updated: 2025-09-08T07:57:11Z
day: '10'
ddc:
- '570'
department:
- _id: RySh
- _id: GaNo
- _id: MaJö
doi: 10.1371/journal.pbio.3002668
ec_funded: 1
external_id:
isi:
- '001246176800003'
pmid:
- '38857283'
file:
- access_level: open_access
checksum: 496e1aa4fd5b92b7e4087ecc2c964133
content_type: application/pdf
creator: dernst
date_created: 2025-01-09T10:39:41Z
date_updated: 2025-01-09T10:39:41Z
file_id: '18805'
file_name: 2024_PloS_Burnett.pdf
file_size: 4016568
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success: 1
file_date_updated: 2025-01-09T10:39:41Z
has_accepted_license: '1'
intvolume: ' 22'
isi: 1
language:
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month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2634E9D2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '756502'
name: Circuits of Visual Attention
publication: PLoS Biology
publication_identifier:
eissn:
- 1545-7885
issn:
- 1544-9173
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
link:
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url: https://doi.org/10.5281/zenodo.11130587
record:
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relation: research_data
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scopus_import: '1'
status: public
title: Shared behavioural impairments in visual perception and place avoidance across
different autism models are driven by periaqueductal grey hypoexcitability in Setd5
haploinsufficient mice
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 22
year: '2024'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '17280'
abstract:
- lang: eng
text: Adherens junction–associated protein 1 (AJAP1) has been implicated in brain
diseases; however, a pathogenic mechanism has not been identified. AJAP1 is widely
expressed in neurons and binds to γ-aminobutyric acid type B receptors (GBRs),
which inhibit neurotransmitter release at most synapses in the brain. Here, we
show that AJAP1 is selectively expressed in dendrites and trans-synaptically recruits
GBRs to presynaptic sites of neurons expressing AJAP1. We have identified several
monoallelic AJAP1 variants in individuals with epilepsy and/or neurodevelopmental
disorders. Specifically, we show that the variant p.(W183C) lacks binding to GBRs,
resulting in the inability to recruit them. Ultrastructural analysis revealed
significantly decreased presynaptic GBR levels in Ajap1−/− and Ajap1W183C/+ mice.
Consequently, these mice exhibited reduced GBR-mediated presynaptic inhibition
at excitatory and inhibitory synapses, along with impaired synaptic plasticity.
Our study reveals that AJAP1 enables the postsynaptic neuron to regulate the level
of presynaptic GBR-mediated inhibition, supporting the clinical relevance of loss-of-function
AJAP1 variants.
acknowledgement: "Ajap1HA/HA and Ajap1W183C/+ mice were generated in collaboration
with Pawel Pelczar at the center for transgenic models at the University of Basel,
Switzerland. We thank the imaging core facility (IMCF, University of Basel) and
in particular A. Ferrand for the technical assistance provided on the OMX 3D-SIM
microscope.\r\nThis work was supported by a grant from the Swiss National Science
Foundation (SNF) to B.B. (31003A-152970, 310030B-201291), an NIH grant to E.A. and
E.H.S. (R01NS058721), DFG grants to B.F. (TRR 152 project ID 239283807, FA 332/15-1,
16-1), and grants to P.S. from AIMS-2-TRIALS, which are supported by the Innovative
Medicines Initiatives from the European Commission joint undertaking under grant
agreement No 777394."
article_number: adk5462
article_processing_charge: Yes
article_type: original
author:
- first_name: Simon
full_name: Früh, Simon
last_name: Früh
- first_name: Sami
full_name: Boudkkazi, Sami
last_name: Boudkkazi
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: Vita
full_name: Sereikaite, Vita
last_name: Sereikaite
- first_name: Li Yuan
full_name: Chen, Li Yuan
last_name: Chen
- first_name: Diego
full_name: Fernandez-Fernandez, Diego
last_name: Fernandez-Fernandez
- first_name: Pascal D.
full_name: Rem, Pascal D.
last_name: Rem
- first_name: Daniel
full_name: Ulrich, Daniel
last_name: Ulrich
- first_name: Jochen
full_name: Schwenk, Jochen
last_name: Schwenk
- first_name: Ziyang
full_name: Chen, Ziyang
last_name: Chen
- first_name: Elodie Le
full_name: Monnier, Elodie Le
last_name: Monnier
- first_name: Thorsten
full_name: Fritzius, Thorsten
last_name: Fritzius
- first_name: Sabrina M.
full_name: Innocenti, Sabrina M.
last_name: Innocenti
- first_name: Valérie
full_name: Besseyrias, Valérie
last_name: Besseyrias
- first_name: Luca
full_name: Trovò, Luca
last_name: Trovò
- first_name: Michal
full_name: Stawarski, Michal
last_name: Stawarski
- first_name: Emanuela
full_name: Argilli, Emanuela
last_name: Argilli
- first_name: Elliott H.
full_name: Sherr, Elliott H.
last_name: Sherr
- first_name: Bregje
full_name: Van Bon, Bregje
last_name: Van Bon
- first_name: Erik Jan
full_name: Kamsteeg, Erik Jan
last_name: Kamsteeg
- first_name: Maria
full_name: Iascone, Maria
last_name: Iascone
- first_name: Alba
full_name: Pilotta, Alba
last_name: Pilotta
- first_name: Maria R.
full_name: Cutrì, Maria R.
last_name: Cutrì
- first_name: Mahshid S.
full_name: Azamian, Mahshid S.
last_name: Azamian
- first_name: Andrés
full_name: Hernández-García, Andrés
last_name: Hernández-García
- first_name: Seema R.
full_name: Lalani, Seema R.
last_name: Lalani
- first_name: Jill A.
full_name: Rosenfeld, Jill A.
last_name: Rosenfeld
- first_name: Xiaonan
full_name: Zhao, Xiaonan
last_name: Zhao
- first_name: Tiphanie P.
full_name: Vogel, Tiphanie P.
last_name: Vogel
- first_name: Herda
full_name: Ona, Herda
last_name: Ona
- first_name: Daryl A.
full_name: Scott, Daryl A.
last_name: Scott
- first_name: Peter
full_name: Scheiffele, Peter
last_name: Scheiffele
- first_name: Kristian
full_name: Strømgaard, Kristian
last_name: Strømgaard
- first_name: Mehdi
full_name: Tafti, Mehdi
last_name: Tafti
- first_name: Martin
full_name: Gassmann, Martin
last_name: Gassmann
- first_name: Bernd
full_name: Fakler, Bernd
last_name: Fakler
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Bernhard
full_name: Bettler, Bernhard
last_name: Bettler
citation:
ama: Früh S, Boudkkazi S, Koppensteiner P, et al. Monoallelic de novo AJAP1 loss-of-
function variants disrupt trans-synaptic control of neurotransmitter release.
Science Advances. 2024;10(28). doi:10.1126/sciadv.adk5462
apa: Früh, S., Boudkkazi, S., Koppensteiner, P., Sereikaite, V., Chen, L. Y., Fernandez-Fernandez,
D., … Bettler, B. (2024). Monoallelic de novo AJAP1 loss-of- function variants
disrupt trans-synaptic control of neurotransmitter release. Science Advances.
American Association for the Advancement of Science. https://doi.org/10.1126/sciadv.adk5462
chicago: Früh, Simon, Sami Boudkkazi, Peter Koppensteiner, Vita Sereikaite, Li Yuan
Chen, Diego Fernandez-Fernandez, Pascal D. Rem, et al. “Monoallelic de Novo AJAP1
Loss-of- Function Variants Disrupt Trans-Synaptic Control of Neurotransmitter
Release.” Science Advances. American Association for the Advancement of
Science, 2024. https://doi.org/10.1126/sciadv.adk5462.
ieee: S. Früh et al., “Monoallelic de novo AJAP1 loss-of- function variants
disrupt trans-synaptic control of neurotransmitter release,” Science Advances,
vol. 10, no. 28. American Association for the Advancement of Science, 2024.
ista: Früh S, Boudkkazi S, Koppensteiner P, Sereikaite V, Chen LY, Fernandez-Fernandez
D, Rem PD, Ulrich D, Schwenk J, Chen Z, Monnier EL, Fritzius T, Innocenti SM,
Besseyrias V, Trovò L, Stawarski M, Argilli E, Sherr EH, Van Bon B, Kamsteeg EJ,
Iascone M, Pilotta A, Cutrì MR, Azamian MS, Hernández-García A, Lalani SR, Rosenfeld
JA, Zhao X, Vogel TP, Ona H, Scott DA, Scheiffele P, Strømgaard K, Tafti M, Gassmann
M, Fakler B, Shigemoto R, Bettler B. 2024. Monoallelic de novo AJAP1 loss-of-
function variants disrupt trans-synaptic control of neurotransmitter release.
Science Advances. 10(28), adk5462.
mla: Früh, Simon, et al. “Monoallelic de Novo AJAP1 Loss-of- Function Variants Disrupt
Trans-Synaptic Control of Neurotransmitter Release.” Science Advances,
vol. 10, no. 28, adk5462, American Association for the Advancement of Science,
2024, doi:10.1126/sciadv.adk5462.
short: S. Früh, S. Boudkkazi, P. Koppensteiner, V. Sereikaite, L.Y. Chen, D. Fernandez-Fernandez,
P.D. Rem, D. Ulrich, J. Schwenk, Z. Chen, E.L. Monnier, T. Fritzius, S.M. Innocenti,
V. Besseyrias, L. Trovò, M. Stawarski, E. Argilli, E.H. Sherr, B. Van Bon, E.J.
Kamsteeg, M. Iascone, A. Pilotta, M.R. Cutrì, M.S. Azamian, A. Hernández-García,
S.R. Lalani, J.A. Rosenfeld, X. Zhao, T.P. Vogel, H. Ona, D.A. Scott, P. Scheiffele,
K. Strømgaard, M. Tafti, M. Gassmann, B. Fakler, R. Shigemoto, B. Bettler, Science
Advances 10 (2024).
date_created: 2024-07-21T22:01:01Z
date_published: 2024-07-12T00:00:00Z
date_updated: 2025-09-08T08:15:54Z
day: '12'
ddc:
- '570'
department:
- _id: RySh
- _id: PreCl
doi: 10.1126/sciadv.adk5462
external_id:
isi:
- '001280159000022'
pmid:
- '38985877'
file:
- access_level: open_access
checksum: 9cbc4501fcd4ba1c0811fd244031422b
content_type: application/pdf
creator: dernst
date_created: 2024-07-22T06:29:27Z
date_updated: 2024-07-22T06:29:27Z
file_id: '17287'
file_name: 2024_ScienceAdv_Früh.pdf
file_size: 7241489
relation: main_file
success: 1
file_date_updated: 2024-07-22T06:29:27Z
has_accepted_license: '1'
intvolume: ' 10'
isi: 1
issue: '28'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: Science Advances
publication_identifier:
eissn:
- 2375-2548
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Monoallelic de novo AJAP1 loss-of- function variants disrupt trans-synaptic
control of neurotransmitter release
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 10
year: '2024'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '17457'
abstract:
- lang: eng
text: "Autoantibodies against the protein leucine-rich glioma inactivated 1 (LGI1)
cause the most\r\ncommon subtype of autoimmune encephalitis with predominant involvement
of the limbic\r\nsystem, associated with seizures and memory deficits. LGI1 and
its receptor ADAM22 are part\r\nof a transsynaptic protein complex that includes
several proteins involved in presynaptic\r\nneurotransmitter release and postsynaptic
glutamate sensing. Autoantibodies against LGI1\r\nincrease excitatory synaptic
strength, but studies that genetically disrupt the LGI1-ADAM22\r\ncomplex report
a reduction in postsynaptic glutamate receptor-mediated responses. Thus, the\r\nmechanisms
underlying the increased synaptic strength induced by LGI1 autoantibodies remain
elusive, and the contributions of presynaptic molecules to the LGI1-transsynaptic
complex remain unclear. We therefore investigated the presynaptic mechanisms that
mediate\r\nautoantibody-induced synaptic strengthening."
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
acknowledgement: 'The authors thank Claudia Sommer for expert technical assistance,
the Electron Microscopy Facility of IST-Austria for resources, and Tereza Belinova
in the Imaging and Optics Facility of IST-Austria for 3D reconstruction. '
article_processing_charge: Yes
article_type: original
author:
- first_name: Andreas
full_name: Ritzau-Jost, Andreas
last_name: Ritzau-Jost
- first_name: Felix
full_name: Gsell, Felix
last_name: Gsell
- first_name: Josefine
full_name: Sell, Josefine
last_name: Sell
- first_name: Stefan
full_name: Sachs, Stefan
last_name: Sachs
- first_name: Jacqueline-Claire
full_name: Montanaro-Punzengruber, Jacqueline-Claire
id: 3786AB44-F248-11E8-B48F-1D18A9856A87
last_name: Montanaro-Punzengruber
- first_name: Toni
full_name: Kirmann, Toni
last_name: Kirmann
- first_name: Sebastian
full_name: Maaß, Sebastian
last_name: Maaß
- first_name: Sarosh R.
full_name: Irani, Sarosh R.
last_name: Irani
- first_name: Christian
full_name: Werner, Christian
last_name: Werner
- first_name: Christian
full_name: Geis, Christian
last_name: Geis
- first_name: Markus
full_name: Sauer, Markus
last_name: Sauer
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Stefan
full_name: Hallermann, Stefan
last_name: Hallermann
citation:
ama: Ritzau-Jost A, Gsell F, Sell J, et al. LGI1 autoantibodies enhance synaptic
transmission by presynaptic Kv1 loss and increased action potential broadening.
