---
OA_embargo: 6 months
OA_place: publisher
OA_type: hybrid
_id: '19498'
abstract:
- lang: eng
text: A dynamic interplay between fast synaptic signals and slower neuromodulatory
signals controls the excitatory/inhibitory (E/I) balance within neuronal circuits.
The mechanisms by which neuropeptide signaling is regulated to maintain E/I balance
remain uncertain. We designed a genetic screen to isolate genes involved in the
peptidergic maintenance of the E/I balance in the C. elegans motor circuit. This
screen identified the C. elegans orthologs of the presynaptic phosphoprotein synapsin
(snn-1) and the protein phosphatase 1 (PP1) regulatory subunit PHACTR1 (phac-1).
We demonstrate that both phac-1 and snn-1 alter the motor behavior of C. elegans,
and genetic interactions suggest that SNN-1 contributes to PP1-PHAC-1 holoenzyme
signaling. De novo variants of human PHACTR1, associated with early-onset epilepsies
[developmental and epileptic encephalopathy 70 (DEE70)], when expressed in C.
elegans resulted in constitutive PP1-PHAC-1 holoenzyme activity. Unregulated PP1-PHAC-1
signaling alters the synapsin and actin cytoskeleton and increases neuropeptide
release by cholinergic motor neurons, which secondarily affects the presynaptic
vesicle cycle. Together, these results clarify the dominant mechanisms of action
of the DEE70 alleles and suggest that altered neuropeptide release may alter E/I
balance in DEE70.
acknowledgement: P.L. is a research associate of the Belgian National Fund for Scientific
Research (FRS-FNRS). K.S., M.S.-G., S.S., and P.L. are supported by grants from
the FRS-FNRS. This work was supported by an Advanced ERC Grant (269058 ACMO) to
M.D.B. We thank the team of Alexander Gottschalk for the snn-1(S9A) strain. We thank
the Imaging Facility of the Faculty of Medicine (LiMiF) of the Universite Libre
de Bruxelles, supported by FRS-FNRS. This work made use of instruments in the Electron
Microscopy Core of the University of Illinois Chicago Research Resources Center
as well as the BioCryo facility of Northwestern University's NUANCE Center, which
has received support from the SHyNE Resource (NSF ECCS-2025633), the IIN, and Northwestern's
MRSEC program (NSF DMR-2308691). Some strains were provided by the CGC, which is
funded by NIH Office of Research Infrastructure Programs (P40 OD010440).
article_number: e1767232024
article_processing_charge: No
article_type: original
author:
- first_name: Aikaterini
full_name: Stratigi, Aikaterini
last_name: Stratigi
- first_name: Miguel
full_name: Soler-García, Miguel
last_name: Soler-García
- first_name: Mia
full_name: Krout, Mia
last_name: Krout
- first_name: Shikha
full_name: Shukla, Shikha
last_name: Shukla
- first_name: Mario
full_name: De Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: De Bono
orcid: 0000-0001-8347-0443
- first_name: Janet E.
full_name: Richmond, Janet E.
last_name: Richmond
- first_name: Patrick
full_name: Laurent, Patrick
last_name: Laurent
citation:
ama: Stratigi A, Soler-García M, Krout M, et al. Neuroendocrine control of synaptic
transmission by PHAC-1 in C. elegans. Journal of Neuroscience. 2025;45(13).
doi:10.1523/JNEUROSCI.1767-23.2024
apa: Stratigi, A., Soler-García, M., Krout, M., Shukla, S., de Bono, M., Richmond,
J. E., & Laurent, P. (2025). Neuroendocrine control of synaptic transmission
by PHAC-1 in C. elegans. Journal of Neuroscience. Society for Neuroscience.
https://doi.org/10.1523/JNEUROSCI.1767-23.2024
chicago: Stratigi, Aikaterini, Miguel Soler-García, Mia Krout, Shikha Shukla, Mario
de Bono, Janet E. Richmond, and Patrick Laurent. “Neuroendocrine Control of Synaptic
Transmission by PHAC-1 in C. Elegans.” Journal of Neuroscience. Society
for Neuroscience, 2025. https://doi.org/10.1523/JNEUROSCI.1767-23.2024.
ieee: A. Stratigi et al., “Neuroendocrine control of synaptic transmission
by PHAC-1 in C. elegans,” Journal of Neuroscience, vol. 45, no. 13. Society
for Neuroscience, 2025.
ista: Stratigi A, Soler-García M, Krout M, Shukla S, de Bono M, Richmond JE, Laurent
P. 2025. Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans.
Journal of Neuroscience. 45(13), e1767232024.
mla: Stratigi, Aikaterini, et al. “Neuroendocrine Control of Synaptic Transmission
by PHAC-1 in C. Elegans.” Journal of Neuroscience, vol. 45, no. 13, e1767232024,
Society for Neuroscience, 2025, doi:10.1523/JNEUROSCI.1767-23.2024.
short: A. Stratigi, M. Soler-García, M. Krout, S. Shukla, M. de Bono, J.E. Richmond,
P. Laurent, Journal of Neuroscience 45 (2025).
date_created: 2025-04-06T22:01:32Z
date_published: 2025-03-26T00:00:00Z
date_updated: 2026-07-28T11:30:41Z
day: '26'
ddc:
- '570'
department:
- _id: MaDe
doi: 10.1523/JNEUROSCI.1767-23.2024
external_id:
isi:
- '001460952700001'
pmid:
- '39919830'
file:
- access_level: open_access
checksum: 7befc0168f4cd5bd2b0fcff9e2a94784
content_type: application/pdf
creator: dernst
date_created: 2025-04-07T11:57:19Z
date_updated: 2025-09-27T22:30:02Z
embargo: 2025-09-27
file_id: '19525'
file_name: 2025_JourNeuroscience_Stratigi.pdf
file_size: 3111735
relation: main_file
file_date_updated: 2025-09-27T22:30:02Z
fulldoi: https://doi.org/10.1523/JNEUROSCI.1767-23.2024
has_accepted_license: '1'
intvolume: ' 45'
isi: 1
issue: '13'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: 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: Neuroendocrine control of synaptic transmission by PHAC-1 in C. elegans
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: 45
year: '2025'
...
---
_id: '17092'
abstract:
- lang: eng
text: Memories are thought to be stored in neural ensembles known as engrams that
are specifically reactivated during memory recall. Recent studies have found that
memory engrams of two events that happened close in time tend to overlap in the
hippocampus and the amygdala, and these overlaps have been shown to support memory
linking. It has been hypothesized that engram overlaps arise from the mechanisms
that regulate memory allocation itself, involving neural excitability, but the
exact process remains unclear. Indeed, most theoretical studies focus on synaptic
plasticity and little is known about the role of intrinsic plasticity, which could
be mediated by neural excitability and serve as a complementary mechanism for
forming memory engrams. Here, we developed a rate-based recurrent neural network
that includes both synaptic plasticity and neural excitability. We obtained structural
and functional overlap of memory engrams for contexts that are presented close
in time, consistent with experimental and computational studies. We then investigated
the role of excitability in memory allocation at the network level and unveiled
competitive mechanisms driven by inhibition. This work suggests mechanisms underlying
the role of intrinsic excitability in memory allocation and linking, and yields
predictions regarding the formation and the overlap of memory engrams.
acknowledgement: We thank Sadra Sadeh and Inês Completo Guerreiro for helpful comments
on the manuscript, Yosif Zaki and Denise J. Cai for useful feedback and members
of the Clopath lab for discussion and support. This work was supported by Biotechnology
and Biological Sciences Research Council (BB/N013956/1 awarded to C.C.), Wellcome
Trust (200790/Z/16/Z awarded to C.C.), the Simons Foundation (564408 awarded to
C.C.), and Engineering and Physical Sciences Research Council (EP/R035806/1 awarded
to C.C.).
article_number: e0846232024
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Geoffroy
full_name: Delamare, Geoffroy
last_name: Delamare
- first_name: Douglas
full_name: Feitosa Tomé, Douglas
id: 0eed2d40-3d48-11ec-8d38-f789cc2e40b2
last_name: Feitosa Tomé
- first_name: Claudia
full_name: Clopath, Claudia
last_name: Clopath
citation:
ama: Delamare G, Feitosa Tomé D, Clopath C. Intrinsic neural excitability biases
allocation and overlap of memory engrams. Journal of Neuroscience. 2024;44(21).
doi:10.1523/JNEUROSCI.0846-23.2024
apa: Delamare, G., Feitosa Tomé, D., & Clopath, C. (2024). Intrinsic neural
excitability biases allocation and overlap of memory engrams. Journal of Neuroscience.
Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.0846-23.2024
chicago: Delamare, Geoffroy, Douglas Feitosa Tomé, and Claudia Clopath. “Intrinsic
Neural Excitability Biases Allocation and Overlap of Memory Engrams.” Journal
of Neuroscience. Society for Neuroscience, 2024. https://doi.org/10.1523/JNEUROSCI.0846-23.2024.
ieee: G. Delamare, D. Feitosa Tomé, and C. Clopath, “Intrinsic neural excitability
biases allocation and overlap of memory engrams,” Journal of Neuroscience,
vol. 44, no. 21. Society for Neuroscience, 2024.
ista: Delamare G, Feitosa Tomé D, Clopath C. 2024. Intrinsic neural excitability
biases allocation and overlap of memory engrams. Journal of Neuroscience. 44(21),
e0846232024.
mla: Delamare, Geoffroy, et al. “Intrinsic Neural Excitability Biases Allocation
and Overlap of Memory Engrams.” Journal of Neuroscience, vol. 44, no. 21,
e0846232024, Society for Neuroscience, 2024, doi:10.1523/JNEUROSCI.0846-23.2024.
short: G. Delamare, D. Feitosa Tomé, C. Clopath, Journal of Neuroscience 44 (2024).
date_created: 2024-06-02T22:00:57Z
date_published: 2024-05-22T00:00:00Z
date_updated: 2025-09-08T07:40:58Z
day: '22'
ddc:
- '570'
department:
- _id: TiVo
doi: 10.1523/JNEUROSCI.0846-23.2024
external_id:
isi:
- '001249681000008'
pmid:
- '38561228'
file:
- access_level: open_access
checksum: 4e19159800db605b802c721e4d4b1ffe
content_type: application/pdf
creator: dernst
date_created: 2024-06-03T06:34:21Z
date_updated: 2024-06-03T06:34:21Z
file_id: '17095'
file_name: 2024_JourNeuroscience_Delamare.pdf
file_size: 920354
relation: main_file
success: 1
file_date_updated: 2024-06-03T06:34:21Z
fulldoi: https://doi.org/10.1523/JNEUROSCI.0846-23.2024
has_accepted_license: '1'
intvolume: ' 44'
isi: 1
issue: '21'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
publication: 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: Intrinsic neural excitability biases allocation and overlap of memory engrams
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: 44
year: '2024'
...