Neurology, Neuroimmunology and Neuroinflammation. 2024;11(5):e200284. doi:10.1212/NXI.0000000000200284
apa: Ritzau-Jost, A., Gsell, F., Sell, J., Sachs, S., Montanaro-Punzengruber, J.-C.,
Kirmann, T., … Hallermann, S. (2024). LGI1 autoantibodies enhance synaptic transmission
by presynaptic Kv1 loss and increased action potential broadening. Neurology,
Neuroimmunology and Neuroinflammation. Wolters Kluwer. https://doi.org/10.1212/NXI.0000000000200284
chicago: Ritzau-Jost, Andreas, Felix Gsell, Josefine Sell, Stefan Sachs, Jacqueline-Claire
Montanaro-Punzengruber, Toni Kirmann, Sebastian Maaß, et al. “LGI1 Autoantibodies
Enhance Synaptic Transmission by Presynaptic Kv1 Loss and Increased Action Potential
Broadening.” Neurology, Neuroimmunology and Neuroinflammation. Wolters
Kluwer, 2024. https://doi.org/10.1212/NXI.0000000000200284.
ieee: A. Ritzau-Jost et al., “LGI1 autoantibodies enhance synaptic transmission
by presynaptic Kv1 loss and increased action potential broadening,” Neurology,
Neuroimmunology and Neuroinflammation, vol. 11, no. 5. Wolters Kluwer, p.
e200284, 2024.
ista: Ritzau-Jost A, Gsell F, Sell J, Sachs S, Montanaro-Punzengruber J-C, Kirmann
T, Maaß S, Irani SR, Werner C, Geis C, Sauer M, Shigemoto R, Hallermann S. 2024.
LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and
increased action potential broadening. Neurology, Neuroimmunology and Neuroinflammation.
11(5), e200284.
mla: Ritzau-Jost, Andreas, et al. “LGI1 Autoantibodies Enhance Synaptic Transmission
by Presynaptic Kv1 Loss and Increased Action Potential Broadening.” Neurology,
Neuroimmunology and Neuroinflammation, vol. 11, no. 5, Wolters Kluwer, 2024,
p. e200284, doi:10.1212/NXI.0000000000200284.
short: A. Ritzau-Jost, F. Gsell, J. Sell, S. Sachs, J.-C. Montanaro-Punzengruber,
T. Kirmann, S. Maaß, S.R. Irani, C. Werner, C. Geis, M. Sauer, R. Shigemoto, S.
Hallermann, Neurology, Neuroimmunology and Neuroinflammation 11 (2024) e200284.
date_created: 2024-08-25T22:01:07Z
date_published: 2024-09-01T00:00:00Z
date_updated: 2025-09-08T08:59:37Z
day: '01'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1212/NXI.0000000000200284
external_id:
isi:
- '001291908600001'
pmid:
- '39141878'
file:
- access_level: open_access
checksum: 1e6d1230e0387f72752e3268f5330c9e
content_type: application/pdf
creator: dernst
date_created: 2025-01-09T13:42:42Z
date_updated: 2025-01-09T13:42:42Z
file_id: '18815'
file_name: 2024_NeurologyNeuroimmNeuroinflamm_RitzauJost.pdf
file_size: 855818
relation: main_file
success: 1
file_date_updated: 2025-01-09T13:42:42Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
issue: '5'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: e200284
pmid: 1
project:
- _id: 05970B30-7A3F-11EA-A408-12923DDC885E
grant_number: I04638
name: LGI1 antibody-induced pathophysiology in synapses
publication: Neurology, Neuroimmunology and Neuroinflammation
publication_identifier:
eissn:
- 2332-7812
publication_status: published
publisher: Wolters Kluwer
quality_controlled: '1'
related_material:
link:
- relation: earlier_version
url: https://doi.org/10.1101/2023.10.04.560631
scopus_import: '1'
status: public
title: LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and
increased action potential broadening
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 11
year: '2024'
...
---
_id: '12875'
abstract:
- lang: eng
text: The superior colliculus (SC) in the mammalian midbrain is essential for multisensory
integration and is composed of a rich diversity of excitatory and inhibitory neurons
and glia. However, the developmental principles directing the generation of SC
cell-type diversity are not understood. Here, we pursued systematic cell lineage
tracing in silico and in vivo, preserving full spatial information, using genetic
mosaic analysis with double markers (MADM)-based clonal analysis with single-cell
sequencing (MADM-CloneSeq). The analysis of clonally related cell lineages revealed
that radial glial progenitors (RGPs) in SC are exceptionally multipotent. Individual
resident RGPs have the capacity to produce all excitatory and inhibitory SC neuron
types, even at the stage of terminal division. While individual clonal units show
no pre-defined cellular composition, the establishment of appropriate relative
proportions of distinct neuronal types occurs in a PTEN-dependent manner. Collectively,
our findings provide an inaugural framework at the single-RGP/-cell level of the
mammalian SC ontogeny.
acknowledged_ssus:
- _id: Bio
- _id: M-Shop
- _id: LifeSc
- _id: PreCl
acknowledgement: "We thank Liqun Luo for his continued support, for providing essential
resources for generating Fzd10-CreER mice which were generated in his laboratory,
and for comments on the manuscript; W. Zhong for providing Nestin-Cre transgenic
mouse line for this study; A. Heger for mouse colony management; R. Beattie and
T. Asenov for designing and producing components of acute slice recovery chamber
for MADM-CloneSeq experiments; and K. Leopold, J. Rodarte and N. Amberg for initial
experiments, technical support and/or assistance. This study was supported by the
Scientific Service Units (SSU) of IST Austria through resources provided by the
Imaging & Optics Facility (IOF), Laboratory Support Facility (LSF), Miba Machine
Shop, and Pre-clinical Facility (PCF). G.C. received funding from European Commission
(IST plus postdoctoral fellowship). This work was supported by ISTA institutional\r\nfunds;
the Austrian Science Fund Special Research Programmes (FWF SFB F78 Neuro Stem Modulation)
to S.H. "
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: Thomas
full_name: Krausgruber, Thomas
last_name: Krausgruber
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Martin
full_name: Schrammel, Martin
id: f13e7cae-e8bd-11ed-841a-96dedf69f46d
last_name: Schrammel
- first_name: Natalie Y
full_name: Özgen, Natalie Y
id: e68ece33-f6e0-11ea-865d-ae1031dcc090
last_name: Özgen
- first_name: Alexis
full_name: Ivec, Alexis
id: 1d144691-e8be-11ed-9b33-bdd3077fad4c
last_name: Ivec
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Cheung GT, Pauler F, Koppensteiner P, et al. Multipotent progenitors instruct
ontogeny of the superior colliculus. Neuron. 2024;112(2):230-246.e11. doi:10.1016/j.neuron.2023.11.009
apa: Cheung, G. T., Pauler, F., Koppensteiner, P., Krausgruber, T., Streicher, C.,
Schrammel, M., … Hippenmeyer, S. (2024). Multipotent progenitors instruct ontogeny
of the superior colliculus. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.11.009
chicago: Cheung, Giselle T, Florian Pauler, Peter Koppensteiner, Thomas Krausgruber,
Carmen Streicher, Martin Schrammel, Natalie Y Özgen, et al. “Multipotent Progenitors
Instruct Ontogeny of the Superior Colliculus.” Neuron. Elsevier, 2024.
https://doi.org/10.1016/j.neuron.2023.11.009.
ieee: G. T. Cheung et al., “Multipotent progenitors instruct ontogeny of
the superior colliculus,” Neuron, vol. 112, no. 2. Elsevier, p. 230–246.e11,
2024.
ista: Cheung GT, Pauler F, Koppensteiner P, Krausgruber T, Streicher C, Schrammel
M, Özgen NY, Ivec A, Bock C, Shigemoto R, Hippenmeyer S. 2024. Multipotent progenitors
instruct ontogeny of the superior colliculus. Neuron. 112(2), 230–246.e11.
mla: Cheung, Giselle T., et al. “Multipotent Progenitors Instruct Ontogeny of the
Superior Colliculus.” Neuron, vol. 112, no. 2, Elsevier, 2024, p. 230–246.e11,
doi:10.1016/j.neuron.2023.11.009.
short: G.T. Cheung, F. Pauler, P. Koppensteiner, T. Krausgruber, C. Streicher, M.
Schrammel, N.Y. Özgen, A. Ivec, C. Bock, R. Shigemoto, S. Hippenmeyer, Neuron
112 (2024) 230–246.e11.
corr_author: '1'
date_created: 2023-04-27T09:41:48Z
date_published: 2024-01-17T00:00:00Z
date_updated: 2025-12-30T10:54:12Z
day: '17'
ddc:
- '570'
department:
- _id: SiHi
- _id: RySh
doi: 10.1016/j.neuron.2023.11.009
external_id:
isi:
- '001163937900001'
pmid:
- '38096816'
file:
- access_level: open_access
checksum: 32b3788f7085cf44a84108d8faaff3ce
content_type: application/pdf
creator: dernst
date_created: 2024-02-06T13:56:15Z
date_updated: 2024-02-06T13:56:15Z
file_id: '14944'
file_name: 2024_Neuron_Cheung.pdf
file_size: 5942467
relation: main_file
success: 1
file_date_updated: 2024-02-06T13:56:15Z
has_accepted_license: '1'
intvolume: ' 112'
isi: 1
issue: '2'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 230-246.e11
pmid: 1
project:
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F7805
name: Stem Cell Modulation in Neural Development and Regeneration/ P05-Molecular
Mechanisms of Neural Stem Cell Lineage Progression
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/the-pedigree-of-brain-cells/
scopus_import: '1'
status: public
title: Multipotent progenitors instruct ontogeny of the superior colliculus
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 112
year: '2024'
...
---
OA_place: publisher
OA_type: hybrid
_id: '14257'
abstract:
- lang: eng
text: Mapping the complex and dense arrangement of cells and their connectivity
in brain tissue demands nanoscale spatial resolution imaging. Super-resolution
optical microscopy excels at visualizing specific molecules and individual cells
but fails to provide tissue context. Here we developed Comprehensive Analysis
of Tissues across Scales (CATS), a technology to densely map brain tissue architecture
from millimeter regional to nanometer synaptic scales in diverse chemically fixed
brain preparations, including rodent and human. CATS uses fixation-compatible
extracellular labeling and optical imaging, including stimulated emission depletion
or expansion microscopy, to comprehensively delineate cellular structures. It
enables three-dimensional reconstruction of single synapses and mapping of synaptic
connectivity by identification and analysis of putative synaptic cleft regions.
Applying CATS to the mouse hippocampal mossy fiber circuitry, we reconstructed
and quantified the synaptic input and output structure of identified neurons.
We furthermore demonstrate applicability to clinically derived human tissue samples,
including formalin-fixed paraffin-embedded routine diagnostic specimens, for visualizing
the cellular architecture of brain tissue in health and disease.
acknowledged_ssus:
- _id: ScienComp
- _id: Bio
- _id: PreCl
- _id: LifeSc
- _id: M-Shop
- _id: E-Lib
acknowledgement: 'We thank J. Vorlaufer, N. Agudelo-Dueñas, W. Jahr and A. Wartak
for microscope maintenance and troubleshooting; C. Kreuzinger, A. Freeman and I.
Erber for technical assistance; and M. Tomschik for support with obtaining human
samples. We gratefully acknowledge E. Miguel for setting up webKnossos and M. Šuplata
for computational support and hardware control. We are grateful to R. Shigemoto
and B. Bickel for generous support and M. Sixt and S. Boyd (Stanford University)
for discussions and critical reading of the paper. PSD95-HaloTag mice were kindly
provided by S. Grant (University of Edinburgh). We acknowledge expert support by
Institute of Science and Technology Austria’s scientific computing, imaging and
optics, preclinical and lab support facilities and by the Miba machine shop and
library. We gratefully acknowledge funding by the following sources: Austrian Science
Fund (FWF) grant I3600-B27 (J.G.D.); Austrian Science Fund (FWF) grant DK W1232
(J.G.D. and J.M.M.); Austrian Science Fund (FWF) grant Z 312-B27, Wittgenstein award
(P.J.); Austrian Science Fund (FWF) projects I4685-B, I6565-B (SYNABS) and DOC 33-B27
(R.H.); Gesellschaft für Forschungsförderung NÖ (NFB) grant LSC18-022 (J.G.D.);
European Union’s Horizon 2020 research and innovation programme, European Research
Council (ERC) grant 715508 – REVERSEAUTISM (G.N.); European Union’s Horizon 2020
research and innovation programme, European Research Council (ERC) grant 692692
– GIANTSYN (P.J.); Marie Skłodowska-Curie Actions Fellowship GA no. 665385 under
the EU Horizon 2020 program (J.M.M. and J.L.); and Marie Skłodowska-Curie Actions
Individual Fellowship no. 101026635 under the EU Horizon 2020 program (J.F.W.).'