---
_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
fulldoi: https://doi.org/10.1523/JNEUROSCI.1514-22.2023
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: '10051'
abstract:
- lang: eng
text: 'Rab-interacting molecule (RIM)-binding protein 2 (BP2) is a multidomain protein
of the presynaptic active zone (AZ). By binding to RIM, bassoon (Bsn), and voltage-gated
Ca2+ channels (CaV), it is considered to be a central organizer of the topography
of CaV and release sites of synaptic vesicles (SVs) at the AZ. Here, we used RIM-BP2
knock-out (KO) mice and their wild-type (WT) littermates of either sex to investigate
the role of RIM-BP2 at the endbulb of Held synapse of auditory nerve fibers (ANFs)
with bushy cells (BCs) of the cochlear nucleus, a fast relay of the auditory pathway
with high release probability. Disruption of RIM-BP2 lowered release probability
altering short-term plasticity and reduced evoked EPSCs. Analysis of SV pool dynamics
during high-frequency train stimulation indicated a reduction of SVs with high
release probability but an overall normal size of the readily releasable SV pool
(RRP). The Ca2+-dependent fast component of SV replenishment after RRP depletion
was slowed. Ultrastructural analysis by superresolution light and electron microscopy
revealed an impaired topography of presynaptic CaV and a reduction of docked and
membrane-proximal SVs at the AZ. We conclude that RIM-BP2 organizes the topography
of CaV, and promotes SV tethering and docking. This way RIM-BP2 is critical for
establishing a high initial release probability as required to reliably signal
sound onset information that we found to be degraded in BCs of RIM-BP2-deficient
mice in vivo. SIGNIFICANCE STATEMENT: Rab-interacting molecule (RIM)-binding proteins
(BPs) are key organizers of the active zone (AZ). Using a multidisciplinary approach
to the calyceal endbulb of Held synapse that transmits auditory information at
rates of up to hundreds of Hertz with submillisecond precision we demonstrate
a requirement for RIM-BP2 for normal auditory signaling. Endbulb synapses lacking
RIM-BP2 show a reduced release probability despite normal whole-terminal Ca2+
influx and abundance of the key priming protein Munc13-1, a reduced rate of SV
replenishment, as well as an altered topography of voltage-gated (CaV)2.1 Ca2+
channels, and fewer docked and membrane proximal synaptic vesicles (SVs). This
hampers transmission of sound onset information likely affecting downstream neural
computations such as of sound localization.'
acknowledgement: This work was supported by the Deutsche Forschungsgemeinschaft (DFG,
German Research Foundation) through the Collaborative Sensory Research Center 1286
[to C.W. (A4) and T.M. (B5)] and under Germany’s Excellence Strategy Grant EXC 2067/1-390729940.
We thank S. Gerke, A.J. Goldak, and C. Senger-Freitag for expert technical assistance;
G. Hoch for developing image analysis routines; and S. Chepurwar and N. Strenzke
for technical support and discussion regarding in vivo experiments. We also thank
Dr. Christian Rosenmund, Dr. Katharina Grauel, and Dr. Stephan Sigrist for providing
RIM-BP2 KO mice and Dr. Masahiko Watanabe for providing the anti-neurexin-antibody,
and Dr. Toshihisa Ohtsuka for the anti-ELKS-antibody. J. Neef for help with the
STED imaging and image analysis; E. Neher and S. Rizzoli for discussion and comments
on the manuscript; K. Eguchi for help with the statistical analysis; and C. H. Huang
and J. Neef for constant support and scientific discussion.
article_processing_charge: No
article_type: original
author:
- first_name: Tanvi
full_name: Butola, Tanvi
last_name: Butola
- first_name: Theocharis
full_name: Alvanos, Theocharis
last_name: Alvanos
- first_name: Anika
full_name: Hintze, Anika
last_name: Hintze
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: David
full_name: Kleindienst, David
id: 42E121A4-F248-11E8-B48F-1D18A9856A87
last_name: Kleindienst
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Carolin
full_name: Wichmann, Carolin
last_name: Wichmann
- first_name: Tobias
full_name: Moser, Tobias
last_name: Moser
citation:
ama: Butola T, Alvanos T, Hintze A, et al. RIM-binding protein 2 organizes Ca21
channel topography and regulates release probability and vesicle replenishment
at a fast central synapse. Journal of Neuroscience. 2021;41(37):7742-7767.
doi:10.1523/JNEUROSCI.0586-21.2021
apa: Butola, T., Alvanos, T., Hintze, A., Koppensteiner, P., Kleindienst, D., Shigemoto,
R., … Moser, T. (2021). RIM-binding protein 2 organizes Ca21 channel
topography and regulates release probability and vesicle replenishment at a fast
central synapse. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.0586-21.2021
chicago: Butola, Tanvi, Theocharis Alvanos, Anika Hintze, Peter Koppensteiner, David
Kleindienst, Ryuichi Shigemoto, Carolin Wichmann, and Tobias Moser. “RIM-Binding
Protein 2 Organizes Ca21 Channel Topography and Regulates Release Probability
and Vesicle Replenishment at a Fast Central Synapse.” Journal of Neuroscience.
Society for Neuroscience, 2021. https://doi.org/10.1523/JNEUROSCI.0586-21.2021.
ieee: T. Butola et al., “RIM-binding protein 2 organizes Ca21
channel topography and regulates release probability and vesicle replenishment
at a fast central synapse,” Journal of Neuroscience, vol. 41, no. 37. Society
for Neuroscience, pp. 7742–7767, 2021.
ista: Butola T, Alvanos T, Hintze A, Koppensteiner P, Kleindienst D, Shigemoto R,
Wichmann C, Moser T. 2021. RIM-binding protein 2 organizes Ca21 channel
topography and regulates release probability and vesicle replenishment at a fast
central synapse. Journal of Neuroscience. 41(37), 7742–7767.
mla: Butola, Tanvi, et al. “RIM-Binding Protein 2 Organizes Ca21 Channel
Topography and Regulates Release Probability and Vesicle Replenishment at a Fast
Central Synapse.” Journal of Neuroscience, vol. 41, no. 37, Society for
Neuroscience, 2021, pp. 7742–67, doi:10.1523/JNEUROSCI.0586-21.2021.
short: T. Butola, T. Alvanos, A. Hintze, P. Koppensteiner, D. Kleindienst, R. Shigemoto,
C. Wichmann, T. Moser, Journal of Neuroscience 41 (2021) 7742–7767.
date_created: 2021-09-27T14:33:13Z
date_published: 2021-09-15T00:00:00Z
date_updated: 2023-08-14T06:56:30Z
day: '15'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1523/JNEUROSCI.0586-21.2021
external_id:
isi:
- '000752287700005'
pmid:
- '34353898'
file:
- access_level: open_access
checksum: 769ab627c7355a50ccfd445e43a5f351
content_type: application/pdf
creator: dernst
date_created: 2022-05-31T09:10:15Z
date_updated: 2022-05-31T09:10:15Z
file_id: '11423'
file_name: 2021_JourNeuroscience_Butola.pdf
file_size: 11571961
relation: main_file
success: 1
file_date_updated: 2022-05-31T09:10:15Z
fulldoi: https://doi.org/10.1523/JNEUROSCI.0586-21.2021
has_accepted_license: '1'
intvolume: ' 41'
isi: 1
issue: '37'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 7742-7767
pmid: 1
publication: 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: RIM-binding protein 2 organizes Ca21 channel topography and regulates
release probability and vesicle replenishment at a fast central 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: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 41
year: '2021'
...
---
_id: '9073'
abstract:
- lang: eng
text: The sensory and cognitive abilities of the mammalian neocortex are underpinned
by intricate columnar and laminar circuits formed from an array of diverse neuronal
populations. One approach to determining how interactions between these circuit
components give rise to complex behavior is to investigate the rules by which
cortical circuits are formed and acquire functionality during development. This
review summarizes recent research on the development of the neocortex, from genetic
determination in neural stem cells through to the dynamic role that specific neuronal
populations play in the earliest circuits of neocortex, and how they contribute
to emergent function and cognition. While many of these endeavors take advantage
of model systems, consideration will also be given to advances in our understanding
of activity in nascent human circuits. Such cross-species perspective is imperative
when investigating the mechanisms underlying the dysfunction of early neocortical
circuits in neurodevelopmental disorders, so that one can identify targets amenable
to therapeutic intervention.
acknowledgement: Work in the I.L.H.-O. laboratory was supported by European Research
Council Grant ERC-2015-CoG 681577 and German Research Foundation Ha 4466/10-1, Ha4466/11-1,
Ha4466/12-1, SPP 1665, and SFB 936B5. Work in the S.J.B.B. laboratory was supported
by Biotechnology and Biological Sciences Research Council BB/P003796/1, Medical
Research Council MR/K004387/1 and MR/T033320/1, Wellcome Trust 215199/Z/19/Z and
102386/Z/13/Z, and John Fell Fund. Work in the S.H. laboratory was supported by
European Research Council Grants ERC-2016-CoG 725780 LinPro and FWF SFB F78. This
work was supported by National Institutes of Health Grant NIMH 1R01MH110553 to N.V.D.M.G.
Work in the J.A.C. laboratory was supported by the Ludwig Family Foundation, Simons
Foundation SFARI Research Award, and National Institutes of Health/National Institute
of Mental Health R01 MH102365 and R01MH113852. The B.V. laboratory was supported
by Whitehall Foundation 2017-12-73, National Science Foundation 1736028, National
Institutes of Health, National Institute of General Medical Sciences R01GM134363-01,
and Halıcıoğlu Data Science Institute Fellowship. This work was supported by the
University of California San Diego School of Medicine.
article_processing_charge: No
article_type: original
author:
- first_name: Ileana L.
full_name: Hanganu-Opatz, Ileana L.
last_name: Hanganu-Opatz
- first_name: Simon J. B.
full_name: Butt, Simon J. B.
last_name: Butt
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Natalia V.
full_name: De Marco García, Natalia V.
last_name: De Marco García
- first_name: Jessica A.
full_name: Cardin, Jessica A.
last_name: Cardin
- first_name: Bradley
full_name: Voytek, Bradley
last_name: Voytek
- first_name: Alysson R.
full_name: Muotri, Alysson R.
last_name: Muotri
citation:
ama: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical
circuits in health and disease. The Journal of Neuroscience. 2021;41(5):813-822.
doi:10.1523/jneurosci.1655-20.2020
apa: Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N.
V., Cardin, J. A., Voytek, B., & Muotri, A. R. (2021). The logic of developing
neocortical circuits in health and disease. The Journal of Neuroscience.
Society for Neuroscience. https://doi.org/10.1523/jneurosci.1655-20.2020
chicago: Hanganu-Opatz, Ileana L., Simon J. B. Butt, Simon Hippenmeyer, Natalia
V. De Marco García, Jessica A. Cardin, Bradley Voytek, and Alysson R. Muotri.
“The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal
of Neuroscience. Society for Neuroscience, 2021. https://doi.org/10.1523/jneurosci.1655-20.2020.
ieee: I. L. Hanganu-Opatz et al., “The logic of developing neocortical circuits
in health and disease,” The Journal of Neuroscience, vol. 41, no. 5. Society
for Neuroscience, pp. 813–822, 2021.
ista: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, De Marco García NV, Cardin JA,
Voytek B, Muotri AR. 2021. The logic of developing neocortical circuits in health
and disease. The Journal of Neuroscience. 41(5), 813–822.
mla: Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits
in Health and Disease.” The Journal of Neuroscience, vol. 41, no. 5, Society
for Neuroscience, 2021, pp. 813–22, doi:10.1523/jneurosci.1655-20.2020.
short: I.L. Hanganu-Opatz, S.J.B. Butt, S. Hippenmeyer, N.V. De Marco García, J.A.
Cardin, B. Voytek, A.R. Muotri, The Journal of Neuroscience 41 (2021) 813–822.
date_created: 2021-02-03T12:23:51Z
date_published: 2021-02-03T00:00:00Z
date_updated: 2025-04-15T08:23:06Z
day: '03'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1523/jneurosci.1655-20.2020
ec_funded: 1
external_id:
isi:
- '000616763400002'
pmid:
- '33431633'
file:
- access_level: open_access
checksum: 578fd7ed1a0aef74bce61bea2d987b33
content_type: application/pdf
creator: dernst
date_created: 2022-05-27T06:59:55Z
date_updated: 2022-05-27T06:59:55Z
file_id: '11414'
file_name: 2021_JourNeuroscience_Hanganu.pdf
file_size: 1031150
relation: main_file
success: 1
file_date_updated: 2022-05-27T06:59:55Z
fulldoi: https://doi.org/10.1523/jneurosci.1655-20.2020
has_accepted_license: '1'
intvolume: ' 41'
isi: 1
issue: '5'
keyword:
- General Neuroscience
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 813-822
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _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: 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: The logic of developing neocortical circuits in health and disease
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 41
year: '2021'
...
---
_id: '8084'
abstract:
- lang: eng
text: Origin and functions of intermittent transitions among sleep stages, including
brief awakenings and arousals, constitute a challenge to the current homeostatic
framework for sleep regulation, focusing on factors modulating sleep over large
time scales. Here we propose that the complex micro-architecture characterizing
sleep on scales of seconds and minutes results from intrinsic non-equilibrium
critical dynamics. We investigate θ- and δ-wave dynamics in control rats and in
rats where the sleep-promoting ventrolateral preoptic nucleus (VLPO) is lesioned
(male Sprague-Dawley rats). We demonstrate that bursts in θ and δ cortical rhythms
exhibit complex temporal organization, with long-range correlations and robust
duality of power-law (θ-bursts, active phase) and exponential-like (δ-bursts,
quiescent phase) duration distributions, features typical of non-equilibrium systems
self-organizing at criticality. We show that such non-equilibrium behavior relates
to anti-correlated coupling between θ- and δ-bursts, persists across a range of
time scales, and is independent of the dominant physiologic state; indications
of a basic principle in sleep regulation. Further, we find that VLPO lesions lead
to a modulation of cortical dynamics resulting in altered dynamical parameters
of θ- and δ-bursts and significant reduction in θ–δ coupling. Our empirical findings
and model simulations demonstrate that θ–δ coupling is essential for the emerging
non-equilibrium critical dynamics observed across the sleep–wake cycle, and indicate
that VLPO neurons may have dual role for both sleep and arousal/brief wake activation.
The uncovered critical behavior in sleep- and wake-related cortical rhythms indicates
a mechanism essential for the micro-architecture of spontaneous sleep-stage and
arousal transitions within a novel, non-homeostatic paradigm of sleep regulation.
article_processing_charge: No
article_type: original
author:
- first_name: Fabrizio
full_name: Lombardi, Fabrizio
id: A057D288-3E88-11E9-986D-0CF4E5697425
last_name: Lombardi
orcid: 0000-0003-2623-5249
- first_name: Manuel
full_name: Gómez-Extremera, Manuel
last_name: Gómez-Extremera
- first_name: Pedro
full_name: Bernaola-Galván, Pedro
last_name: Bernaola-Galván
- first_name: Ramalingam
full_name: Vetrivelan, Ramalingam
last_name: Vetrivelan
- first_name: Clifford B.
full_name: Saper, Clifford B.
last_name: Saper
- first_name: Thomas E.
full_name: Scammell, Thomas E.
last_name: Scammell
- first_name: Plamen Ch.
full_name: Ivanov, Plamen Ch.
last_name: Ivanov
citation:
ama: Lombardi F, Gómez-Extremera M, Bernaola-Galván P, et al. Critical dynamics
and coupling in bursts of cortical rhythms indicate non-homeostatic mechanism
for sleep-stage transitions and dual role of VLPO neurons in both sleep and wake.
Journal of Neuroscience. 2020;40(1):171-190. doi:10.1523/jneurosci.1278-19.2019
apa: Lombardi, F., Gómez-Extremera, M., Bernaola-Galván, P., Vetrivelan, R., Saper,
C. B., Scammell, T. E., & Ivanov, P. C. (2020). Critical dynamics and coupling
in bursts of cortical rhythms indicate non-homeostatic mechanism for sleep-stage
transitions and dual role of VLPO neurons in both sleep and wake. Journal of
Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.1278-19.2019
chicago: Lombardi, Fabrizio, Manuel Gómez-Extremera, Pedro Bernaola-Galván, Ramalingam
Vetrivelan, Clifford B. Saper, Thomas E. Scammell, and Plamen Ch. Ivanov. “Critical
Dynamics and Coupling in Bursts of Cortical Rhythms Indicate Non-Homeostatic Mechanism
for Sleep-Stage Transitions and Dual Role of VLPO Neurons in Both Sleep and Wake.”
Journal of Neuroscience. Society for Neuroscience, 2020. https://doi.org/10.1523/jneurosci.1278-19.2019.
ieee: F. Lombardi et al., “Critical dynamics and coupling in bursts of cortical
rhythms indicate non-homeostatic mechanism for sleep-stage transitions and dual
role of VLPO neurons in both sleep and wake,” Journal of Neuroscience,
vol. 40, no. 1. Society for Neuroscience, pp. 171–190, 2020.
ista: Lombardi F, Gómez-Extremera M, Bernaola-Galván P, Vetrivelan R, Saper CB,
Scammell TE, Ivanov PC. 2020. Critical dynamics and coupling in bursts of cortical
rhythms indicate non-homeostatic mechanism for sleep-stage transitions and dual
role of VLPO neurons in both sleep and wake. Journal of Neuroscience. 40(1), 171–190.
mla: Lombardi, Fabrizio, et al. “Critical Dynamics and Coupling in Bursts of Cortical
Rhythms Indicate Non-Homeostatic Mechanism for Sleep-Stage Transitions and Dual
Role of VLPO Neurons in Both Sleep and Wake.” Journal of Neuroscience,
vol. 40, no. 1, Society for Neuroscience, 2020, pp. 171–90, doi:10.1523/jneurosci.1278-19.2019.
short: F. Lombardi, M. Gómez-Extremera, P. Bernaola-Galván, R. Vetrivelan, C.B.
Saper, T.E. Scammell, P.C. Ivanov, Journal of Neuroscience 40 (2020) 171–190.
date_created: 2020-07-05T15:24:51Z
date_published: 2020-01-02T00:00:00Z
date_updated: 2025-04-14T07:44:04Z
day: '02'
ddc:
- '570'
department:
- _id: GaTk
doi: 10.1523/jneurosci.1278-19.2019
ec_funded: 1
external_id:
isi:
- '000505167600016'
pmid:
- '31694962'
file:
- access_level: open_access
content_type: application/pdf
creator: dernst
date_created: 2020-07-22T11:44:48Z
date_updated: 2020-07-22T11:44:48Z
file_id: '8150'
file_name: 2020_JournNeuroscience_Lombardi.pdf
file_size: 6646046
relation: main_file
success: 1
file_date_updated: 2020-07-22T11:44:48Z
fulldoi: https://doi.org/10.1523/jneurosci.1278-19.2019
has_accepted_license: '1'
intvolume: ' 40'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 171-190
pmid: 1
project:
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
publication: 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: Critical dynamics and coupling in bursts of cortical rhythms indicate non-homeostatic
mechanism for sleep-stage transitions and dual role of VLPO neurons in both sleep
and wake
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 40
year: '2020'
...
---
_id: '7339'
abstract:
- lang: eng
text: Cytoskeletal filaments such as microtubules (MTs) and filamentous actin (F-actin)
dynamically support cell structure and functions. In central presynaptic terminals,
F-actin is expressed along the release edge and reportedly plays diverse functional
roles, but whether axonal MTs extend deep into terminals and play any physiological
role remains controversial. At the calyx of Held in rats of either sex, confocal
and high-resolution microscopy revealed that MTs enter deep into presynaptic terminal
swellings and partially colocalize with a subset of synaptic vesicles (SVs). Electrophysiological
analysis demonstrated that depolymerization of MTs specifically prolonged the
slow-recovery time component of EPSCs from short-term depression induced by a
train of high-frequency stimulation, whereas depolymerization of F-actin specifically
prolonged the fast-recovery component. In simultaneous presynaptic and postsynaptic
action potential recordings, depolymerization of MTs or F-actin significantly
impaired the fidelity of high-frequency neurotransmission. We conclude that MTs
and F-actin differentially contribute to slow and fast SV replenishment, thereby
maintaining high-frequency neurotransmission.
article_processing_charge: No
article_type: original
author:
- first_name: Lashmi
full_name: Piriya Ananda Babu, Lashmi
last_name: Piriya Ananda Babu
- first_name: Han Ying
full_name: Wang, Han Ying
last_name: Wang
- first_name: Kohgaku
full_name: Eguchi, Kohgaku
id: 2B7846DC-F248-11E8-B48F-1D18A9856A87
last_name: Eguchi
orcid: 0000-0002-6170-2546
- first_name: Laurent
full_name: Guillaud, Laurent
last_name: Guillaud
- first_name: Tomoyuki
full_name: Takahashi, Tomoyuki
last_name: Takahashi
citation:
ama: Piriya Ananda Babu L, Wang HY, Eguchi K, Guillaud L, Takahashi T. Microtubule
and actin differentially regulate synaptic vesicle cycling to maintain high-frequency
neurotransmission. Journal of neuroscience. 2020;40(1):131-142. doi:10.1523/JNEUROSCI.1571-19.2019
apa: Piriya Ananda Babu, L., Wang, H. Y., Eguchi, K., Guillaud, L., & Takahashi,
T. (2020). Microtubule and actin differentially regulate synaptic vesicle cycling
to maintain high-frequency neurotransmission. Journal of Neuroscience.
Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1571-19.2019
chicago: Piriya Ananda Babu, Lashmi, Han Ying Wang, Kohgaku Eguchi, Laurent Guillaud,
and Tomoyuki Takahashi. “Microtubule and Actin Differentially Regulate Synaptic
Vesicle Cycling to Maintain High-Frequency Neurotransmission.” Journal of Neuroscience.
Society for Neuroscience, 2020. https://doi.org/10.1523/JNEUROSCI.1571-19.2019.
ieee: L. Piriya Ananda Babu, H. Y. Wang, K. Eguchi, L. Guillaud, and T. Takahashi,
“Microtubule and actin differentially regulate synaptic vesicle cycling to maintain
high-frequency neurotransmission,” Journal of neuroscience, vol. 40, no.
1. Society for Neuroscience, pp. 131–142, 2020.
ista: Piriya Ananda Babu L, Wang HY, Eguchi K, Guillaud L, Takahashi T. 2020. Microtubule
and actin differentially regulate synaptic vesicle cycling to maintain high-frequency
neurotransmission. Journal of neuroscience. 40(1), 131–142.
mla: Piriya Ananda Babu, Lashmi, et al. “Microtubule and Actin Differentially Regulate
Synaptic Vesicle Cycling to Maintain High-Frequency Neurotransmission.” Journal
of Neuroscience, vol. 40, no. 1, Society for Neuroscience, 2020, pp. 131–42,
doi:10.1523/JNEUROSCI.1571-19.2019.
short: L. Piriya Ananda Babu, H.Y. Wang, K. Eguchi, L. Guillaud, T. Takahashi, Journal
of Neuroscience 40 (2020) 131–142.
date_created: 2020-01-19T23:00:38Z
date_published: 2020-01-02T00:00:00Z
date_updated: 2026-04-16T08:27:29Z
day: '02'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1523/JNEUROSCI.1571-19.2019
external_id:
isi:
- '000505167600013'
pmid:
- '31767677'
file:
- access_level: open_access
checksum: 92f5e8a47f454fc131fb94cd7f106e60
content_type: application/pdf
creator: dernst
date_created: 2020-01-20T14:44:10Z
date_updated: 2020-07-14T12:47:56Z
file_id: '7345'
file_name: 2020_JourNeuroscience_Piriya.pdf
file_size: 4460781
relation: main_file
file_date_updated: 2020-07-14T12:47:56Z
fulldoi: https://doi.org/10.1523/JNEUROSCI.1571-19.2019
has_accepted_license: '1'
intvolume: ' 40'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 131-142
pmid: 1
publication: 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: Microtubule and actin differentially regulate synaptic vesicle cycling to maintain
high-frequency neurotransmission
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 40
year: '2020'
...
---
_id: '6126'
abstract:
- lang: eng
text: Aerobic animals constantly monitor and adapt to changes in O2 levels. The
molecular mechanisms involved in sensing O2 are, however, incompletely understood.
Previous studies showed that a hexacoordinated globin called GLB-5 tunes the dynamic
range of O2-sensing neurons in natural C. elegans isolates, but is defective in
the N2 lab reference strain (McGrath et al., 2009; Persson et al., 2009). GLB-5
enables a sharp behavioral switch when O2 changes between 21 and 17%. Here, we
show that GLB-5 also confers rapid behavioral and cellular recovery from exposure
to hypoxia. Hypoxia reconfigures O2-evoked Ca2+ responses in the URX O2 sensors,
and GLB-5 enables rapid recovery of these responses upon re-oxygenation. Forward
genetic screens indicate that GLB-5's effects on O2 sensing require PDL-1, the
C. elegans ortholog of mammalian PrBP/PDE6δ protein. In mammals, PDE6δ regulates
the traffic and activity of prenylated proteins (Zhang et al., 2004; Norton et
al., 2005). PDL-1 promotes localization of GCY-33 and GCY-35, atypical soluble
guanylate cyclases that act as O2 sensors, to the dendritic endings of URX and
BAG neurons, where they colocalize with GLB-5. Both GCY-33 and GCY-35 are predicted
to be prenylated. Dendritic localization is not essential for GCY-35 to function
as an O2 sensor, but disrupting pdl-1 alters the URX neuron's O2 response properties.
Functional GLB-5 can restore dendritic localization of GCY-33 in pdl-1 mutants,
suggesting GCY-33 and GLB-5 are in a complex. Our data suggest GLB-5 and the soluble
guanylate cyclases operate in close proximity to sculpt O2 responses.
author:
- first_name: E.
full_name: Gross, E.
last_name: Gross
- first_name: Z.
full_name: Soltesz, Z.
last_name: Soltesz
- first_name: S.
full_name: Oda, S.
last_name: Oda
- first_name: V.
full_name: Zelmanovich, V.
last_name: Zelmanovich
- first_name: Z.
full_name: Abergel, Z.
last_name: Abergel
- first_name: Mario
full_name: de Bono, Mario
id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87
last_name: de Bono
orcid: 0000-0001-8347-0443
citation:
ama: Gross E, Soltesz Z, Oda S, Zelmanovich V, Abergel Z, de Bono M. GLOBIN-5-dependent
O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate
cyclases to dendritic endings. Journal of Neuroscience. 2014;34(50):16726-16738.
doi:10.1523/jneurosci.5368-13.2014
apa: Gross, E., Soltesz, Z., Oda, S., Zelmanovich, V., Abergel, Z., & de Bono,
M. (2014). GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets
prenylated soluble guanylate cyclases to dendritic endings. Journal of Neuroscience.
Society for Neuroscience. https://doi.org/10.1523/jneurosci.5368-13.2014
chicago: Gross, E., Z. Soltesz, S. Oda, V. Zelmanovich, Z. Abergel, and Mario de
Bono. “GLOBIN-5-Dependent O2 Responses Are Regulated by PDL-1/PrBP That Targets
Prenylated Soluble Guanylate Cyclases to Dendritic Endings.” Journal of Neuroscience.
Society for Neuroscience, 2014. https://doi.org/10.1523/jneurosci.5368-13.2014.
ieee: E. Gross, Z. Soltesz, S. Oda, V. Zelmanovich, Z. Abergel, and M. de Bono,
“GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated
soluble guanylate cyclases to dendritic endings,” Journal of Neuroscience,
vol. 34, no. 50. Society for Neuroscience, pp. 16726–16738, 2014.
ista: Gross E, Soltesz Z, Oda S, Zelmanovich V, Abergel Z, de Bono M. 2014. GLOBIN-5-dependent
O2 responses are regulated by PDL-1/PrBP that targets prenylated soluble guanylate
cyclases to dendritic endings. Journal of Neuroscience. 34(50), 16726–16738.
mla: Gross, E., et al. “GLOBIN-5-Dependent O2 Responses Are Regulated by PDL-1/PrBP
That Targets Prenylated Soluble Guanylate Cyclases to Dendritic Endings.” Journal
of Neuroscience, vol. 34, no. 50, Society for Neuroscience, 2014, pp. 16726–38,
doi:10.1523/jneurosci.5368-13.2014.
short: E. Gross, Z. Soltesz, S. Oda, V. Zelmanovich, Z. Abergel, M. de Bono, Journal
of Neuroscience 34 (2014) 16726–16738.
date_created: 2019-03-19T14:52:26Z
date_published: 2014-12-10T00:00:00Z
date_updated: 2021-01-12T08:06:14Z
day: '10'
ddc:
- '570'
doi: 10.1523/jneurosci.5368-13.2014
extern: '1'
external_id:
pmid:
- '25505325'
file:
- access_level: open_access
checksum: a3dd71969f94c43909327cd083283d4b
content_type: application/pdf
creator: kschuh
date_created: 2019-03-19T14:55:58Z
date_updated: 2020-07-14T12:47:20Z
file_id: '6127'
file_name: 2014_SFN_Gross.pdf
file_size: 3263422
relation: main_file
file_date_updated: 2020-07-14T12:47:20Z
fulldoi: https://doi.org/10.1523/jneurosci.5368-13.2014
has_accepted_license: '1'
intvolume: ' 34'
issue: '50'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 16726-16738
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
issn:
- 0270-6474
- 1529-2401
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
status: public
title: GLOBIN-5-dependent O2 responses are regulated by PDL-1/PrBP that targets prenylated
soluble guanylate cyclases to dendritic endings
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: 34
year: '2014'
...
---
_id: '2018'
abstract:
- lang: eng
text: Synaptic cell adhesion molecules are increasingly gaining attention for conferring
specific properties to individual synapses. Netrin-G1 and netrin-G2 are trans-synaptic
adhesion molecules that distribute on distinct axons, and their presence restricts
the expression of their cognate receptors, NGL1 and NGL2, respectively, to specific
subdendritic segments of target neurons. However, the neural circuits and functional
roles of netrin-G isoform complexes remain unclear. Here, we use netrin-G-KO and
NGL-KO mice to reveal that netrin-G1/NGL1 and netrin-G2/NGL2 interactions specify
excitatory synapses in independent hippocampal pathways. In the hippocampal CA1
area, netrin-G1/NGL1 and netrin-G2/NGL2 were expressed in the temporoammonic and
Schaffer collateral pathways, respectively. The lack of presynaptic netrin-Gs
led to the dispersion of NGLs from postsynaptic membranes. In accord, netrin-G
mutant synapses displayed opposing phenotypes in long-term and short-term plasticity
through discrete biochemical pathways. The plasticity phenotypes in netrin-G-KOs
were phenocopied in NGL-KOs, with a corresponding loss of netrin-Gs from presynaptic
membranes. Our findings show that netrin-G/NGL interactions differentially control
synaptic plasticity in distinct circuits via retrograde signaling mechanisms and
explain how synaptic inputs are diversified to control neuronal activity.
acknowledgement: This work was supported by “Funding Program for World-Leading Innovative
R&D on Science and Technology (FIRST Program)” initiated by the Council for Science
and Technology Policy.