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Julia M
full_name: Michalska, Julia M
id: 443DB6DE-F248-11E8-B48F-1D18A9856A87
last_name: Michalska
orcid: 0000-0003-3862-1235
- first_name: Julia
full_name: Lyudchik, Julia
id: 46E28B80-F248-11E8-B48F-1D18A9856A87
last_name: Lyudchik
- first_name: Philipp
full_name: Velicky, Philipp
id: 39BDC62C-F248-11E8-B48F-1D18A9856A87
last_name: Velicky
orcid: 0000-0002-2340-7431
- first_name: Hana
full_name: Korinkova, Hana
id: ee3cb6ca-ec98-11ea-ae11-ff703e2254ed
last_name: Korinkova
- first_name: Jake
full_name: Watson, Jake
id: 63836096-4690-11EA-BD4E-32803DDC885E
last_name: Watson
orcid: 0000-0002-8698-3823
- first_name: Alban
full_name: Cenameri, Alban
id: 9ac8f577-2357-11eb-997a-e566c5550886
last_name: Cenameri
- first_name: Christoph M
full_name: Sommer, Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Alessandro
full_name: Venturino, Alessandro
id: 41CB84B2-F248-11E8-B48F-1D18A9856A87
last_name: Venturino
orcid: 0000-0003-2356-9403
- first_name: Karl
full_name: Roessler, Karl
last_name: Roessler
- first_name: Thomas
full_name: Czech, Thomas
last_name: Czech
- first_name: Romana
full_name: Höftberger, Romana
last_name: Höftberger
- first_name: Sandra
full_name: Siegert, Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Johann G
full_name: Danzl, Johann G
id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
last_name: Danzl
orcid: 0000-0001-8559-3973
citation:
ama: Michalska JM, Lyudchik J, Velicky P, et al. Imaging brain tissue architecture
across millimeter to nanometer scales. Nature Biotechnology. 2024;42:1051-1064.
doi:10.1038/s41587-023-01911-8
apa: Michalska, J. M., Lyudchik, J., Velicky, P., Korinkova, H., Watson, J., Cenameri,
A., … Danzl, J. G. (2024). Imaging brain tissue architecture across millimeter
to nanometer scales. Nature Biotechnology. Springer Nature. https://doi.org/10.1038/s41587-023-01911-8
chicago: Michalska, Julia M, Julia Lyudchik, Philipp Velicky, Hana Korinkova, Jake
Watson, Alban Cenameri, Christoph M Sommer, et al. “Imaging Brain Tissue Architecture
across Millimeter to Nanometer Scales.” Nature Biotechnology. Springer
Nature, 2024. https://doi.org/10.1038/s41587-023-01911-8.
ieee: J. M. Michalska et al., “Imaging brain tissue architecture across millimeter
to nanometer scales,” Nature Biotechnology, vol. 42. Springer Nature, pp.
1051–1064, 2024.
ista: Michalska JM, Lyudchik J, Velicky P, Korinkova H, Watson J, Cenameri A, Sommer
CM, Amberg N, Venturino A, Roessler K, Czech T, Höftberger R, Siegert S, Novarino
G, Jonas PM, Danzl JG. 2024. Imaging brain tissue architecture across millimeter
to nanometer scales. Nature Biotechnology. 42, 1051–1064.
mla: Michalska, Julia M., et al. “Imaging Brain Tissue Architecture across Millimeter
to Nanometer Scales.” Nature Biotechnology, vol. 42, Springer Nature, 2024,
pp. 1051–64, doi:10.1038/s41587-023-01911-8.
short: J.M. Michalska, J. Lyudchik, P. Velicky, H. Korinkova, J. Watson, A. Cenameri,
C.M. Sommer, N. Amberg, A. Venturino, K. Roessler, T. Czech, R. Höftberger, S.
Siegert, G. Novarino, P.M. Jonas, J.G. Danzl, Nature Biotechnology 42 (2024) 1051–1064.
corr_author: '1'
date_created: 2023-09-03T22:01:15Z
date_published: 2024-07-01T00:00:00Z
date_updated: 2026-04-14T08:34:35Z
day: '01'
ddc:
- '570'
department:
- _id: SaSi
- _id: GaNo
- _id: PeJo
- _id: JoDa
- _id: Bio
- _id: RySh
doi: 10.1038/s41587-023-01911-8
ec_funded: 1
external_id:
isi:
- '001065254200001'
pmid:
- '37653226'
file:
- access_level: open_access
checksum: 57d5fafb16f02dcb9f7dddb1bd7e2a71
content_type: application/pdf
creator: dernst
date_created: 2025-01-09T07:48:01Z
date_updated: 2025-01-09T07:48:01Z
file_id: '18784'
file_name: 2024_NatureBiotech_Michalska.pdf
file_size: 26065165
relation: main_file
success: 1
file_date_updated: 2025-01-09T07:48:01Z
has_accepted_license: '1'
intvolume: ' 42'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 1051-1064
pmid: 1
project:
- _id: 265CB4D0-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I03600
name: Optical control of synaptic function via adhesion molecules
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232
name: Molecular Drug Targets
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: Synaptic communication in neuronal microcircuits
- _id: 23889792-32DE-11EA-91FC-C7463DDC885E
grant_number: LS18-022
name: High content imaging to decode human immune cell interactions in health and
allergic disease
- _id: 25444568-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715508'
name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
and in vitro Models
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glutamatergic synapse
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
- _id: fc2be41b-9c52-11eb-aca3-faa90aa144e9
call_identifier: H2020
grant_number: '101026635'
name: Synaptic computations of the hippocampal CA3 circuitry
publication: Nature Biotechnology
publication_identifier:
eissn:
- 1546-1696
issn:
- 1087-0156
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: software
url: https://github.com/danzllab/CATS
record:
- id: '18660'
relation: dissertation_contains
status: deleted
- id: '13126'
relation: research_data
status: public
- id: '18674'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Imaging brain tissue architecture across millimeter to nanometer scales
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 42
year: '2024'
...
---
APC_amount: 6248,82 EUR
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '18603'
abstract:
- lang: eng
text: It is widely believed that information storage in neuronal circuits involves
nanoscopic structural changes at synapses, resulting in the formation of synaptic
engrams. However, direct evidence for this hypothesis is lacking. To test this
conjecture, we combined chemical potentiation, functional analysis by paired pre-postsynaptic
recordings, and structural analysis by electron microscopy (EM) and freeze-fracture
replica labeling (FRL) at the rodent hippocampal mossy fiber synapse, a key synapse
in the trisynaptic circuit of the hippocampus. Biophysical analysis of synaptic
transmission revealed that forskolin-induced chemical potentiation increased the
readily releasable vesicle pool size and vesicular release probability by 146%
and 49%, respectively. Structural analysis of mossy fiber synapses by EM and FRL
demonstrated an increase in the number of vesicles close to the plasma membrane
and the number of clusters of the priming protein Munc13-1, indicating an increase
in the number of both docked and primed vesicles. Furthermore, FRL analysis revealed
a significant reduction of the distance between Munc13-1 and CaV2.1 Ca2+ channels,
suggesting reconfiguration of the channel-vesicle coupling nanotopography. Our
results indicate that presynaptic plasticity is associated with structural reorganization
of active zones. We propose that changes in potential nanoscopic organization
at synaptic vesicle release sites may be correlates of learning and memory at
a plastic central synapse.
acknowledged_ssus:
- _id: EM-Fac
- _id: PreCl
acknowledgement: "We thank Carolina Borges-Merjane, Jing-Jing Chen, Katharina Lichter,
and Samuel Young for critically reading the manuscript; the Electron Microscopy
Facility of ISTA, in particular Vanessa Zheden, for extensive support, advice, and
experimental assistance; the Preclinical Facility of ISTA, in particular Victoria
Wimmer and Michael Schunn, for experimental assistance; Florian Marr and Christina
Altmutter for technical support; Alois Schlögl for help with analysis; and Eleftheria
Kralli-Beller for manuscript editing. We also thank Cordelia Imig for providing
Munc13-1cKO-Munc13-2/3(−/−) mutant mice. Part of the work has been published in
O.K.’s thesis in partial fulfillment of the requirements for the degree of Doctor
of Philosophy.\r\nThis project received funding from the European Research Council
and European Union’s Horizon 2020 research and innovation programme (ERC 692692
to P.J.; https://cordis.europa.eu/project/id/692692/de) and from the Fond zur Förderung
der Wissenschaftlichen Forschung (Z312-B27 Wittgenstein award to P.J., https://www.fwf.ac.at/en/funding/portfolio/projects/fwf-wittgenstein-award;
W1205-B09 and P36232-B to P.J., https://www.fwf.ac.at/en/funding; I6166-B to R.S.;
https://www.fwf.ac.at/en/funding). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the manuscript."
article_number: e3002879
article_processing_charge: Yes
article_type: original
author:
- first_name: Olena
full_name: Kim, Olena
id: 3F8ABDDA-F248-11E8-B48F-1D18A9856A87
last_name: Kim
orcid: 0000-0003-2344-1039
- first_name: Yuji
full_name: Okamoto, Yuji
id: 3337E116-F248-11E8-B48F-1D18A9856A87
last_name: Okamoto
orcid: 0000-0003-0408-6094
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Nils
full_name: Brose, Nils
last_name: Brose
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Kim O, Okamoto Y, Kaufmann W, Brose N, Shigemoto R, Jonas PM. Presynaptic cAMP-PKA-mediated
potentiation induces reconfiguration of synaptic vesicle pools and channel-vesicle
coupling at hippocampal mossy fiber boutons. PLoS Biology. 2024;22(11).
doi:10.1371/journal.pbio.3002879
apa: Kim, O., Okamoto, Y., Kaufmann, W., Brose, N., Shigemoto, R., & Jonas,
P. M. (2024). Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration
of synaptic vesicle pools and channel-vesicle coupling at hippocampal mossy fiber
boutons. PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.3002879
chicago: Kim, Olena, Yuji Okamoto, Walter Kaufmann, Nils Brose, Ryuichi Shigemoto,
and Peter M Jonas. “Presynaptic CAMP-PKA-Mediated Potentiation Induces Reconfiguration
of Synaptic Vesicle Pools and Channel-Vesicle Coupling at Hippocampal Mossy Fiber
Boutons.” PLoS Biology. Public Library of Science, 2024. https://doi.org/10.1371/journal.pbio.3002879.
ieee: O. Kim, Y. Okamoto, W. Kaufmann, N. Brose, R. Shigemoto, and P. M. Jonas,
“Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration of synaptic
vesicle pools and channel-vesicle coupling at hippocampal mossy fiber boutons,”
PLoS Biology, vol. 22, no. 11. Public Library of Science, 2024.
ista: Kim O, Okamoto Y, Kaufmann W, Brose N, Shigemoto R, Jonas PM. 2024. Presynaptic
cAMP-PKA-mediated potentiation induces reconfiguration of synaptic vesicle pools
and channel-vesicle coupling at hippocampal mossy fiber boutons. PLoS Biology.
22(11), e3002879.
mla: Kim, Olena, et al. “Presynaptic CAMP-PKA-Mediated Potentiation Induces Reconfiguration
of Synaptic Vesicle Pools and Channel-Vesicle Coupling at Hippocampal Mossy Fiber
Boutons.” PLoS Biology, vol. 22, no. 11, e3002879, Public Library of Science,
2024, doi:10.1371/journal.pbio.3002879.
short: O. Kim, Y. Okamoto, W. Kaufmann, N. Brose, R. Shigemoto, P.M. Jonas, PLoS
Biology 22 (2024).
corr_author: '1'
date_created: 2024-12-01T23:01:54Z
date_published: 2024-11-18T00:00:00Z
date_updated: 2026-04-16T12:20:34Z
day: '18'
ddc:
- '570'
department:
- _id: PeJo
- _id: EM-Fac
- _id: RySh
doi: 10.1371/journal.pbio.3002879
ec_funded: 1
external_id:
isi:
- '001358568700003'
pmid:
- '39556620'
file:
- access_level: open_access
checksum: 7de2dcb50deb65dde05c80082bb85a82
content_type: application/pdf
creator: dernst
date_created: 2024-12-03T08:56:53Z
date_updated: 2024-12-03T08:56:53Z
file_id: '18608'
file_name: 2024_PloSBio_Kim.pdf
file_size: 3057631
relation: main_file
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file_date_updated: 2024-12-03T08:56:53Z
has_accepted_license: '1'
intvolume: ' 22'
isi: 1
issue: '11'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glutamatergic synapse
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: Synaptic communication in neuronal microcircuits
- _id: bd88be38-d553-11ed-ba76-81d5a70a6ef5
grant_number: P36232
name: Mechanisms of GABA release in hippocampal circuits
- _id: b1b85715-d554-11ed-a5ad-84a07fc9f18e
grant_number: I06166
name: Structural & functional basis of presynaptic plasticity
- _id: 25C3DBB6-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W01205
name: Zellkommunikation in Gesundheit und Krankheit
- _id: 3AC91DDA-15DF-11EA-824D-93A3E7B544D1
call_identifier: FWF
name: FWF Open Access Fund
publication: PLoS Biology
publication_identifier:
eissn:
- 1545-7885
issn:
- 1544-9173
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
related_material:
record:
- id: '18296'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration of synaptic
vesicle pools and channel-vesicle coupling at hippocampal mossy fiber boutons
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 22
year: '2024'
...
---
_id: '18296'
abstract:
- lang: eng
text: It is widely believed that information storage in neuronal circuits involves
nanoscopic structural changes at synapses, resulting in the formation of synaptic
engrams. However, direct evidence for this hypothesis is lacking. To test this
conjecture, we combined chemical potentiation, functional analysis by paired pre-postsynaptic
recordings, and structural analysis by electron microscopy (EM) and freeze-fracture
replica labeling (FRL) at the murine hippocampal mossy fiber synapse, a key synapse
in the trisynaptic circuit of the hippocampus. Biophysical analysis of synaptic
transmission revealed that forskolin-induced chemical potentiation increased the
readily releasable vesicle pool size and vesicular release probability by 146%
and 49%, respectively. Structural analysis of mossy fiber synapses by EM and FRL
demonstrated an increase in the number of vesicles close to the plasma membrane
and the number of clusters of the priming protein Munc13-1, indicating an increase
in the number of both docked and primed vesicles. Furthermore, FRL analysis revealed
a significant reduction of the distance between Munc13-1 and CaV2.1 Ca2+ channels,
suggesting reconfiguration of the channel-vesicle coupling nanotopography. Our
results indicate that presynaptic plasticity is associated with structural reorganization
of active zones. We propose that changes in potential nanoscopic organization
at synaptic vesicle release sites may be correlates of learning and memory at
a plastic central synapse.
article_processing_charge: No
author:
- first_name: Olena
full_name: Kim, Olena
id: 3F8ABDDA-F248-11E8-B48F-1D18A9856A87
last_name: Kim
orcid: 0000-0003-2344-1039
citation:
ama: Kim O. Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration of
synaptic vesicle pools and channel-vesicle coupling at hippocampal mossy fiber
boutons. 2024. doi:10.15479/AT:ISTA:18296
apa: Kim, O. (2024). Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration
of synaptic vesicle pools and channel-vesicle coupling at hippocampal mossy fiber
boutons. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:18296
chicago: Kim, Olena. “Presynaptic CAMP-PKA-Mediated Potentiation Induces Reconfiguration
of Synaptic Vesicle Pools and Channel-Vesicle Coupling at Hippocampal Mossy Fiber
Boutons.” Institute of Science and Technology Austria, 2024. https://doi.org/10.15479/AT:ISTA:18296.
ieee: O. Kim, “Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration
of synaptic vesicle pools and channel-vesicle coupling at hippocampal mossy fiber
boutons.” Institute of Science and Technology Austria, 2024.
ista: Kim O. 2024. Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration
of synaptic vesicle pools and channel-vesicle coupling at hippocampal mossy fiber
boutons, Institute of Science and Technology Austria, 10.15479/AT:ISTA:18296.
mla: Kim, Olena. Presynaptic CAMP-PKA-Mediated Potentiation Induces Reconfiguration
of Synaptic Vesicle Pools and Channel-Vesicle Coupling at Hippocampal Mossy Fiber
Boutons. Institute of Science and Technology Austria, 2024, doi:10.15479/AT:ISTA:18296.
short: O. Kim, (2024).
contributor:
- contributor_type: researcher
first_name: Olena
id: 3F8ABDDA-F248-11E8-B48F-1D18A9856A87
last_name: Kim
- contributor_type: researcher
first_name: Yuji
id: 3337E116-F248-11E8-B48F-1D18A9856A87
last_name: Okamoto
orcid: 0000-0003-0408-6094
- contributor_type: researcher
first_name: Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- contributor_type: researcher
first_name: 'Nils '
last_name: Brose
- contributor_type: researcher
first_name: Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- contributor_type: supervisor
first_name: Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
corr_author: '1'
date_created: 2024-10-11T10:12:17Z
date_published: 2024-10-11T00:00:00Z
date_updated: 2026-04-16T12:20:33Z
day: '11'
ddc:
- '570'
department:
- _id: PeJo
- _id: RySh
- _id: EM-Fac
doi: 10.15479/AT:ISTA:18296
ec_funded: 1
file:
- access_level: open_access
checksum: 0a977e7df54c418251b10dfd3f8a015c
content_type: application/zip
creator: okim
date_created: 2024-10-11T10:04:19Z
date_updated: 2024-10-11T10:04:19Z
file_id: '18297'
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file_size: 164382
relation: main_file
success: 1
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checksum: 5b9343d6b2035ac3185e390fad4d3830
content_type: text/plain
creator: okim
date_created: 2024-10-11T10:04:23Z
date_updated: 2024-10-11T10:04:23Z
file_id: '18298'
file_name: info.txt
file_size: 654
relation: main_file
success: 1
file_date_updated: 2024-10-11T10:04:23Z
has_accepted_license: '1'
keyword:
- Hippocampal mossy fiber synapses
- short-term potentiation
- long-term potentiation
- presynaptic plasticity
- electron microscopy
- freeze-fracture replica labeling
- paired recordings
- forskolin
- cyclic adenosine monophosphate (cAMP)
- protein kinase A (PKA)
- neuromodulation
- synaptic vesicle pools
- presynaptic Ca2+ channels
- Munc13
- docking
- priming
- active zone
month: '10'
oa: 1
oa_version: Submitted Version
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glutamatergic synapse
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '18603'
relation: used_in_publication
status: public
status: public
title: Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration of synaptic
vesicle pools and channel-vesicle coupling at hippocampal mossy fiber boutons
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: research_data
user_id: 68b8ca59-c5b3-11ee-8790-cd641c68093d
year: '2024'
...
---
APC_amount: 5887,8 EUR
OA_place: publisher
OA_type: hybrid
_id: '15084'
abstract:
- lang: eng
text: "GABAB receptor (GBR) activation inhibits neurotransmitter release in axon
terminals in the brain, except in medial habenula (MHb) terminals, which show
robust potentiation. However, mechanisms underlying this enigmatic potentiation
remain elusive. Here, we report that GBR activation on MHb terminals induces an
activity-dependent transition from a facilitating, tonic to a depressing, phasic
neurotransmitter release mode. This transition is accompanied by a 4.1-fold increase
in readily releasable vesicle pool (RRP) size and a 3.5-fold increase of docked
synaptic vesicles (SVs) at the presynaptic active zone (AZ). Strikingly, the depressing
phasic release exhibits looser coupling distance than the tonic release. Furthermore,
the tonic and phasic release are selectively affected by deletion of synaptoporin
(SPO) and Ca\r\n 2+\r\n -dependent
activator protein for secretion 2 (CAPS2), respectively. SPO modulates augmentation,
the short-term plasticity associated with tonic release, and CAPS2 retains the
increased RRP for initial responses in phasic response trains. The cytosolic protein
CAPS2 showed a SV-associated distribution similar to the vesicular transmembrane
protein SPO, and they were colocalized in the same terminals. We developed the
“Flash and Freeze-fracture” method, and revealed the release of SPO-associated
vesicles in both tonic and phasic modes and activity-dependent recruitment of
CAPS2 to the AZ during phasic release, which lasted several minutes. Overall,
these results indicate that GBR activation translocates CAPS2 to the AZ along
with the fusion of CAPS2-associated SVs, contributing to persistency of the RRP
increase. Thus, we identified structural and molecular mechanisms underlying tonic
and phasic neurotransmitter release and their transition by GBR activation in
MHb terminals."
acknowledged_ssus:
- _id: M-Shop
- _id: PreCl
- _id: EM-Fac
acknowledgement: We thank Erwin Neher and Ipe Ninan for critical comments on the manuscript.
This project has received funding from the European Research Council (ERC) and European
Commission, under the European Union’s Horizon 2020 research and innovation program
(ERC grant agreement no. 694539 to R.S. and the Marie Skłodowska-Curie grant agreement
no. 665385 to C.Ö.). This study was supported by the Cooperative Study Program of
Center for Animal Resources and Collaborative Study of NINS. We thank Kohgaku Eguchi
for statistical analysis, Yu Kasugai for additional EM imaging, Robert Beattie for
the design of the slice recovery chamber for Flash and Freeze experiments, Todor
Asenov from the ISTA machine shop for custom part preparations for high-pressure
freezing, the ISTA preclinical facility for animal caretaking, and the ISTA EM facilities
for technical support.
article_number: e2301449121
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: Pradeep
full_name: Bhandari, Pradeep
id: 45EDD1BC-F248-11E8-B48F-1D18A9856A87
last_name: Bhandari
orcid: 0000-0003-0863-4481
- first_name: Hüseyin C
full_name: Önal, Hüseyin C
id: 4659D740-F248-11E8-B48F-1D18A9856A87
last_name: Önal
orcid: 0000-0002-2771-2011
- first_name: Carolina
full_name: Borges Merjane, Carolina
id: 4305C450-F248-11E8-B48F-1D18A9856A87
last_name: Borges Merjane
orcid: 0000-0003-0005-401X
- first_name: Elodie
full_name: Le Monnier, Elodie
id: 3B59276A-F248-11E8-B48F-1D18A9856A87
last_name: Le Monnier
- first_name: Utsa
full_name: Roy, Utsa
id: 4d26cf11-5355-11ee-ae5a-eb05e255b9b2
last_name: Roy
- first_name: Yukihiro
full_name: Nakamura, Yukihiro
last_name: Nakamura
- first_name: Tetsushi
full_name: Sadakata, Tetsushi
last_name: Sadakata
- first_name: Makoto
full_name: Sanbo, Makoto
last_name: Sanbo
- first_name: Masumi
full_name: Hirabayashi, Masumi
last_name: Hirabayashi
- first_name: JeongSeop
full_name: Rhee, JeongSeop
last_name: Rhee
- first_name: Nils
full_name: Brose, Nils
last_name: Brose
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Koppensteiner P, Bhandari P, Önal C, et al. GABAB receptors induce phasic release
from medial habenula terminals through activity-dependent recruitment of release-ready
vesicles. Proceedings of the National Academy of Sciences of the United States
of America. 2024;121(8). doi:10.1073/pnas.2301449121
apa: Koppensteiner, P., Bhandari, P., Önal, C., Borges Merjane, C., Le Monnier,
E., Roy, U., … Shigemoto, R. (2024). GABAB receptors induce phasic release from
medial habenula terminals through activity-dependent recruitment of release-ready
vesicles. Proceedings of the National Academy of Sciences of the United States
of America. National Academy of Sciences. https://doi.org/10.1073/pnas.2301449121
chicago: Koppensteiner, Peter, Pradeep Bhandari, Cihan Önal, Carolina Borges Merjane,
Elodie Le Monnier, Utsa Roy, Yukihiro Nakamura, et al. “GABAB Receptors Induce
Phasic Release from Medial Habenula Terminals through Activity-Dependent Recruitment
of Release-Ready Vesicles.” Proceedings of the National Academy of Sciences
of the United States of America. National Academy of Sciences, 2024. https://doi.org/10.1073/pnas.2301449121.
ieee: P. Koppensteiner et al., “GABAB receptors induce phasic release from
medial habenula terminals through activity-dependent recruitment of release-ready
vesicles,” Proceedings of the National Academy of Sciences of the United States
of America, vol. 121, no. 8. National Academy of Sciences, 2024.
ista: Koppensteiner P, Bhandari P, Önal C, Borges Merjane C, Le Monnier E, Roy U,
Nakamura Y, Sadakata T, Sanbo M, Hirabayashi M, Rhee J, Brose N, Jonas PM, Shigemoto
R. 2024. GABAB receptors induce phasic release from medial habenula terminals
through activity-dependent recruitment of release-ready vesicles. Proceedings
of the National Academy of Sciences of the United States of America. 121(8), e2301449121.
mla: Koppensteiner, Peter, et al. “GABAB Receptors Induce Phasic Release from Medial
Habenula Terminals through Activity-Dependent Recruitment of Release-Ready Vesicles.”
Proceedings of the National Academy of Sciences of the United States of America,
vol. 121, no. 8, e2301449121, National Academy of Sciences, 2024, doi:10.1073/pnas.2301449121.
short: P. Koppensteiner, P. Bhandari, C. Önal, C. Borges Merjane, E. Le Monnier,
U. Roy, Y. Nakamura, T. Sadakata, M. Sanbo, M. Hirabayashi, J. Rhee, N. Brose,
P.M. Jonas, R. Shigemoto, Proceedings of the National Academy of Sciences of the
United States of America 121 (2024).
corr_author: '1'
date_created: 2024-03-05T09:23:55Z
date_published: 2024-02-20T00:00:00Z
date_updated: 2026-04-27T22:30:21Z
day: '20'
ddc:
- '570'
department:
- _id: RySh
- _id: PeJo
doi: 10.1073/pnas.2301449121
ec_funded: 1
external_id:
isi:
- '001208567300006'
pmid:
- '38346189'
file:
- access_level: open_access
checksum: b25b2a057c266ff317a48b0d54d6fc8a
content_type: application/pdf
creator: dernst
date_created: 2024-03-12T13:42:42Z
date_updated: 2024-03-12T13:42:42Z
file_id: '15110'
file_name: 2024_PNAS_Koppensteiner.pdf
file_size: 13648221
relation: main_file
success: 1
file_date_updated: 2024-03-12T13:42:42Z
has_accepted_license: '1'
intvolume: ' 121'
isi: 1
issue: '8'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25CA28EA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '694539'
name: 'In situ analysis of single channel subunit composition in neurons: physiological
implication in synaptic plasticity and behaviour'
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '665385'
name: International IST Doctoral Program
publication: Proceedings of the National Academy of Sciences of the United States
of America
publication_identifier:
eissn:
- 1091-6490
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
link:
- description: News on ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/neuronal-insights-flash-and-freeze-fracture/
record:
- id: '13173'
relation: research_data
status: public
- id: '19271'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: GABAB receptors induce phasic release from medial habenula terminals through
activity-dependent recruitment of release-ready vesicles
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 121
year: '2024'
...
---
OA_place: publisher
OA_type: hybrid
PlanS_conform: '1'
_id: '14843'
abstract:
- lang: eng
text: The coupling between Ca2+ channels and release sensors is a key factor defining
the signaling properties of a synapse. However, the coupling nanotopography at
many synapses remains unknown, and it is unclear how it changes during development.