article_processing_charge: No
article_type: original
author:
- first_name: Hiroshi
full_name: Matsukawa, Hiroshi
last_name: Matsukawa
- first_name: Sachiko
full_name: Akiyoshi Nishimura, Sachiko
last_name: Akiyoshi Nishimura
- first_name: Qi
full_name: Zhang, Qi
last_name: Zhang
- first_name: Rafael
full_name: Luján, Rafael
last_name: Luján
- first_name: Kazuhiko
full_name: Yamaguchi, Kazuhiko
last_name: Yamaguchi
- first_name: Hiromichi
full_name: Goto, Hiromichi
last_name: Goto
- first_name: Kunio
full_name: Yaguchi, Kunio
last_name: Yaguchi
- first_name: Tsutomu
full_name: Hashikawa, Tsutomu
last_name: Hashikawa
- first_name: Chie
full_name: Sano, Chie
last_name: Sano
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Toshiaki
full_name: Nakashiba, Toshiaki
last_name: Nakashiba
- first_name: Shigeyoshi
full_name: Itohara, Shigeyoshi
last_name: Itohara
citation:
ama: Matsukawa H, Akiyoshi Nishimura S, Zhang Q, et al. Netrin-G/NGL complexes encode
functional synaptic diversification. Journal of Neuroscience. 2014;34(47):15779-15792.
doi:10.1523/JNEUROSCI.1141-14.2014
apa: Matsukawa, H., Akiyoshi Nishimura, S., Zhang, Q., Luján, R., Yamaguchi, K.,
Goto, H., … Itohara, S. (2014). Netrin-G/NGL complexes encode functional synaptic
diversification. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1141-14.2014
chicago: Matsukawa, Hiroshi, Sachiko Akiyoshi Nishimura, Qi Zhang, Rafael Luján,
Kazuhiko Yamaguchi, Hiromichi Goto, Kunio Yaguchi, et al. “Netrin-G/NGL Complexes
Encode Functional Synaptic Diversification.” Journal of Neuroscience. Society
for Neuroscience, 2014. https://doi.org/10.1523/JNEUROSCI.1141-14.2014.
ieee: H. Matsukawa et al., “Netrin-G/NGL complexes encode functional synaptic
diversification,” Journal of Neuroscience, vol. 34, no. 47. Society for
Neuroscience, pp. 15779–15792, 2014.
ista: Matsukawa H, Akiyoshi Nishimura S, Zhang Q, Luján R, Yamaguchi K, Goto H,
Yaguchi K, Hashikawa T, Sano C, Shigemoto R, Nakashiba T, Itohara S. 2014. Netrin-G/NGL
complexes encode functional synaptic diversification. Journal of Neuroscience.
34(47), 15779–15792.
mla: Matsukawa, Hiroshi, et al. “Netrin-G/NGL Complexes Encode Functional Synaptic
Diversification.” Journal of Neuroscience, vol. 34, no. 47, Society for
Neuroscience, 2014, pp. 15779–92, doi:10.1523/JNEUROSCI.1141-14.2014.
short: H. Matsukawa, S. Akiyoshi Nishimura, Q. Zhang, R. Luján, K. Yamaguchi, H.
Goto, K. Yaguchi, T. Hashikawa, C. Sano, R. Shigemoto, T. Nakashiba, S. Itohara,
Journal of Neuroscience 34 (2014) 15779–15792.
date_created: 2018-12-11T11:55:14Z
date_published: 2014-11-19T00:00:00Z
date_updated: 2025-09-29T12:00:37Z
day: '19'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1523/JNEUROSCI.1141-14.2014
external_id:
isi:
- '000345907500026'
pmid:
- '25411505'
file:
- access_level: open_access
checksum: 6913e9bc26e9fc1c0441a739a4199229
content_type: application/pdf
creator: dernst
date_created: 2022-05-24T08:41:41Z
date_updated: 2022-05-24T08:41:41Z
file_id: '11410'
file_name: 2014_JournNeuroscience_Matsukawa.pdf
file_size: 3963728
relation: main_file
success: 1
file_date_updated: 2022-05-24T08:41:41Z
fulldoi: https://doi.org/10.1523/JNEUROSCI.1141-14.2014
has_accepted_license: '1'
intvolume: ' 34'
isi: 1
issue: '47'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 15779 - 15792
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '5054'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Netrin-G/NGL complexes encode functional synaptic diversification
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 34
year: '2014'
...
---
_id: '8025'
abstract:
- lang: eng
text: Chandelier (axoaxonic) cells (ChCs) are a distinct group of GABAergic interneurons
that innervate the axon initial segments of pyramidal cells. However, their circuit
role and the function of their clearly defined anatomical specificity remain unclear.
Recent work has demonstrated that chandelier cells can produce depolarizing GABAergic
PSPs, occasionally driving postsynaptic targets to spike. On the other hand, other
work suggests that ChCs are hyperpolarizing and may have an inhibitory role. These
disparate functional effects may reflect heterogeneity among ChCs. Here, using
brain slices from transgenic mouse strains, we first demonstrate that, across
different neocortical areas and genetic backgrounds, upper Layer 2/3 ChCs belong
to a single electrophysiologically and morphologically defined population, extensively
sampling Layer 1 inputs with asymmetric dendrites. Consistent with being a single
cell type, we find electrical coupling between ChCs. We then investigate the effect
of chandelier cell activation on pyramidal neuron spiking in several conditions,
ranging from the resting membrane potential to stimuli designed to approximate
in vivo membrane potential dynamics. We find that under quiescent conditions,
chandelier cells are capable of both promoting and inhibiting spike generation,
depending on the postsynaptic membrane potential. However, during in vivo-like
membrane potential fluctuations, the dominant postsynaptic effect was a strong
inhibition. Thus, neocortical chandelier cells, even from within a homogeneous
population, appear to play a dual role in the circuit, helping to activate quiescent
pyramidal neurons, while at the same time inhibiting active ones.
article_processing_charge: No
article_type: original
author:
- first_name: A. R.
full_name: Woodruff, A. R.
last_name: Woodruff
- first_name: L. M.
full_name: McGarry, L. M.
last_name: McGarry
- first_name: Tim P
full_name: Vogels, Tim P
id: CB6FF8D2-008F-11EA-8E08-2637E6697425
last_name: Vogels
orcid: 0000-0003-3295-6181
- first_name: M.
full_name: Inan, M.
last_name: Inan
- first_name: S. A.
full_name: Anderson, S. A.
last_name: Anderson
- first_name: R.
full_name: Yuste, R.
last_name: Yuste
citation:
ama: Woodruff AR, McGarry LM, Vogels TP, Inan M, Anderson SA, Yuste R. State-dependent
function of neocortical chandelier cells. Journal of Neuroscience. 2011;31(49):17872-17886.
doi:10.1523/jneurosci.3894-11.2011
apa: Woodruff, A. R., McGarry, L. M., Vogels, T. P., Inan, M., Anderson, S. A.,
& Yuste, R. (2011). State-dependent function of neocortical chandelier cells.
Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/jneurosci.3894-11.2011
chicago: Woodruff, A. R., L. M. McGarry, Tim P Vogels, M. Inan, S. A. Anderson,
and R. Yuste. “State-Dependent Function of Neocortical Chandelier Cells.” Journal
of Neuroscience. Society for Neuroscience, 2011. https://doi.org/10.1523/jneurosci.3894-11.2011.
ieee: A. R. Woodruff, L. M. McGarry, T. P. Vogels, M. Inan, S. A. Anderson, and
R. Yuste, “State-dependent function of neocortical chandelier cells,” Journal
of Neuroscience, vol. 31, no. 49. Society for Neuroscience, pp. 17872–17886,
2011.
ista: Woodruff AR, McGarry LM, Vogels TP, Inan M, Anderson SA, Yuste R. 2011. State-dependent
function of neocortical chandelier cells. Journal of Neuroscience. 31(49), 17872–17886.
mla: Woodruff, A. R., et al. “State-Dependent Function of Neocortical Chandelier
Cells.” Journal of Neuroscience, vol. 31, no. 49, Society for Neuroscience,
2011, pp. 17872–86, doi:10.1523/jneurosci.3894-11.2011.
short: A.R. Woodruff, L.M. McGarry, T.P. Vogels, M. Inan, S.A. Anderson, R. Yuste,
Journal of Neuroscience 31 (2011) 17872–17886.
date_created: 2020-06-25T13:09:49Z
date_published: 2011-12-07T00:00:00Z
date_updated: 2021-01-12T08:16:36Z
day: '7'
doi: 10.1523/jneurosci.3894-11.2011
extern: '1'
external_id:
pmid:
- '22159102'
fulldoi: https://doi.org/10.1523/jneurosci.3894-11.2011
intvolume: ' 31'
issue: '49'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071969/
month: '12'
oa: 1
oa_version: Published Version
page: 17872-17886
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
issn:
- 0270-6474
- 1529-2401
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
status: public
title: State-dependent function of neocortical chandelier cells
type: journal_article
user_id: D865714E-FA4E-11E9-B85B-F5C5E5697425
volume: 31
year: '2011'
...
---
OA_type: closed access
_id: '3826'
abstract:
- lang: eng
text: Gamma frequency (30-100 Hz) oscillations in the mature cortex underlie higher
cognitive functions. Fast signaling in GABAergic interneuron networks plays a
key role in the generation of these oscillations. During development of the rodent
brain, gamma activity appears at the end of the first postnatal week, but frequency
and synchrony reach adult levels only by the fourth week. However, the mechanisms
underlying the maturation of gamma activity are unclear. Here we demonstrate that
hippocampal basket cells (BCs), the proposed cellular substrate of gamma oscillations,
undergo marked changes in their morphological, intrinsic, and synaptic properties
between postnatal day 6 (P6) and P25. During maturation, action potential duration,
propagation time, duration of the release period, and decay time constant of IPSCs
decreases by approximately 30-60%. Thus, postnatal development converts BCs from
slow into fast signaling devices. Computational analysis reveals that BC networks
with young intrinsic and synaptic properties as well as reduced connectivity generate
oscillations with moderate coherence in the lower gamma frequency range. In contrast,
BC networks with mature properties and increased connectivity generate highly
coherent activity in the upper gamma frequency band. Thus, late postnatal maturation
of BCs enhances coherence in neuronal networks and will thereby contribute to
the development of cognitive brain functions.
article_processing_charge: No
article_type: original
author:
- first_name: Daniel
full_name: Doischer, Daniel
last_name: Doischer
- first_name: Jonas
full_name: Hosp, Jonas
last_name: Hosp
- first_name: Yuchio
full_name: Yanagawa, Yuchio
last_name: Yanagawa
- first_name: Kunihiko
full_name: Obata, Kunihiko
last_name: Obata
- 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: Imre
full_name: Vida, Imre
last_name: Vida
- first_name: Marlene
full_name: Bartos, Marlene
last_name: Bartos
citation:
ama: Doischer D, Hosp J, Yanagawa Y, et al. Postnatal differentiation of basket
cells from slow to fast signaling devices. The Journal of Neuroscience.