To address these questions, we examined coupling at the cerebellar inhibitory
basket cell (BC)-Purkinje cell (PC) synapse. Biophysical analysis of transmission
by paired recording and intracellular pipette perfusion revealed that the effects
of exogenous Ca2+ chelators decreased during development, despite constant reliance
of release on P/Q-type Ca2+ channels. Structural analysis by freeze-fracture replica
labeling (FRL) and transmission electron microscopy (EM) indicated that presynaptic
P/Q-type Ca2+ channels formed nanoclusters throughout development, whereas docked
vesicles were only clustered at later developmental stages. Modeling suggested
a developmental transformation from a more random to a more clustered coupling
nanotopography. Thus, presynaptic signaling developmentally approaches a point-to-point
configuration, optimizing speed, reliability, and energy efficiency of synaptic
transmission.
acknowledged_ssus:
- _id: EM-Fac
- _id: PreCl
- _id: M-Shop
acknowledgement: We thank Drs. David DiGregorio and Erwin Neher for critically reading
an earlier version of the manuscript, Ralf Schneggenburger for helpful discussions,
Benjamin Suter and Katharina Lichter for support with image analysis, Chris Wojtan
for advice on numerical solution of partial differential equations, Maria Reva for
help with Ripley analysis, Alois Schlögl for programming, and Akari Hagiwara and
Toshihisa Ohtsuka for anti-ELKS antibody. We are grateful to Florian Marr, Christina
Altmutter, and Vanessa Zheden for excellent technical assistance and to Eleftheria
Kralli-Beller for manuscript editing. This research was supported by the Scientific
Services Units (SSUs) of ISTA (Electron Microscopy Facility, Preclinical Facility,
and Machine Shop). The project received funding from the European Research Council
(ERC) under the European Union’s Horizon 2020 research and innovation program (grant
agreement no. 692692), the Fonds zur Förderung der Wissenschaftlichen Forschung
(Z 312-B27, Wittgenstein award; P 36232-B), all to P.J., and a DOC fellowship of
the Austrian Academy of Sciences to J.-J.C.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: JingJing
full_name: Chen, JingJing
id: 2C4E65C8-F248-11E8-B48F-1D18A9856A87
last_name: Chen
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Chong
full_name: Chen, Chong
id: 3DFD581A-F248-11E8-B48F-1D18A9856A87
last_name: Chen
- first_name: Itaru
full_name: Arai, Itaru
id: 32A73F6C-F248-11E8-B48F-1D18A9856A87
last_name: Arai
- first_name: Olena
full_name: Kim, Olena
id: 3F8ABDDA-F248-11E8-B48F-1D18A9856A87
last_name: Kim
orcid: 0000-0003-2344-1039
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Peter M
full_name: Jonas, Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
citation:
ama: Chen J, Kaufmann W, Chen C, et al. Developmental transformation of Ca2+ channel-vesicle
nanotopography at a central GABAergic synapse. Neuron. 2024;112(5):755-771.e9.
doi:10.1016/j.neuron.2023.12.002
apa: Chen, J., Kaufmann, W., Chen, C., Arai, itaru, Kim, O., Shigemoto, R., &
Jonas, P. M. (2024). Developmental transformation of Ca2+ channel-vesicle nanotopography
at a central GABAergic synapse. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.12.002
chicago: Chen, JingJing, Walter Kaufmann, Chong Chen, itaru Arai, Olena Kim, Ryuichi
Shigemoto, and Peter M Jonas. “Developmental Transformation of Ca2+ Channel-Vesicle
Nanotopography at a Central GABAergic Synapse.” Neuron. Elsevier, 2024.
https://doi.org/10.1016/j.neuron.2023.12.002.
ieee: J. Chen et al., “Developmental transformation of Ca2+ channel-vesicle
nanotopography at a central GABAergic synapse,” Neuron, vol. 112, no. 5.
Elsevier, p. 755–771.e9, 2024.
ista: Chen J, Kaufmann W, Chen C, Arai itaru, Kim O, Shigemoto R, Jonas PM. 2024.
Developmental transformation of Ca2+ channel-vesicle nanotopography at a central
GABAergic synapse. Neuron. 112(5), 755–771.e9.
mla: Chen, JingJing, et al. “Developmental Transformation of Ca2+ Channel-Vesicle
Nanotopography at a Central GABAergic Synapse.” Neuron, vol. 112, no. 5,
Elsevier, 2024, p. 755–771.e9, doi:10.1016/j.neuron.2023.12.002.
short: J. Chen, W. Kaufmann, C. Chen, itaru Arai, O. Kim, R. Shigemoto, P.M. Jonas,
Neuron 112 (2024) 755–771.e9.
corr_author: '1'
date_created: 2024-01-21T23:00:56Z
date_published: 2024-03-06T00:00:00Z
date_updated: 2026-04-27T22:30:23Z
day: '06'
ddc:
- '570'
department:
- _id: PeJo
- _id: EM-Fac
- _id: RySh
doi: 10.1016/j.neuron.2023.12.002
ec_funded: 1
external_id:
isi:
- '001202925700001'
pmid:
- '38215739'
file:
- access_level: open_access
checksum: 30098b4f0209556ddfb3540a23d07ca5
content_type: application/pdf
creator: dernst
date_created: 2025-04-23T14:02:08Z
date_updated: 2025-04-23T14:02:08Z
file_id: '19614'
file_name: 2024_Neuron_Chen.pdf
file_size: 8192355
relation: main_file
success: 1
file_date_updated: 2025-04-23T14:02:08Z
has_accepted_license: '1'
intvolume: ' 112'
isi: 1
issue: '5'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 755-771.e9
pmid: 1
project:
- _id: 25B7EB9E-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '692692'
name: Biophysics and circuit function of a giant cortical glutamatergic synapse
- _id: 25C5A090-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: Z00312
name: Synaptic communication in neuronal microcircuits
- _id: bd88be38-d553-11ed-ba76-81d5a70a6ef5
grant_number: P36232
name: Mechanisms of GABA release in hippocampal circuits
- _id: 26B66A3E-B435-11E9-9278-68D0E5697425
grant_number: '25383'
name: Development of nanodomain coupling between Ca2+ channels and release sensors
at a central inhibitory synapse
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/synapses-brought-to-the-point/
record:
- id: '15101'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Developmental transformation of Ca2+ channel-vesicle nanotopography at a central
GABAergic synapse
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 112
year: '2024'
...
---
_id: '14253'
abstract:
- lang: eng
text: Junctions between the endoplasmic reticulum (ER) and the plasma membrane (PM)
are specialized membrane contacts ubiquitous in eukaryotic cells. Concentration
of intracellular signaling machinery near ER-PM junctions allows these domains
to serve critical roles in lipid and Ca2+ signaling and homeostasis. Subcellular
compartmentalization of protein kinase A (PKA) signaling also regulates essential
cellular functions, however, no specific association between PKA and ER-PM junctional
domains is known. Here, we show that in brain neurons type I PKA is directed to
Kv2.1 channel-dependent ER-PM junctional domains via SPHKAP, a type I PKA-specific
anchoring protein. SPHKAP association with type I PKA regulatory subunit RI and
ER-resident VAP proteins results in the concentration of type I PKA between stacked
ER cisternae associated with ER-PM junctions. This ER-associated PKA signalosome
enables reciprocal regulation between PKA and Ca2+ signaling machinery to support
Ca2+ influx and excitation-transcription coupling. These data reveal that neuronal
ER-PM junctions support a receptor-independent form of PKA signaling driven by
membrane depolarization and intracellular Ca2+, allowing conversion of information
encoded in electrical signals into biochemical changes universally recognized
throughout the cell.
acknowledgement: We thank Kayla Templeton and Peter Turcanu for technical assistance,
Michelle Salemi for assistance with LC-MS data acquisition and analysis, Dr. Belvin
Gong for advice on monoclonal antibody generation, Drs. Maria Casas Prat and Eamonn
Dickson for assistance with super-resolution TIRF microscopy, Dr. Oscar Cerda for
assistance with the design of TAT-FFAT peptides, Dr. Fernando Santana for helpful
discussions, and Dr. Jodi Nunnari for a careful reading of our manuscript. We also
thank Dr. Alan Howe, Dr. Sohum Mehta, and Dr. Jin Zhang for providing plasmids used
in this study. This project was funded by NIH Grants R01NS114210 and R21NS101648
(J.S.T.), and F32NS108519 (N.C.V.).
article_number: '5231'
article_processing_charge: Yes
article_type: original
author:
- first_name: Nicholas C.
full_name: Vierra, Nicholas C.
last_name: Vierra
- first_name: Luisa
full_name: Ribeiro-Silva, Luisa
last_name: Ribeiro-Silva
- first_name: Michael
full_name: Kirmiz, Michael
last_name: Kirmiz
- first_name: Deborah
full_name: Van Der List, Deborah
last_name: Van Der List
- first_name: Pradeep
full_name: Bhandari, Pradeep
id: 45EDD1BC-F248-11E8-B48F-1D18A9856A87
last_name: Bhandari
orcid: 0000-0003-0863-4481
- first_name: Olivia A.
full_name: Mack, Olivia A.
last_name: Mack
- first_name: James
full_name: Carroll, James
last_name: Carroll
- first_name: Elodie
full_name: Le Monnier, Elodie
id: 3B59276A-F248-11E8-B48F-1D18A9856A87
last_name: Le Monnier
- first_name: Sue A.
full_name: Aicher, Sue A.
last_name: Aicher
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: James S.
full_name: Trimmer, James S.
last_name: Trimmer
citation:
ama: Vierra NC, Ribeiro-Silva L, Kirmiz M, et al. Neuronal ER-plasma membrane junctions
couple excitation to Ca2+-activated PKA signaling. Nature Communications.
2023;14. doi:10.1038/s41467-023-40930-6
apa: Vierra, N. C., Ribeiro-Silva, L., Kirmiz, M., Van Der List, D., Bhandari, P.,
Mack, O. A., … Trimmer, J. S. (2023). Neuronal ER-plasma membrane junctions couple
excitation to Ca2+-activated PKA signaling. Nature Communications. Springer
Nature. https://doi.org/10.1038/s41467-023-40930-6
chicago: Vierra, Nicholas C., Luisa Ribeiro-Silva, Michael Kirmiz, Deborah Van Der
List, Pradeep Bhandari, Olivia A. Mack, James Carroll, et al. “Neuronal ER-Plasma
Membrane Junctions Couple Excitation to Ca2+-Activated PKA Signaling.” Nature
Communications. Springer Nature, 2023. https://doi.org/10.1038/s41467-023-40930-6.
ieee: N. C. Vierra et al., “Neuronal ER-plasma membrane junctions couple
excitation to Ca2+-activated PKA signaling,” Nature Communications, vol.
14. Springer Nature, 2023.
ista: Vierra NC, Ribeiro-Silva L, Kirmiz M, Van Der List D, Bhandari P, Mack OA,
Carroll J, Le Monnier E, Aicher SA, Shigemoto R, Trimmer JS. 2023. Neuronal ER-plasma
membrane junctions couple excitation to Ca2+-activated PKA signaling. Nature Communications.
14, 5231.
mla: Vierra, Nicholas C., et al. “Neuronal ER-Plasma Membrane Junctions Couple Excitation
to Ca2+-Activated PKA Signaling.” Nature Communications, vol. 14, 5231,
Springer Nature, 2023, doi:10.1038/s41467-023-40930-6.
short: N.C. Vierra, L. Ribeiro-Silva, M. Kirmiz, D. Van Der List, P. Bhandari, O.A.
Mack, J. Carroll, E. Le Monnier, S.A. Aicher, R. Shigemoto, J.S. Trimmer, Nature
Communications 14 (2023).
date_created: 2023-09-03T22:01:14Z
date_published: 2023-08-26T00:00:00Z
date_updated: 2025-09-09T12:50:49Z
day: '26'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1038/s41467-023-40930-6
external_id:
isi:
- '001064563400013'
pmid:
- '37633939'
file:
- access_level: open_access
checksum: 6ab8aab4e957f626a09a1c73db3388fb
content_type: application/pdf
creator: dernst
date_created: 2023-09-06T06:50:07Z
date_updated: 2023-09-06T06:50:07Z
file_id: '14270'
file_name: 2023_NatureComm_Vierra.pdf
file_size: 9412549
relation: main_file
success: 1
file_date_updated: 2023-09-06T06:50:07Z
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
eissn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neuronal ER-plasma membrane junctions couple excitation to Ca2+-activated PKA
signaling
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 14
year: '2023'
...
---
_id: '13173'
abstract:
- lang: eng
text: GABAB receptor (GBR) activation inhibits neurotransmitter release in axon
terminals in the brain, except in medial habenula (MHb) terminals, which show
robust potentiation. However, mechanisms underlying this enigmatic potentiation
remain elusive. Here, we report that GBR activation on MHb terminals induces an
activity-dependent transition from a facilitating, tonic to a depressing, phasic
neurotransmitter release mode. This transition is accompanied by a 4.1-fold increase
in readily releasable vesicle pool (RRP) size and a 3.5-fold increase of docked
synaptic vesicles at the presynaptic active zone (AZ). Strikingly, tonic and phasic
release exhibit distinct coupling distances and are selectively affected by deletion
of synaptoporin (SPO) and Ca2+-dependent activator protein for secretion 2 (CAPS2),
respectively. SPO modulates augmentation, the short-term plasticity associated
with tonic release, and CAPS2 retains the increased RRP for initial responses
in phasic response trains. Double pre-embedding immunolabeling confirmed the co-localization
of CAPS2 and SPO inside the same terminal. The cytosolic protein CAPS2 showed
a synaptic vesicle (SV)-associated distribution similar to the vesicular transmembrane
protein SPO. A newly developed “Flash and Freeze-fracture” method revealed the
release of SPO-associated vesicles in both tonic and phasic modes and activity-dependent
recruitment of CAPS2 to the AZ during phasic release, which lasted several minutes.