2008;28(48):12956-12968. doi:10.1523/JNEUROSCI.2890-08.2008
apa: Doischer, D., Hosp, J., Yanagawa, Y., Obata, K., Jonas, P. M., Vida, I., &
Bartos, M. (2008). Postnatal differentiation of basket cells from slow to fast
signaling devices. The Journal of Neuroscience. Society for Neuroscience.
https://doi.org/10.1523/JNEUROSCI.2890-08.2008
chicago: Doischer, Daniel, Jonas Hosp, Yuchio Yanagawa, Kunihiko Obata, Peter M
Jonas, Imre Vida, and Marlene Bartos. “Postnatal Differentiation of Basket Cells
from Slow to Fast Signaling Devices.” The Journal of Neuroscience. Society
for Neuroscience, 2008. https://doi.org/10.1523/JNEUROSCI.2890-08.2008.
ieee: D. Doischer et al., “Postnatal differentiation of basket cells from
slow to fast signaling devices,” The Journal of Neuroscience, vol. 28,
no. 48. Society for Neuroscience, pp. 12956–68, 2008.
ista: Doischer D, Hosp J, Yanagawa Y, Obata K, Jonas PM, Vida I, Bartos M. 2008.
Postnatal differentiation of basket cells from slow to fast signaling devices.
The Journal of Neuroscience. 28(48), 12956–68.
mla: Doischer, Daniel, et al. “Postnatal Differentiation of Basket Cells from Slow
to Fast Signaling Devices.” The Journal of Neuroscience, vol. 28, no. 48,
Society for Neuroscience, 2008, pp. 12956–68, doi:10.1523/JNEUROSCI.2890-08.2008.
short: D. Doischer, J. Hosp, Y. Yanagawa, K. Obata, P.M. Jonas, I. Vida, M. Bartos,
The Journal of Neuroscience 28 (2008) 12956–68.
date_created: 2018-12-11T12:05:23Z
date_published: 2008-01-01T00:00:00Z
date_updated: 2026-05-29T10:46:21Z
day: '01'
doi: 10.1523/JNEUROSCI.2890-08.2008
extern: '1'
external_id:
pmid:
- '19036989'
fulldoi: https://doi.org/10.1523/JNEUROSCI.2890-08.2008
intvolume: ' 28'
issue: '48'
language:
- iso: eng
month: '01'
oa_version: None
page: 12956 - 68
pmid: 1
publication: The Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '2383'
status: public
title: Postnatal differentiation of basket cells from slow to fast signaling devices
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 28
year: '2008'
...
---
OA_type: closed access
_id: '3545'
abstract:
- lang: eng
text: The functional organization of the basal ganglia ( BG) is often defined according
to one of two opposing schemes. The first proposes multiple, essentially independent
channels of information processing. The second posits convergence and lateral
integration of striatal channels at the level of the globus pallidus ( GP). We
tested the hypothesis that these proposed aspects of functional connectivity within
the striatopallidal axis are dynamic and related to brain state. Local field potentials
( LFPs) were simultaneously recorded from multiple sites in striatum and GP in
anesthetized rats during slow-wave activity( SWA) and during global activation
evoked by sensory stimulation. Functional connectivity was inferred from comparative
analyses of the internuclear and intranuclear coherence between bipolar derivations
of LFPs. During prominent SWA, as shown in the electrocorticogram and local field
potentials in the basal ganglia, intranuclear coherence, and, thus, lateral functional
connectivity within striatum or globus pallidus was relatively weak. Furthermore,
the temporal coupling of LFPs recorded across these two nuclei involved functional
convergence at the level of GP. Global activation, indicated by a loss of SWA,
was accompanied by a rapid functional reorganization of the striatopallidal axis.
Prominent lateral functional connectivity developed within GP and, to a significantly
more constrained spatial extent, striatum. Additionally, functional convergence
on GP was no longer apparent, despite increased internuclear coherence. These
data demonstrate that functional connectivity within the BG is highly dynamic
and suggest that the relative expression of organizational principles, such as
parallel, independent processing channels, striatopallidal convergence, and lateral
integration within BG nuclei, is dependent on brain state.
article_processing_charge: No
article_type: original
author:
- first_name: Peter
full_name: Magill, Peter
last_name: Magill
- first_name: Alek
full_name: Pogosyan, Alek
last_name: Pogosyan
- first_name: Andrew
full_name: Sharott, Andrew
last_name: Sharott
- first_name: Jozsef L
full_name: Csicsvari, Jozsef L
id: 3FA14672-F248-11E8-B48F-1D18A9856A87
last_name: Csicsvari
orcid: 0000-0002-5193-4036
- first_name: John
full_name: Bolam, John
last_name: Bolam
- first_name: Peter
full_name: Brown, Peter
last_name: Brown
citation:
ama: Magill P, Pogosyan A, Sharott A, Csicsvari JL, Bolam J, Brown P. Changes in
functional connectivity within the rat striatopallidal axis during global brain
activation in vivo. Journal of Neuroscience. 2006;26(23):6318-6329. doi:10.1523/JNEUROSCI.0620-06.2006
apa: Magill, P., Pogosyan, A., Sharott, A., Csicsvari, J. L., Bolam, J., & Brown,
P. (2006). Changes in functional connectivity within the rat striatopallidal axis
during global brain activation in vivo. Journal of Neuroscience. Society
for Neuroscience. https://doi.org/10.1523/JNEUROSCI.0620-06.2006
chicago: Magill, Peter, Alek Pogosyan, Andrew Sharott, Jozsef L Csicsvari, John
Bolam, and Peter Brown. “Changes in Functional Connectivity within the Rat Striatopallidal
Axis during Global Brain Activation in Vivo.” Journal of Neuroscience.
Society for Neuroscience, 2006. https://doi.org/10.1523/JNEUROSCI.0620-06.2006.
ieee: P. Magill, A. Pogosyan, A. Sharott, J. L. Csicsvari, J. Bolam, and P. Brown,
“Changes in functional connectivity within the rat striatopallidal axis during
global brain activation in vivo,” Journal of Neuroscience, vol. 26, no.
23. Society for Neuroscience, pp. 6318–6329, 2006.
ista: Magill P, Pogosyan A, Sharott A, Csicsvari JL, Bolam J, Brown P. 2006. Changes
in functional connectivity within the rat striatopallidal axis during global brain
activation in vivo. Journal of Neuroscience. 26(23), 6318–6329.
mla: Magill, Peter, et al. “Changes in Functional Connectivity within the Rat Striatopallidal
Axis during Global Brain Activation in Vivo.” Journal of Neuroscience,
vol. 26, no. 23, Society for Neuroscience, 2006, pp. 6318–29, doi:10.1523/JNEUROSCI.0620-06.2006.
short: P. Magill, A. Pogosyan, A. Sharott, J.L. Csicsvari, J. Bolam, P. Brown, Journal
of Neuroscience 26 (2006) 6318–6329.
date_created: 2018-12-11T12:03:53Z
date_published: 2006-06-07T00:00:00Z
date_updated: 2026-08-28T11:11:24Z
day: '07'
doi: 10.1523/JNEUROSCI.0620-06.2006
extern: '1'
external_id:
pmid:
- '16763040'
fulldoi: https://doi.org/10.1523/JNEUROSCI.0620-06.2006
intvolume: ' 26'
issue: '23'
language:
- iso: eng
month: '06'
oa_version: None
page: 6318 - 6329
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '2840'
status: public
title: Changes in functional connectivity within the rat striatopallidal axis during
global brain activation in vivo
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 26
year: '2006'
...
---
_id: '8028'
abstract:
- lang: eng
text: 'Transmission of signals within the brain is essential for cognitive function,
but it is not clear how neural circuits support reliable and accurate signal propagation
over a sufficiently large dynamic range. Two modes of propagation have been studied:
synfire chains, in which synchronous activity travels through feedforward layers
of a neuronal network, and the propagation of fluctuations in firing rate across
these layers. In both cases, a sufficient amount of noise, which was added to
previous models from an external source, had to be included to support stable
propagation. Sparse, randomly connected networks of spiking model neurons can
generate chaotic patterns of activity. We investigate whether this activity, which
is a more realistic noise source, is sufficient to allow for signal transmission.
We find that, for rate-coded signals but not for synfire chains, such networks
support robust and accurate signal reproduction through up to six layers if appropriate
adjustments are made in synaptic strengths. We investigate the factors affecting
transmission and show that multiple signals can propagate simultaneously along
different pathways. Using this feature, we show how different types of logic gates
can arise within the architecture of the random network through the strengthening
of specific synapses.'
article_processing_charge: No
article_type: original
author:
- first_name: Tim P
full_name: Vogels, Tim P
id: CB6FF8D2-008F-11EA-8E08-2637E6697425
last_name: Vogels
orcid: 0000-0003-3295-6181
- first_name: L. F.
full_name: Abbott, L. F.
last_name: Abbott
citation:
ama: Vogels TP, Abbott LF. Signal propagation and logic gating in networks of integrate-and-fire
neurons. Journal of Neuroscience. 2005;25(46):10786-10795. doi:10.1523/jneurosci.3508-05.2005
apa: Vogels, T. P., & Abbott, L. F. (2005). Signal propagation and logic gating
in networks of integrate-and-fire neurons. Journal of Neuroscience. Society
for Neuroscience. https://doi.org/10.1523/jneurosci.3508-05.2005
chicago: Vogels, Tim P, and L. F. Abbott. “Signal Propagation and Logic Gating in
Networks of Integrate-and-Fire Neurons.” Journal of Neuroscience. Society
for Neuroscience, 2005. https://doi.org/10.1523/jneurosci.3508-05.2005.
ieee: T. P. Vogels and L. F. Abbott, “Signal propagation and logic gating in networks
of integrate-and-fire neurons,” Journal of Neuroscience, vol. 25, no. 46.
Society for Neuroscience, pp. 10786–10795, 2005.
ista: Vogels TP, Abbott LF. 2005. Signal propagation and logic gating in networks
of integrate-and-fire neurons. Journal of Neuroscience. 25(46), 10786–10795.
mla: Vogels, Tim P., and L. F. Abbott. “Signal Propagation and Logic Gating in Networks
of Integrate-and-Fire Neurons.” Journal of Neuroscience, vol. 25, no. 46,
Society for Neuroscience, 2005, pp. 10786–95, doi:10.1523/jneurosci.3508-05.2005.
short: T.P. Vogels, L.F. Abbott, Journal of Neuroscience 25 (2005) 10786–10795.
date_created: 2020-06-25T13:12:33Z
date_published: 2005-11-16T00:00:00Z
date_updated: 2021-01-12T08:16:37Z
day: '16'
doi: 10.1523/jneurosci.3508-05.2005
extern: '1'
external_id:
pmid:
- '16291952'
fulldoi: https://doi.org/10.1523/jneurosci.3508-05.2005
intvolume: ' 25'
issue: '46'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6725859/
month: '11'
oa: 1
oa_version: Published Version
page: 10786-10795
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
issn:
- 0270-6474
- 1529-2401
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
status: public
title: Signal propagation and logic gating in networks of integrate-and-fire neurons
type: journal_article
user_id: D865714E-FA4E-11E9-B85B-F5C5E5697425
volume: 25
year: '2005'
...
---
OA_type: closed access
_id: '2654'
abstract:
- lang: eng
text: Presynaptic metabotropic glutamate receptors (mGluRs) show a highly selective
expression and subcellular location in nerve terminals modulating neurotransmitter
release. We have demonstrated that alternatively spliced variants of mGluR8, mGluR8a
and mGluR8b, have an overlapping distribution in the hippocampus, and besides
perforant path terminals, they are expressed in the presynaptic active zone of
boutons making synapses selectively with several types of GABAergic interneurons,
primarily in the stratum oriens. Boutons labeled for mGluR8 formed either type
I or type II synapses, and the latter were GABAergic. Some mGluR8-positive boutons
also expressed mGluR7 or vasoactive intestinal polypeptide. Interneurons strongly
immunopositive for the muscarinic M2 or the mGlu1 receptors were the primary targets
of mGluR8-containing terminals in the stratum oriens, but only neurochemically
distinct subsets were innervated by mGluR8-enriched terminals. The majority of
M2-positive neurons were mGluR8 innervated, but a minority, which expresses somatostatin,
was not. Rare neurons coexpressing calretinin and M2 were consistently targeted
by mGluR8-positive boutons. In vivo recording and labeling of an mGluR8-decorated
and strongly M2-positive interneuron revealed a trilaminar cell with complex spike
bursts during theta oscillations and strong discharge during sharp wave/ripple
events. The trilaminar cell had a large projection from the CA1 area to the subiculum
and a preferential innervation of interneurons in the CA1 area in addition to
pyramidal cell somata and dendrites. The postsynaptic interneuron type-specific
expression of the high-efficacy presynaptic mGluR8 in both putative glutamatergic
and in identified GABAergic terminals predicts a role in adjusting the activity
of interneurons depending on the level of network activity.
article_processing_charge: No
article_type: original
author:
- first_name: Francesco
full_name: Ferraguti, Francesco
last_name: Ferraguti
- first_name: Thomas
full_name: Klausberger, Thomas
last_name: Klausberger
- first_name: Philip
full_name: Cobden, Philip
last_name: Cobden
- first_name: Agnès
full_name: Baude, Agnès
last_name: Baude
- first_name: John
full_name: Roberts, John
last_name: Roberts
- first_name: Péter
full_name: Szűcs, Péter
last_name: Szűcs
- first_name: Ayae
full_name: Kinoshita, Ayae
last_name: Kinoshita
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Péter
full_name: Somogyi, Péter
last_name: Somogyi
- first_name: Yannis
full_name: Dalezios, Yannis
last_name: Dalezios
citation:
ama: Ferraguti F, Klausberger T, Cobden P, et al. Metabotropic glutamate receptor
8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus.
Journal of Neuroscience. 2005;25(45):10520-10536. doi:10.1523/JNEUROSCI.2547-05.2005
apa: Ferraguti, F., Klausberger, T., Cobden, P., Baude, A., Roberts, J., Szűcs,
P., … Dalezios, Y. (2005). Metabotropic glutamate receptor 8-expressing nerve
terminals target subsets of GABAergic neurons in the hippocampus. Journal of
Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2547-05.2005
chicago: Ferraguti, Francesco, Thomas Klausberger, Philip Cobden, Agnès Baude, John
Roberts, Péter Szűcs, Ayae Kinoshita, Ryuichi Shigemoto, Péter Somogyi, and Yannis
Dalezios. “ Metabotropic Glutamate Receptor 8-Expressing Nerve Terminals Target
Subsets of GABAergic Neurons in the Hippocampus.” Journal of Neuroscience.
Society for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.2547-05.2005.
ieee: F. Ferraguti et al., “ Metabotropic glutamate receptor 8-expressing
nerve terminals target subsets of GABAergic neurons in the hippocampus,” Journal
of Neuroscience, vol. 25, no. 45. Society for Neuroscience, pp. 10520–10536,
2005.
ista: Ferraguti F, Klausberger T, Cobden P, Baude A, Roberts J, Szűcs P, Kinoshita
A, Shigemoto R, Somogyi P, Dalezios Y. 2005. Metabotropic glutamate receptor
8-expressing nerve terminals target subsets of GABAergic neurons in the hippocampus.
Journal of Neuroscience. 25(45), 10520–10536.
mla: Ferraguti, Francesco, et al. “ Metabotropic Glutamate Receptor 8-Expressing
Nerve Terminals Target Subsets of GABAergic Neurons in the Hippocampus.” Journal
of Neuroscience, vol. 25, no. 45, Society for Neuroscience, 2005, pp. 10520–36,
doi:10.1523/JNEUROSCI.2547-05.2005.
short: F. Ferraguti, T. Klausberger, P. Cobden, A. Baude, J. Roberts, P. Szűcs,
A. Kinoshita, R. Shigemoto, P. Somogyi, Y. Dalezios, Journal of Neuroscience 25
(2005) 10520–10536.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-11-09T00:00:00Z
date_updated: 2026-07-29T13:10:21Z
day: '09'
doi: 10.1523/JNEUROSCI.2547-05.2005
extern: '1'
external_id:
pmid:
- '16280590'
fulldoi: https://doi.org/10.1523/JNEUROSCI.2547-05.2005
intvolume: ' 25'
issue: '45'
language:
- iso: eng
month: '11'
oa_version: None
page: 10520 - 10536
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '4242'
status: public
title: ' Metabotropic glutamate receptor 8-expressing nerve terminals target subsets
of GABAergic neurons in the hippocampus'
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 25
year: '2005'
...
---
OA_type: closed access
_id: '2652'
abstract:
- lang: eng
text: We studied neurogliaform neurons in the stratum lacunosum moleculare of the
CA1 hippocampal area. These interneurons have short stellate dendrites and an
extensive axonal arbor mainly located in the stratum lacunosum moleculare. Single-cell
reverse transcription-PCR showed that these neurons were GABAergic and that the
majority expressed mRNA for neuropeptide Y. Most neurogliaform neurons tested
were immunoreactive for α-actinin-2, and many stratum lacunosum moleculare interneurons
coexpressed α-actinin-2 and neuropeptide Y. Neurogliaform neurons received monosynaptic,
DNQX-sensitive excitatory input from the perforant path, and 40 Hz stimulation
of this input evoked EPSCs displaying either depression or initial facilitation,
followed by depression. Paired recordings performed between neurogliaform neurons
showed that 85% of pairs were electrically connected and 70% were also connected
via GABAergic synapses. Injection of sine waveforms into neurons during paired
recordings resulted in transmission of the waveforms through the electrical synapse.
Unitary IPSCs recorded from neurogliaform pairs readily fatigued, had a slow decay,
and had a strong depression of the synaptic response at a 5 Hz stimulation frequency
that was antagonized by the GABA B antagonist (2S)-3-[[(1S)-1-(3,4-dichlorophenyl)ethyl]amino-2-hydroxypropyl](phenylmethyl)
phosphinic acid (CGP55845). The amplitude of the first IPSC during the 5 Hz stimulation
was also increased by CGP55845, suggesting a tonic inhibition of synaptic transmission.
A small unitary GABA B-mediated IPSC could also be detected, providing the first
evidence for such a component between GABAergic interneurons. Electron microscopic
localization of the GABA B1 subunit at neurogliaform synapses revealed the protein
in both presynaptic and postsynaptic membranes. Our data disclose a novel interneuronal
network well suited for modulating the flow of information between the entorhinal
cortex and CA1 hippocampus.
article_processing_charge: No
article_type: original
author:
- first_name: Christopher
full_name: Price, Christopher
last_name: Price
- first_name: Bruno
full_name: Cauli, Bruno
last_name: Cauli
- first_name: Endre
full_name: Kovács, Endre
last_name: Kovács
- first_name: Ákos
full_name: Kulik, Ákos
last_name: Kulik
- first_name: Bertrand
full_name: Lambolez, Bertrand
last_name: Lambolez
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Marco
full_name: Capogna, Marco
last_name: Capogna
citation:
ama: Price C, Cauli B, Kovács E, et al. Neurogliaform neurons form a novel inhibitory
network in the hippocampal CA1 area. Journal of Neuroscience. 2005;25(29):6775-6786.
doi:10.1523/JNEUROSCI.1135-05.2005
apa: Price, C., Cauli, B., Kovács, E., Kulik, Á., Lambolez, B., Shigemoto, R., &
Capogna, M. (2005). Neurogliaform neurons form a novel inhibitory network in the
hippocampal CA1 area. Journal of Neuroscience. Society for Neuroscience.
https://doi.org/10.1523/JNEUROSCI.1135-05.2005
chicago: Price, Christopher, Bruno Cauli, Endre Kovács, Ákos Kulik, Bertrand Lambolez,
Ryuichi Shigemoto, and Marco Capogna. “Neurogliaform Neurons Form a Novel Inhibitory
Network in the Hippocampal CA1 Area.” Journal of Neuroscience. Society
for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.1135-05.2005.
ieee: C. Price et al., “Neurogliaform neurons form a novel inhibitory network
in the hippocampal CA1 area,” Journal of Neuroscience, vol. 25, no. 29.
Society for Neuroscience, pp. 6775–6786, 2005.
ista: Price C, Cauli B, Kovács E, Kulik Á, Lambolez B, Shigemoto R, Capogna M. 2005.
Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1 area.