Overall, these results indicate that GBR activation translocates CAPS2 to the
AZ along with the fusion of CAPS2-associated SVs, contributing to a persistent
RRP increase. Thus, we discovered structural and molecular mechanisms underlying
tonic and phasic neurotransmitter release and their transition by GBR activation
in MHb terminals.
article_processing_charge: No
author:
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Shigemoto R. Transition from tonic to phasic neurotransmitter release by presynaptic
GABAB receptor activation in medial habenula terminals. 2023. doi:10.15479/AT:ISTA:13173
apa: Shigemoto, R. (2023). Transition from tonic to phasic neurotransmitter release
by presynaptic GABAB receptor activation in medial habenula terminals. Institute
of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:13173
chicago: Shigemoto, Ryuichi. “Transition from Tonic to Phasic Neurotransmitter Release
by Presynaptic GABAB Receptor Activation in Medial Habenula Terminals.” Institute
of Science and Technology Austria, 2023. https://doi.org/10.15479/AT:ISTA:13173.
ieee: R. Shigemoto, “Transition from tonic to phasic neurotransmitter release by
presynaptic GABAB receptor activation in medial habenula terminals.” Institute
of Science and Technology Austria, 2023.
ista: Shigemoto R. 2023. Transition from tonic to phasic neurotransmitter release
by presynaptic GABAB receptor activation in medial habenula terminals, Institute
of Science and Technology Austria, 10.15479/AT:ISTA:13173.
mla: Shigemoto, Ryuichi. Transition from Tonic to Phasic Neurotransmitter Release
by Presynaptic GABAB Receptor Activation in Medial Habenula Terminals. Institute
of Science and Technology Austria, 2023, doi:10.15479/AT:ISTA:13173.
short: R. Shigemoto, (2023).
corr_author: '1'
date_created: 2023-06-29T13:16:42Z
date_published: 2023-07-29T00:00:00Z
date_updated: 2025-09-04T12:16:24Z
day: '29'
ddc:
- '571'
department:
- _id: RySh
doi: 10.15479/AT:ISTA:13173
file:
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content_type: application/x-zip-compressed
creator: shigemot
date_created: 2023-06-29T13:11:22Z
date_updated: 2023-11-17T14:30:44Z
description: After review an updated version of the data is provided
file_id: '13174'
file_name: Raw data for Koppensteiner et al.zip
file_size: 542873672
relation: main_file
title: Outdated Version
- access_level: open_access
checksum: c07860eb82b4d367245f1b589fe5c250
content_type: application/vnd.openxmlformats-officedocument.spreadsheetml.sheet
creator: patrickd
date_created: 2023-11-17T14:13:02Z
date_updated: 2023-11-17T14:13:02Z
file_id: '14550'
file_name: 11-17-23 Updated Koppensteiner et al. raw data.xlsx
file_size: 915079
relation: main_file
success: 1
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checksum: abf84b1699edac4349dc3a92d466fb7b
content_type: application/x-zip-compressed
creator: dernst
date_created: 2024-02-06T07:21:43Z
date_updated: 2024-02-06T07:21:43Z
file_id: '14942'
file_name: EM_Images.zip
file_size: 544868924
relation: main_file
success: 1
file_date_updated: 2024-02-06T07:21:43Z
has_accepted_license: '1'
keyword:
- medial habenula
- GABAB receptor
- vesicle release
- Flash and Freeze
- Flash and Freeze-fracture
month: '07'
oa: 1
oa_version: Published Version
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '15084'
relation: used_in_publication
status: public
status: public
title: Transition from tonic to phasic neurotransmitter release by presynaptic GABAB
receptor activation in medial habenula terminals
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: research_data
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '13202'
abstract:
- lang: eng
text: Phosphatidylinositol-4,5-bisphosphate (PI(4,5)P2) plays an essential role
in neuronal activities through interaction with various proteins involved in signaling
at membranes. However, the distribution pattern of PI(4,5)P2 and the association
with these proteins on the neuronal cell membranes remain elusive. In this study,
we established a method for visualizing PI(4,5)P2 by SDS-digested freeze-fracture
replica labeling (SDS-FRL) to investigate the quantitative nanoscale distribution
of PI(4,5)P2 in cryo-fixed brain. We demonstrate that PI(4,5)P2 forms tiny clusters
with a mean size of ∼1000 nm2 rather than randomly distributed in cerebellar neuronal
membranes in male C57BL/6J mice. These clusters show preferential accumulation
in specific membrane compartments of different cell types, in particular, in Purkinje
cell (PC) spines and granule cell (GC) presynaptic active zones. Furthermore,
we revealed extensive association of PI(4,5)P2 with CaV2.1 and GIRK3 across different
membrane compartments, whereas its association with mGluR1α was compartment specific.
These results suggest that our SDS-FRL method provides valuable insights into
the physiological functions of PI(4,5)P2 in neurons.
acknowledged_ssus:
- _id: EM-Fac
acknowledgement: This work was supported by The Institute of Science and Technology
(IST) Austria, the European Union's Horizon 2020 Research and Innovation Program
under the Marie Skłodowska-Curie Grant Agreement No. 793482 (to K.E.) and by the
European Research Council (ERC) Grant Agreement No. 694539 (to R.S.). We thank Nicoleta
Condruz (IST Austria, Klosterneuburg, Austria) for technical assistance with sample
preparation, the Electron Microscopy Facility of IST Austria (Klosterneuburg, Austria)
for technical support with EM works, Natalia Baranova (University of Vienna, Vienna,
Austria) and Martin Loose (IST Austria, Klosterneuburg, Austria) for advice on liposome
preparation, and Yugo Fukazawa (University of Fukui, Fukui, Japan) for comments.
article_processing_charge: No
article_type: original
author:
- first_name: Kohgaku
full_name: Eguchi, Kohgaku
id: 2B7846DC-F248-11E8-B48F-1D18A9856A87
last_name: Eguchi
orcid: 0000-0002-6170-2546
- first_name: Elodie
full_name: Le Monnier, Elodie
id: 3B59276A-F248-11E8-B48F-1D18A9856A87
last_name: Le Monnier
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Eguchi K, Le Monnier E, Shigemoto R. Nanoscale phosphoinositide distribution
on cell membranes of mouse cerebellar neurons. The Journal of Neuroscience.
2023;43(23):4197-4216. doi:10.1523/JNEUROSCI.1514-22.2023
apa: Eguchi, K., Le Monnier, E., & Shigemoto, R. (2023). Nanoscale phosphoinositide
distribution on cell membranes of mouse cerebellar neurons. The Journal of
Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1514-22.2023
chicago: Eguchi, Kohgaku, Elodie Le Monnier, and Ryuichi Shigemoto. “Nanoscale Phosphoinositide
Distribution on Cell Membranes of Mouse Cerebellar Neurons.” The Journal of
Neuroscience. Society for Neuroscience, 2023. https://doi.org/10.1523/JNEUROSCI.1514-22.2023.
ieee: K. Eguchi, E. Le Monnier, and R. Shigemoto, “Nanoscale phosphoinositide distribution
on cell membranes of mouse cerebellar neurons,” The Journal of Neuroscience,
vol. 43, no. 23. Society for Neuroscience, pp. 4197–4216, 2023.
ista: Eguchi K, Le Monnier E, Shigemoto R. 2023. Nanoscale phosphoinositide distribution
on cell membranes of mouse cerebellar neurons. The Journal of Neuroscience. 43(23),
4197–4216.
mla: Eguchi, Kohgaku, et al. “Nanoscale Phosphoinositide Distribution on Cell Membranes
of Mouse Cerebellar Neurons.” The Journal of Neuroscience, vol. 43, no.
23, Society for Neuroscience, 2023, pp. 4197–216, doi:10.1523/JNEUROSCI.1514-22.2023.
short: K. Eguchi, E. Le Monnier, R. Shigemoto, The Journal of Neuroscience 43 (2023)
4197–4216.
corr_author: '1'
date_created: 2023-07-09T22:01:12Z
date_published: 2023-06-07T00:00:00Z
date_updated: 2025-04-14T07:27:15Z
day: '07'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1523/JNEUROSCI.1514-22.2023
ec_funded: 1
external_id:
isi:
- '001020132100005'
pmid:
- '37160366'
file:
- access_level: open_access
checksum: 70b2141870e0bf1c94fd343e18fdbc32
content_type: application/pdf
creator: alisjak
date_created: 2023-07-10T09:04:58Z
date_updated: 2023-07-10T09:04:58Z
file_id: '13205'
file_name: 2023_JN_Eguchi.pdf
file_size: 7794425
relation: main_file
success: 1
file_date_updated: 2023-07-10T09:04:58Z
has_accepted_license: '1'
intvolume: ' 43'
isi: 1
issue: '23'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 4197-4216
pmid: 1
project:
- _id: 2659CC84-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '793482'
name: 'Ultrastructural analysis of phosphoinositides in nerve terminals: distribution,
dynamics and physiological roles in synaptic transmission'
- _id: 25CA28EA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '694539'
name: 'In situ analysis of single channel subunit composition in neurons: physiological
implication in synaptic plasticity and behaviour'
publication: The Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar
neurons
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 43
year: '2023'
...
---
_id: '13126'
abstract:
- lang: eng
text: Mapping the complex and dense arrangement of cells and their connectivity
in brain tissue demands nanoscale spatial resolution imaging. Super-resolution
optical microscopy excels at visualizing specific molecules and individual cells
but fails to provide tissue context. Here, we developed Comprehensive Analysis
of Tissues across Scales (CATS), a technology to densely map brain tissue architecture
from millimeter regional to nanometer synaptic scales in diverse chemically fixed
brain preparations, including rodent and human. CATS uses fixation-compatible
extracellular labeling and optical imaging, including stimulated emission depletion
or expansion microscopy, to comprehensively delineate cellular structures. It
enables three-dimensional reconstruction of single synapses and mapping of synaptic
connectivity by identification and analysis of putative synaptic cleft regions.
Applying CATS to the mouse hippocampal mossy fiber circuitry, we reconstructed
and quantified the synaptic input and output structure of identified neurons.
We furthermore demonstrate applicability to clinically derived human tissue samples,
including formalin-fixed paraffin-embedded routine diagnostic specimens, for visualizing
the cellular architecture of brain tissue in health and disease.
acknowledged_ssus:
- _id: ScienComp
- _id: Bio
- _id: PreCl
- _id: LifeSc
- _id: M-Shop
- _id: E-Lib
acknowledgement: "We thank Jakob Vorlaufer, Nathalie Agudelo-Dueñas, Wiebke Jahr,
Andreas Wartak for microscope maintenance and troubleshooting, Caroline Kreuzinger,
Anna Freeman, and Irene Erber for technical assistance and Matthias Tomschik for
support with obtaining human samples. We gratefully acknowledge Eder Miguel for
setting up webKnossos and Marek Šuplata for computational support and hardware control.
We are grateful to Ryuichi Shigemoto and Bernd Bickel for generous support, and
Michael Sixt and Scott Boyd (Stanford University) for discussions and critical reading
of the manuscript. PSD95-HaloTag mice were kindly provided by Seth Grant (University
of Edinburgh). We acknowledge expert support by IST Austria’s scientific computing,
imaging and optics, preclinical, and lab support facilities, and by the Library
and Miba machine shop.\r\nWe gratefully acknowledge funding by the following sources:
\r\nAustrian Science Fund (FWF) grant I3600-B27 (JGD)\r\nAustrian Science Fund (FWF)
grant DK W1232 (JGD, JMM)\r\nAustrian Science Fund (FWF) grant Z 312-B27, Wittgenstein
award (PJ)\r\nAustrian Science Funds (FWF) projects I4685-B, I6565-B (SYNABS) and
DOC 33-B27 (RH)\r\nGesellschaft für Forschungsförderung NÖ (NFB) grant LSC18-022
(JGD)\r\nEuropean Union’s Horizon 2020 research and innovation programme, European
Research Council (ERC) grant 715508 – REVERSEAUTISM (GN)\r\nEuropean Union’s Horizon
2020 research and innovation programme, European Research Council (ERC) grant 692692
– GIANTSYN (PJ)\r\nMarie Skłodowska-Curie Actions Fellowship GA no. 665385 under
the EU Horizon 2020 program (JMM, JL)\r\nMarie Skłodowska-Curie Actions Individual
Fellowship 101026635 under the EU Horizon 2020 program (JFW)"
article_processing_charge: No
author:
- first_name: Johann G
full_name: Danzl, Johann G
id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87
last_name: Danzl
orcid: 0000-0001-8559-3973
citation:
ama: Danzl JG. Research data for the publication “Imaging brain tissue architecture
across millimeter to nanometer scales.” 2023. doi:10.15479/AT:ISTA:13126
apa: Danzl, J. G. (2023). Research data for the publication “Imaging brain tissue
architecture across millimeter to nanometer scales.” Institute of Science and
Technology Austria. https://doi.org/10.15479/AT:ISTA:13126
chicago: Danzl, Johann G. “Research Data for the Publication ‘Imaging Brain Tissue
Architecture across Millimeter to Nanometer Scales.’” Institute of Science and
Technology Austria, 2023. https://doi.org/10.15479/AT:ISTA:13126.
ieee: J. G. Danzl, “Research data for the publication ‘Imaging brain tissue architecture
across millimeter to nanometer scales.’” Institute of Science and Technology Austria,
2023.
ista: Danzl JG. 2023. Research data for the publication ‘Imaging brain tissue architecture
across millimeter to nanometer scales’, Institute of Science and Technology Austria,
10.15479/AT:ISTA:13126.
mla: Danzl, Johann G. Research Data for the Publication “Imaging Brain Tissue
Architecture across Millimeter to Nanometer Scales.” Institute of Science
and Technology Austria, 2023, doi:10.15479/AT:ISTA:13126.
short: J.G. Danzl, (2023).
contributor:
- first_name: Julia M
id: 443DB6DE-F248-11E8-B48F-1D18A9856A87
last_name: Michalska
- first_name: Julia
id: 46E28B80-F248-11E8-B48F-1D18A9856A87
last_name: Lyudchik
- first_name: Philipp
id: 39BDC62C-F248-11E8-B48F-1D18A9856A87
last_name: Velicky
orcid: 0000-0002-2340-7431
- first_name: Hana
id: ee3cb6ca-ec98-11ea-ae11-ff703e2254ed
last_name: Stefanickova
- first_name: Jake
id: 63836096-4690-11EA-BD4E-32803DDC885E
last_name: Watson
orcid: 0000-0002-8698-3823
- first_name: Alban
id: 9ac8f577-2357-11eb-997a-e566c5550886
last_name: Cenameri
- first_name: Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Alessandro
id: 41CB84B2-F248-11E8-B48F-1D18A9856A87
last_name: Venturino
orcid: 0000-0003-2356-9403
- first_name: Karl
last_name: Roessler
- first_name: Thomas
last_name: Czech
- first_name: Romana
last_name: Höftberger
- first_name: Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
- first_name: Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
- first_name: Peter M
id: 353C1B58-F248-11E8-B48F-1D18A9856A87
last_name: Jonas
orcid: 0000-0001-5001-4804
corr_author: '1'
date_created: 2023-06-07T07:15:12Z
date_published: 2023-08-04T00:00:00Z
date_updated: 2026-04-14T08:34:35Z
day: '04'
ddc:
- '610'
department:
- _id: JoDa
- _id: SaSi
- _id: GaNo
- _id: PeJo
- _id: Bio
- _id: RySh
doi: 10.15479/AT:ISTA:13126
ec_funded: 1
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- description: 'Original data for Fig. 5d, Fig. 5d (N2V) and Fig. 5f-i, provided
via an external link due to the large size (>10GB) of the datasets. '
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image: /images/cc_by_nc_sa.png
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...
---
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abstract:
- lang: eng
text: "Understanding the mechanisms of learning and memory formation has always
been one of\r\nthe main goals in neuroscience. Already Pavlov (1927) in his early
days has used his classic\r\nconditioning experiments to study the neural mechanisms
governing behavioral adaptation.\r\nWhat was not known back then was that the
part of the brain that is largely responsible for\r\nthis type of associative
learning is the cerebellum.\r\nSince then, plenty of theories on cerebellar learning
have emerged. Despite their differences,\r\none thing they all have in common
is that learning relies on synaptic and intrinsic plasticity.\r\nThe goal of my
PhD project was to unravel the molecular mechanisms underlying synaptic\r\nplasticity
in two synapses that have been shown to be implicated in motor learning, in an\r\neffort
to understand how learning and memory formation are processed in the cerebellum.\r\nOne
of the earliest and most well-known cerebellar theories postulates that motor
learning\r\nlargely depends on long-term depression at the parallel fiber-Purkinje
cell (PC-PC) synapse.\r\nHowever, the discovery of other types of plasticity in
the cerebellar circuitry, like long-term\r\npotentiation (LTP) at the PC-PC synapse,
potentiation of molecular layer interneurons (MLIs),\r\nand plasticity transfer
from the cortex to the cerebellar/ vestibular nuclei has increased the\r\npopularity
of the idea that multiple sites of plasticity might be involved in learning.\r\nStill
a lot remains unknown about the molecular mechanisms responsible for these types
of\r\nplasticity and whether they occur during physiological learning.\r\nIn the
first part of this thesis we have analyzed the variation and nanodistribution
of voltagegated calcium channels (VGCCs) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic
acid\r\ntype glutamate receptors (AMPARs) on the parallel fiber-Purkinje cell
synapse after vestibuloocular reflex phase reversal adaptation, a behavior that
has been suggested to rely on PF-PC\r\nLTP. We have found that on the last day
of adaptation there is no learning trace in form of\r\nVGCCs nor AMPARs variation
at the PF-PC synapse, but instead a decrease in the number of\r\nPF-PC synapses.
These data seem to support the view that learning is only stored in the\r\ncerebellar
cortex in an initial learning phase, being transferred later to the vestibular
nuclei.\r\nNext, we have studied the role of MLIs in motor learning using a relatively
simple and well characterized behavioral paradigm – horizontal optokinetic reflex
(HOKR) adaptation. We\r\nhave found behavior-induced MLI potentiation in form
of release probability increase that\r\ncould be explained by the increase of
VGCCs at the presynaptic side. Our results strengthen\r\nthe idea of distributed
cerebellar plasticity contributing to learning and provide a novel\r\nmechanism
for release probability increase. "
acknowledged_ssus:
- _id: EM-Fac
- _id: Bio
- _id: PreCl
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Catarina
full_name: Alcarva, Catarina
id: 3A96634C-F248-11E8-B48F-1D18A9856A87
last_name: Alcarva
citation:
ama: 'Alcarva C. Plasticity in the cerebellum: What molecular mechanisms are behind
physiological learning. 2023. doi:10.15479/at:ista:12809'
apa: 'Alcarva, C. (2023). Plasticity in the cerebellum: What molecular mechanisms
are behind physiological learning. Institute of Science and Technology Austria.
https://doi.org/10.15479/at:ista:12809'
chicago: 'Alcarva, Catarina. “Plasticity in the Cerebellum: What Molecular Mechanisms
Are behind Physiological Learning.” Institute of Science and Technology Austria,
2023. https://doi.org/10.15479/at:ista:12809.'
ieee: 'C. Alcarva, “Plasticity in the cerebellum: What molecular mechanisms are
behind physiological learning,” Institute of Science and Technology Austria, 2023.'
ista: 'Alcarva C. 2023. Plasticity in the cerebellum: What molecular mechanisms
are behind physiological learning. Institute of Science and Technology Austria.'
mla: 'Alcarva, Catarina. Plasticity in the Cerebellum: What Molecular Mechanisms
Are behind Physiological Learning. Institute of Science and Technology Austria,
2023, doi:10.15479/at:ista:12809.'
short: 'C. Alcarva, Plasticity in the Cerebellum: What Molecular Mechanisms Are
behind Physiological Learning, Institute of Science and Technology Austria, 2023.'
corr_author: '1'
date_created: 2023-04-06T07:54:09Z
date_published: 2023-04-06T00:00:00Z
date_updated: 2026-04-07T13:53:28Z
day: '06'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: RySh
doi: 10.15479/at:ista:12809
file:
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creator: cchlebak
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date_updated: 2024-04-08T22:30:03Z
embargo: 2024-04-07
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file_size: 9881969
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date_updated: 2024-04-08T22:30:03Z
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creator: cchlebak
date_created: 2023-04-07T06:18:05Z
date_updated: 2024-04-08T22:30:03Z
embargo_to: open_access
file_id: '12816'
file_name: Thesis_CatarinaAlcarva_final.docx
file_size: 84731244
relation: source_file
file_date_updated: 2024-04-08T22:30:03Z
has_accepted_license: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: '115'
project:
- _id: 267DFB90-B435-11E9-9278-68D0E5697425
name: 'Plasticity in the cerebellum: Which molecular mechanisms are behind physiological
learning?'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
status: public
supervisor:
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
title: 'Plasticity in the cerebellum: What molecular mechanisms are behind physiological
learning'
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2023'
...
---
_id: '12212'
abstract:
- lang: eng
text: Alzheimer’s disease (AD) is characterized by a reorganization of brain activity
determining network hyperexcitability and loss of synaptic plasticity. Precisely,
a dysfunction in metabotropic GABAB receptor signalling through G protein-gated
inwardly rectifying K+ (GIRK or Kir3) channels on the hippocampus has been postulated.
Thus, we determined the impact of amyloid-β (Aβ) pathology in GIRK channel density,
subcellular distribution, and its association with GABAB receptors in hippocampal
CA1 pyramidal neurons from the APP/PS1 mouse model using quantitative SDS-digested
freeze-fracture replica labelling (SDS-FRL) and proximity ligation in situ assay
(P-LISA). In wild type mice, single SDS-FRL detection revealed a similar dendritic
gradient for GIRK1 and GIRK2 in CA1 pyramidal cells, with higher densities in
spines, and GIRK3 showed a lower and uniform distribution. Double SDS-FRL showed
a co-clustering of GIRK2 and GIRK1 in post- and presynaptic compartments, but
not for GIRK2 and GIRK3. Likewise, double GABAB1 and GIRK2 SDS-FRL detection displayed
a high degree of co-clustering in nanodomains (40–50 nm) mostly in spines and
axon terminals. In APP/PS1 mice, the density of GIRK2 and GIRK1, but not for GIRK3,
was significantly reduced along the neuronal surface of CA1 pyramidal cells and
in axon terminals contacting them. Importantly, GABAB1 and GIRK2 co-clustering
was not present in APP/PS1 mice. Similarly, P-LISA experiments revealed a significant
reduction in GABAB1 and GIRK2 interaction on the hippocampus of this animal model.
Overall, our results provide compelling evidence showing a significant reduction
on the cell surface density of pre- and postsynaptic GIRK1 and GIRK2, but not
GIRK3, and a decline in GABAB receptors and GIRK2 channels co-clustering in hippocampal
pyramidal neurons from APP/PS1 mice, thus suggesting that a disruption in the
GABAB receptor–GIRK channel membrane assembly causes dysregulation in the GABAB
signalling via GIRK channels in this AD animal model.
acknowledgement: "We thank Ms. Diane Latawiec for the English revision of the manuscript.
Funding sources were the Spanish Ministerio de Economía y Competitividad, Junta
de Comunidades de Castilla-La Mancha (Spain), and Life Science Innovation Center
at University of Fukui. We thank Centres de Recerca de Catalunya (CERCA) Programme/Generalitat
de Catalunya for IDIBELL institutional support. We thank Hitoshi Takagi and Takako
Maegawa at the University of Fukui for their technical assistance on SDS-FRL experiments.\r\nThis
work was supported by grants from the Spanish Ministerio de Economía y Competitividad
(BFU2015-63769-R, RTI2018-095812-B-I00, and PID2021-125875OB-I00) and Junta de Comunidades
de Castilla-La Mancha (SBPLY/17/180501/000229 and SBPLY/21/180501/000064) to RL,
Life Science Innovation Center at University of Fukui and JSPS KAKENHI (Grant Numbers
16H04662, 19H03323, and 20H05058) to YF, and Margarita Salas fellowship from Ministerio
de Universidades and Universidad de Castilla-La Mancha to AMB."
article_number: '136'
article_processing_charge: No
article_type: original
author:
- first_name: Alejandro
full_name: Martín-Belmonte, Alejandro
last_name: Martín-Belmonte
- first_name: Carolina
full_name: Aguado, Carolina
last_name: Aguado
- first_name: Rocío
full_name: Alfaro-Ruiz, Rocío
last_name: Alfaro-Ruiz
- first_name: Ana Esther
full_name: Moreno-Martínez, Ana Esther
last_name: Moreno-Martínez
- first_name: Luis
full_name: de la Ossa, Luis
last_name: de la Ossa
- first_name: Ester
full_name: Aso, Ester
last_name: Aso
- first_name: Laura
full_name: Gómez-Acero, Laura
last_name: Gómez-Acero
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Yugo
full_name: Fukazawa, Yugo
last_name: Fukazawa
- first_name: Francisco
full_name: Ciruela, Francisco
last_name: Ciruela
- first_name: Rafael
full_name: Luján, Rafael
last_name: Luján
citation:
ama: Martín-Belmonte A, Aguado C, Alfaro-Ruiz R, et al. Nanoscale alterations in
GABAB receptors and GIRK channel organization on the hippocampus of APP/PS1 mice.
Alzheimer’s Research & Therapy. 2022;14. doi:10.1186/s13195-022-01078-5
apa: Martín-Belmonte, A., Aguado, C., Alfaro-Ruiz, R., Moreno-Martínez, A. E., de
la Ossa, L., Aso, E., … Luján, R. (2022). Nanoscale alterations in GABAB receptors
and GIRK channel organization on the hippocampus of APP/PS1 mice. Alzheimer’s
Research & Therapy. Springer Nature. https://doi.org/10.1186/s13195-022-01078-5
chicago: Martín-Belmonte, Alejandro, Carolina Aguado, Rocío Alfaro-Ruiz, Ana Esther
Moreno-Martínez, Luis de la Ossa, Ester Aso, Laura Gómez-Acero, et al. “Nanoscale
Alterations in GABAB Receptors and GIRK Channel Organization on the Hippocampus
of APP/PS1 Mice.” Alzheimer’s Research & Therapy. Springer Nature,
2022. https://doi.org/10.1186/s13195-022-01078-5.
ieee: A. Martín-Belmonte et al., “Nanoscale alterations in GABAB receptors
and GIRK channel organization on the hippocampus of APP/PS1 mice,” Alzheimer’s
Research & Therapy, vol. 14. Springer Nature, 2022.
ista: Martín-Belmonte A, Aguado C, Alfaro-Ruiz R, Moreno-Martínez AE, de la Ossa
L, Aso E, Gómez-Acero L, Shigemoto R, Fukazawa Y, Ciruela F, Luján R. 2022. Nanoscale
alterations in GABAB receptors and GIRK channel organization on the hippocampus
of APP/PS1 mice. Alzheimer’s Research & Therapy. 14, 136.
mla: Martín-Belmonte, Alejandro, et al. “Nanoscale Alterations in GABAB Receptors
and GIRK Channel Organization on the Hippocampus of APP/PS1 Mice.” Alzheimer’s
Research & Therapy, vol. 14, 136, Springer Nature, 2022, doi:10.1186/s13195-022-01078-5.
short: A. Martín-Belmonte, C. Aguado, R. Alfaro-Ruiz, A.E. Moreno-Martínez, L. de
la Ossa, E. Aso, L. Gómez-Acero, R. Shigemoto, Y. Fukazawa, F. Ciruela, R. Luján,
Alzheimer’s Research & Therapy 14 (2022).
date_created: 2023-01-16T09:45:51Z
date_published: 2022-09-21T00:00:00Z
date_updated: 2025-06-11T13:40:00Z
day: '21'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1186/s13195-022-01078-5
external_id:
isi:
- '000857985500001'
pmid:
- '36131327'
file:
- access_level: open_access
checksum: 88e49715ad6a1abf0fdb27efd65368dc
content_type: application/pdf
creator: dernst
date_created: 2023-01-27T07:53:18Z
date_updated: 2023-01-27T07:53:18Z
file_id: '12413'
file_name: 2022_AlzheimersResearch_MartinBelmont.pdf
file_size: 11013325
relation: main_file
success: 1
file_date_updated: 2023-01-27T07:53:18Z
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
keyword:
- Cognitive Neuroscience
- Neurology (clinical)
- Neurology
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
publication: Alzheimer's Research & Therapy
publication_identifier:
issn:
- 1758-9193
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nanoscale alterations in GABAB receptors and GIRK channel organization on the
hippocampus of APP/PS1 mice
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2022'
...
---
_id: '10889'
abstract:
- lang: eng
text: Genetically encoded tags have introduced extensive lines of application from
purification of tagged proteins to their visualization at the single molecular,
cellular, histological and whole-body levels. Combined with other rapidly developing
technologies such as clustered regularly interspaced palindromic repeats (CRISPR)/CRISPR-associated
protein 9 (Cas9) system, proteomics, super-resolution microscopy and proximity
labeling, a large variety of genetically encoded tags have been developed in the
last two decades. In this review, I focus on the current status of tag development
for electron microscopic (EM) visualization of proteins with metal particle labeling.
Compared with conventional immunoelectron microscopy using gold particles, tag-mediated
metal particle labeling has several advantages that could potentially improve
the sensitivity, spatial and temporal resolution, and applicability to a wide
range of proteins of interest (POIs). It may enable researchers to detect single
molecules in situ, allowing the quantitative measurement of absolute numbers and
exact localization patterns of POI in the ultrastructural context. Thus, genetically
encoded tags for EM could revolutionize the field as green fluorescence protein
did for light microscopy, although we still have many challenges to overcome before
reaching this goal.
acknowledgement: European Research Council Advanced Grant (694539 to R.S.).
article_processing_charge: No
article_type: original
author:
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Shigemoto R. Electron microscopic visualization of single molecules by tag-mediated
metal particle labeling. Microscopy. 2022;71(Supplement_1):i72-i80. doi:10.1093/jmicro/dfab048
apa: Shigemoto, R. (2022). Electron microscopic visualization of single molecules
by tag-mediated metal particle labeling. Microscopy. Oxford University
Press. https://doi.org/10.1093/jmicro/dfab048
chicago: Shigemoto, Ryuichi. “Electron Microscopic Visualization of Single Molecules
by Tag-Mediated Metal Particle Labeling.” Microscopy. Oxford University
Press, 2022. https://doi.org/10.1093/jmicro/dfab048.
ieee: R. Shigemoto, “Electron microscopic visualization of single molecules by tag-mediated
metal particle labeling,” Microscopy, vol. 71, no. Supplement_1. Oxford
University Press, pp. i72–i80, 2022.
ista: Shigemoto R. 2022. Electron microscopic visualization of single molecules
by tag-mediated metal particle labeling. Microscopy. 71(Supplement_1), i72–i80.
mla: Shigemoto, Ryuichi. “Electron Microscopic Visualization of Single Molecules
by Tag-Mediated Metal Particle Labeling.” Microscopy, vol. 71, no. Supplement_1,
Oxford University Press, 2022, pp. i72–80, doi:10.1093/jmicro/dfab048.
short: R. Shigemoto, Microscopy 71 (2022) i72–i80.
corr_author: '1'
date_created: 2022-03-20T23:01:39Z
date_published: 2022-03-01T00:00:00Z
date_updated: 2025-05-14T11:05:40Z
day: '01'
department:
- _id: RySh
doi: 10.1093/jmicro/dfab048
ec_funded: 1
external_id:
isi:
- '000768384100011'
pmid:
- '35275179'
intvolume: ' 71'
isi: 1
issue: Supplement_1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1093/jmicro/dfab048
month: '03'
oa: 1
oa_version: Published Version
page: i72-i80
pmid: 1
project:
- _id: 25CA28EA-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '694539'
name: 'In situ analysis of single channel subunit composition in neurons: physiological
implication in synaptic plasticity and behaviour'
publication: Microscopy
publication_identifier:
eissn:
- 2050-5701
issn:
- 2050-5698
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Electron microscopic visualization of single molecules by tag-mediated metal
particle labeling
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 71
year: '2022'
...
---
_id: '11419'
abstract:
- lang: eng
text: Elevation of soluble wild-type (WT) tau occurs in synaptic compartments in
Alzheimer’s disease. We addressed whether tau elevation affects synaptic transmission
at the calyx of Held in slices from mice brainstem. Whole-cell loading of WT human
tau (h-tau) in presynaptic terminals at 10–20 µM caused microtubule (MT) assembly
and activity-dependent rundown of excitatory neurotransmission. Capacitance measurements
revealed that the primary target of WT h-tau is vesicle endocytosis. Blocking
MT assembly using nocodazole prevented tau-induced impairments of endocytosis
and neurotransmission. Immunofluorescence imaging analyses revealed that MT assembly
by WT h-tau loading was associated with an increased MT-bound fraction of the
endocytic protein dynamin. A synthetic dodecapeptide corresponding to dynamin
1-pleckstrin-homology domain inhibited MT-dynamin interaction and rescued tau-induced
impairments of endocytosis and neurotransmission. We conclude that elevation of
presynaptic WT tau induces de novo assembly of MTs, thereby sequestering free
dynamins. As a result, endocytosis and subsequent vesicle replenishment are impaired,
causing activity-dependent rundown of neurotransmission.
acknowledgement: We thank Yasuo Ihara, Nobuyuki Nukina, and Takeshi Sakaba for comments
and Patrick Stoney for editing this paper. We also thank Shota Okuda and Mikako
Matsubara for their contributions in the early stage of this study, and Satoko Wada-Kakuda
for technical assistant with in vitro analysis of tau. This research was supported
by funding from Okinawa Institute of Science and Technology and from Technology
(OIST) and Core Research for the Evolutional Science and Technology of Japan Science
and Technology Agency (CREST) to TT, and by Scientific Research on Innovative Areas
to TM (Brain Protein Aging and Dementia Control 26117004).
article_number: e73542
article_processing_charge: No
article_type: original
author:
- first_name: Tetsuya
full_name: Hori, Tetsuya
last_name: Hori
- first_name: Kohgaku
full_name: Eguchi, Kohgaku
id: 2B7846DC-F248-11E8-B48F-1D18A9856A87
last_name: Eguchi
orcid: 0000-0002-6170-2546
- first_name: Han Ying
full_name: Wang, Han Ying
last_name: Wang
- first_name: Tomohiro
full_name: Miyasaka, Tomohiro
last_name: Miyasaka
- first_name: Laurent
full_name: Guillaud, Laurent
last_name: Guillaud
- first_name: Zacharie
full_name: Taoufiq, Zacharie
last_name: Taoufiq
- first_name: Satyajit
full_name: Mahapatra, Satyajit
last_name: Mahapatra
- first_name: Hiroshi
full_name: Yamada, Hiroshi
last_name: Yamada
- first_name: Kohji
full_name: Takei, Kohji
last_name: Takei
- first_name: Tomoyuki
full_name: Takahashi, Tomoyuki
last_name: Takahashi
citation:
ama: Hori T, Eguchi K, Wang HY, et al. Microtubule assembly by tau impairs endocytosis
and neurotransmission via dynamin sequestration in Alzheimer’s disease synapse
model. eLife. 2022;11. doi:10.7554/eLife.73542
apa: Hori, T., Eguchi, K., Wang, H. Y., Miyasaka, T., Guillaud, L., Taoufiq, Z.,
… Takahashi, T. (2022). Microtubule assembly by tau impairs endocytosis and neurotransmission
via dynamin sequestration in Alzheimer’s disease synapse model. ELife.
eLife Sciences Publications. https://doi.org/10.7554/eLife.73542
chicago: Hori, Tetsuya, Kohgaku Eguchi, Han Ying Wang, Tomohiro Miyasaka, Laurent
Guillaud, Zacharie Taoufiq, Satyajit Mahapatra, Hiroshi Yamada, Kohji Takei, and
Tomoyuki Takahashi. “Microtubule Assembly by Tau Impairs Endocytosis and Neurotransmission
via Dynamin Sequestration in Alzheimer’s Disease Synapse Model.” ELife.
eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.73542.
ieee: T. Hori et al., “Microtubule assembly by tau impairs endocytosis and
neurotransmission via dynamin sequestration in Alzheimer’s disease synapse model,”
eLife, vol. 11. eLife Sciences Publications, 2022.
ista: Hori T, Eguchi K, Wang HY, Miyasaka T, Guillaud L, Taoufiq Z, Mahapatra S,
Yamada H, Takei K, Takahashi T. 2022. Microtubule assembly by tau impairs endocytosis
and neurotransmission via dynamin sequestration in Alzheimer’s disease synapse
model. eLife. 11, e73542.
mla: Hori, Tetsuya, et al. “Microtubule Assembly by Tau Impairs Endocytosis and
Neurotransmission via Dynamin Sequestration in Alzheimer’s Disease Synapse Model.”
ELife, vol. 11, e73542, eLife Sciences Publications, 2022, doi:10.7554/eLife.73542.
short: T. Hori, K. Eguchi, H.Y. Wang, T. Miyasaka, L. Guillaud, Z. Taoufiq, S. Mahapatra,
H. Yamada, K. Takei, T. Takahashi, ELife 11 (2022).
date_created: 2022-05-29T22:01:54Z
date_published: 2022-05-05T00:00:00Z
date_updated: 2023-08-03T07:15:49Z
day: '05'
ddc:
- '616'
department:
- _id: RySh
doi: 10.7554/eLife.73542
external_id:
isi:
- '000876231600001'
pmid:
- '35471147 '
file:
- access_level: open_access
checksum: ccddbd167e00ff8375f12998af497152
content_type: application/pdf
creator: cchlebak
date_created: 2022-05-30T08:09:16Z
date_updated: 2022-05-30T08:09:16Z
file_id: '11421'
file_name: elife-73542-v2.pdf
file_size: 2466296
relation: main_file
success: 1
file_date_updated: 2022-05-30T08:09:16Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
eissn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Microtubule assembly by tau impairs endocytosis and neurotransmission via dynamin
sequestration in Alzheimer's disease synapse model
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2022'
...
---
_id: '11333'
abstract:
- lang: eng
text: Adenosine triphosphate (ATP) is the energy source for various biochemical
processes and biomolecular motors in living things. Development of ATP antagonists
and their stimuli-controlled actions offer a novel approach to regulate biological
processes. Herein, we developed azobenzene-based photoswitchable ATP antagonists
for controlling the activity of motor proteins; cytoplasmic and axonemal dyneins.
The new ATP antagonists showed reversible photoswitching of cytoplasmic dynein
activity in an in vitro dynein-microtubule system due to the trans and cis photoisomerization
of their azobenzene segment. Importantly, our ATP antagonists reversibly regulated
the axonemal dynein motor activity for the force generation in a demembranated
model of Chlamydomonas reinhardtii. We found that the trans and cis isomers of
ATP antagonists significantly differ in their affinity to the ATP binding site.
article_number: e202200807
article_processing_charge: No
article_type: original
author:
- first_name: Sampreeth
full_name: Thayyil, Sampreeth
last_name: Thayyil
- first_name: Yukinori
full_name: Nishigami, Yukinori
last_name: Nishigami
- first_name: Muhammad J
full_name: Islam, Muhammad J
id: C94881D2-008F-11EA-8E08-2637E6697425
last_name: Islam
- first_name: P. K.
full_name: Hashim, P. K.
last_name: Hashim
- first_name: Ken'Ya
full_name: Furuta, Ken'Ya
last_name: Furuta
- first_name: Kazuhiro
full_name: Oiwa, Kazuhiro
last_name: Oiwa
- first_name: Jian
full_name: Yu, Jian
last_name: Yu
- first_name: Min
full_name: Yao, Min
last_name: Yao
- first_name: Toshiyuki
full_name: Nakagaki, Toshiyuki
last_name: Nakagaki
- first_name: Nobuyuki
full_name: Tamaoki, Nobuyuki
last_name: Tamaoki
citation:
ama: Thayyil S, Nishigami Y, Islam MJ, et al. Dynamic control of microbial movement
by photoswitchable ATP antagonists. Chemistry - A European Journal. 2022;28(30).
doi:10.1002/chem.202200807
apa: Thayyil, S., Nishigami, Y., Islam, M. J., Hashim, P. K., Furuta, K., Oiwa,
K., … Tamaoki, N. (2022). Dynamic control of microbial movement by photoswitchable
ATP antagonists. Chemistry - A European Journal. Wiley. https://doi.org/10.1002/chem.202200807
chicago: Thayyil, Sampreeth, Yukinori Nishigami, Muhammad J Islam, P. K. Hashim,
Ken’Ya Furuta, Kazuhiro Oiwa, Jian Yu, Min Yao, Toshiyuki Nakagaki, and Nobuyuki
Tamaoki. “Dynamic Control of Microbial Movement by Photoswitchable ATP Antagonists.”
Chemistry - A European Journal. Wiley, 2022. https://doi.org/10.1002/chem.202200807.
ieee: S. Thayyil et al., “Dynamic control of microbial movement by photoswitchable
ATP antagonists,” Chemistry - A European Journal, vol. 28, no. 30. Wiley,
2022.
ista: Thayyil S, Nishigami Y, Islam MJ, Hashim PK, Furuta K, Oiwa K, Yu J, Yao M,
Nakagaki T, Tamaoki N. 2022. Dynamic control of microbial movement by photoswitchable
ATP antagonists. Chemistry - A European Journal. 28(30), e202200807.
mla: Thayyil, Sampreeth, et al. “Dynamic Control of Microbial Movement by Photoswitchable
ATP Antagonists.” Chemistry - A European Journal, vol. 28, no. 30, e202200807,
Wiley, 2022, doi:10.1002/chem.202200807.
short: S. Thayyil, Y. Nishigami, M.J. Islam, P.K. Hashim, K. Furuta, K. Oiwa, J.
Yu, M. Yao, T. Nakagaki, N. Tamaoki, Chemistry - A European Journal 28 (2022).
date_created: 2022-04-24T22:01:44Z
date_published: 2022-05-25T00:00:00Z
date_updated: 2026-04-02T11:59:00Z
day: '25'
department:
- _id: RySh
doi: 10.1002/chem.202200807
external_id:
isi:
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pmid:
- '35332959'
intvolume: ' 28'
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issue: '30'
language:
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main_file_link:
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url: https://doi.org/10.1002/chem.202200807
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: Chemistry - A European Journal
publication_identifier:
eissn:
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issn:
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publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dynamic control of microbial movement by photoswitchable ATP antagonists
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 28
year: '2022'
...