Journal of Neuroscience. 25(29), 6775–6786.
mla: Price, Christopher, et al. “Neurogliaform Neurons Form a Novel Inhibitory Network
in the Hippocampal CA1 Area.” Journal of Neuroscience, vol. 25, no. 29,
Society for Neuroscience, 2005, pp. 6775–86, doi:10.1523/JNEUROSCI.1135-05.2005.
short: C. Price, B. Cauli, E. Kovács, Á. Kulik, B. Lambolez, R. Shigemoto, M. Capogna,
Journal of Neuroscience 25 (2005) 6775–6786.
date_created: 2018-12-11T11:58:53Z
date_published: 2005-07-20T00:00:00Z
date_updated: 2026-08-06T13:38:49Z
day: '20'
doi: 10.1523/JNEUROSCI.1135-05.2005
extern: '1'
external_id:
pmid:
- '16033887'
fulldoi: https://doi.org/10.1523/JNEUROSCI.1135-05.2005
intvolume: ' 25'
issue: '29'
language:
- iso: eng
month: '07'
oa_version: None
page: 6775 - 6786
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '4245'
status: public
title: Neurogliaform neurons form a novel inhibitory network in the hippocampal CA1
area
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 25
year: '2005'
...
---
OA_type: closed access
_id: '2655'
abstract:
- lang: eng
text: Input-dependent left-right asymmetry of NMDA receptor ε2 (NR2B) subunit allocation
was discovered in hippocampal Schaffer collateral (Sch) and commissural fiber
pyramidal cell synapses (Kawakami et al., 2003). To investigate whether this asymmetrical
ε2 allocation is also related to the types of the postsynaptic cells, we compared
postembedding immunogold labeling for ε2 in left and right Sch synapses on pyramidal
cells and interneurons. To facilitate the detection of ε2 density difference,
we used ε1 (NR2A) knock-out (KO) mice, which have a simplified NMDA receptor subunit
composition. The labeling density for ε2 but not ζ1 (NR1) and subtype 2/3 glutamate
receptor (GluR2/3) in Sch-CA1 pyramidal cell synapses was significantly different
between the left and right hippocampus with opposite directions in strata oriens
and radiatum; the left to right ratio of ε2 labeling density was 1:1.50 in stratum
oriens and 1.44:1 in stratum radiatum. No significant difference, however, was
detected in CA1 stratum radiatum between the left and right Sch-GluR4-positive
(mostly parvalbumin-positive) and Sch-GluR4-negative interneuron synapses. Consistent
with the anatomical asymmetry, the amplitude ratio of NMDA EPSCs to non-NMDA EPSCs
in pyramidal cells was approximately two times larger in right than left stratum
radiatum and vice versa in stratum oriens of ε1 KO mice. Moreover, the amplitude
of long-term potentiation in the Sch-CA1 synapses of left stratum radiatum was
significantly larger than that in the right corresponding synapses. These results
indicate that the asymmetry of ε2 distribution is target cell specific, resulting
in the left-right difference in NMDA receptor content and plasticity in Sch-CA1
pyramidal cell synapses in ε1 KO mice.
article_processing_charge: No
article_type: original
author:
- first_name: Yue
full_name: Wu, Yue
last_name: Wu
- first_name: Ryosuke
full_name: Kawakami, Ryosuke
last_name: Kawakami
- first_name: Yoshiaki
full_name: Shinohara, Yoshiaki
last_name: Shinohara
- first_name: Masahiro
full_name: Fukaya, Masahiro
last_name: Fukaya
- first_name: Kenji
full_name: Sakimura, Kenji
last_name: Sakimura
- first_name: Masayoshi
full_name: Mishina, Masayoshi
last_name: Mishina
- first_name: Masahiko
full_name: Watanabe, Masahiko
last_name: Watanabe
- first_name: Isao
full_name: Ito, Isao
last_name: Ito
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Wu Y, Kawakami R, Shinohara Y, et al. Target-cell-specific left-right asymmetry
of NMDA receptor content in Schaffer collateral synapses in ε1/NR2A knock-out
mice. Journal of Neuroscience. 2005;25(40):9213-9226. doi:10.1523/JNEUROSCI.2134-05.2005
apa: Wu, Y., Kawakami, R., Shinohara, Y., Fukaya, M., Sakimura, K., Mishina, M.,
… Shigemoto, R. (2005). Target-cell-specific left-right asymmetry of NMDA receptor
content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal
of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2134-05.2005
chicago: Wu, Yue, Ryosuke Kawakami, Yoshiaki Shinohara, Masahiro Fukaya, Kenji Sakimura,
Masayoshi Mishina, Masahiko Watanabe, Isao Ito, and Ryuichi Shigemoto. “Target-Cell-Specific
Left-Right Asymmetry of NMDA Receptor Content in Schaffer Collateral Synapses
in Ε1/NR2A Knock-out Mice.” Journal of Neuroscience. Society for Neuroscience,
2005. https://doi.org/10.1523/JNEUROSCI.2134-05.2005.
ieee: Y. Wu et al., “Target-cell-specific left-right asymmetry of NMDA receptor
content in Schaffer collateral synapses in ε1/NR2A knock-out mice,” Journal
of Neuroscience, vol. 25, no. 40. Society for Neuroscience, pp. 9213–9226,
2005.
ista: Wu Y, Kawakami R, Shinohara Y, Fukaya M, Sakimura K, Mishina M, Watanabe M,
Ito I, Shigemoto R. 2005. Target-cell-specific left-right asymmetry of NMDA receptor
content in Schaffer collateral synapses in ε1/NR2A knock-out mice. Journal of
Neuroscience. 25(40), 9213–9226.
mla: Wu, Yue, et al. “Target-Cell-Specific Left-Right Asymmetry of NMDA Receptor
Content in Schaffer Collateral Synapses in Ε1/NR2A Knock-out Mice.” Journal
of Neuroscience, vol. 25, no. 40, Society for Neuroscience, 2005, pp. 9213–26,
doi:10.1523/JNEUROSCI.2134-05.2005.
short: Y. Wu, R. Kawakami, Y. Shinohara, M. Fukaya, K. Sakimura, M. Mishina, M.
Watanabe, I. Ito, R. Shigemoto, Journal of Neuroscience 25 (2005) 9213–9226.
date_created: 2018-12-11T11:58:54Z
date_published: 2005-10-05T00:00:00Z
date_updated: 2026-08-06T13:30:33Z
day: '05'
doi: 10.1523/JNEUROSCI.2134-05.2005
extern: '1'
external_id:
pmid:
- '16207881 '
fulldoi: https://doi.org/10.1523/JNEUROSCI.2134-05.2005
intvolume: ' 25'
issue: '40'
language:
- iso: eng
month: '10'
oa_version: None
page: 9213 - 9226
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '4243'
status: public
title: Target-cell-specific left-right asymmetry of NMDA receptor content in Schaffer
collateral synapses in ε1/NR2A knock-out mice
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 25
year: '2005'
...
---
OA_type: closed access
_id: '1298'
abstract:
- lang: eng
text: Genetically encoded fluorescent probes of neural activity represent new promising
tools for systems neuroscience. Here, we present a comparative in vivo analysis
of 10 different genetically encoded calcium indicators, as well as the pH-sensitive
synapto-pHluorin. We analyzed their fluorescence changes in presynaptic boutons
of the Drosophila larval neuromuscular junction. Robust neural activity did not
result in any or noteworthy fluorescence changes when Flash-Pericam, Camgaroo-1,
and Camgaroo-2 were expressed. However, calculated on the raw data, fractional
fluorescence changes up to 18% were reported by synapto-pHluorin, Yellow Cameleon
2.0, 2.3, and 3.3, Inverse-Pericam, GCaMP1.3, GCaMP1.6, and the troponin C-based
calcium sensor TN-L15. The response characteristics of all of these indicators
differed considerably from each other, with GCaMP1.6 reporting high rates of neural
activity with the largest and fastest fluorescence changes. However, GCaMP1.6
suffered from photobleaching, whereas the fluorescence signals of the double-chromophore
indicators were in general smaller but more photostable and reproducible, with
TN-L15 showing the fastest rise of the signals at lower activity rates. We show
for GCaMP1.3 and YC3.3 that an expanded range of neural activity evoked fairly
linear fluorescence changes and a corresponding linear increase in the signal-to-noise
ratio (SNR). The expression level of the indicator biased the signal kinetics
and SNR, whereas the signal amplitude was independent. The presented data will
be useful for in vivo experiments with respect to the selection of an appropriate
indicator, as well as for the correct interpretation of the optical signals.
acknowledgement: This work was supported by the Max-Planck-Society.
article_processing_charge: No
article_type: original
author:
- first_name: Dierk
full_name: Reiff, Dierk
last_name: Reiff
- first_name: Alexandra
full_name: Ihring, Alexandra
last_name: Ihring
- first_name: Giovanna
full_name: Guerrero, Giovanna
last_name: Guerrero
- first_name: Ehud
full_name: Isacoff, Ehud
last_name: Isacoff
- first_name: Maximilian A
full_name: Jösch, Maximilian A
id: 2BD278E6-F248-11E8-B48F-1D18A9856A87
last_name: Jösch
orcid: 0000-0002-3937-1330
- first_name: Junichi
full_name: Nakai, Junichi
last_name: Nakai
- first_name: Alexander
full_name: Borst, Alexander
last_name: Borst
citation:
ama: Reiff D, Ihring A, Guerrero G, et al. In vivo performance of genetically encoded
indicators of neural activity in flies. Journal of Neuroscience. 2005;25(19):4766-4778.
doi:10.1523/JNEUROSCI.4900-04.2005
apa: Reiff, D., Ihring, A., Guerrero, G., Isacoff, E., Jösch, M. A., Nakai, J.,
& Borst, A. (2005). In vivo performance of genetically encoded indicators
of neural activity in flies. Journal of Neuroscience. Society for Neuroscience.
https://doi.org/10.1523/JNEUROSCI.4900-04.2005
chicago: Reiff, Dierk, Alexandra Ihring, Giovanna Guerrero, Ehud Isacoff, Maximilian
A Jösch, Junichi Nakai, and Alexander Borst. “In Vivo Performance of Genetically
Encoded Indicators of Neural Activity in Flies.” Journal of Neuroscience.
Society for Neuroscience, 2005. https://doi.org/10.1523/JNEUROSCI.4900-04.2005.
ieee: D. Reiff et al., “In vivo performance of genetically encoded indicators
of neural activity in flies,” Journal of Neuroscience, vol. 25, no. 19.
Society for Neuroscience, pp. 4766–4778, 2005.
ista: Reiff D, Ihring A, Guerrero G, Isacoff E, Jösch MA, Nakai J, Borst A. 2005.
In vivo performance of genetically encoded indicators of neural activity in flies.
Journal of Neuroscience. 25(19), 4766–4778.
mla: Reiff, Dierk, et al. “In Vivo Performance of Genetically Encoded Indicators
of Neural Activity in Flies.” Journal of Neuroscience, vol. 25, no. 19,
Society for Neuroscience, 2005, pp. 4766–78, doi:10.1523/JNEUROSCI.4900-04.2005.
short: D. Reiff, A. Ihring, G. Guerrero, E. Isacoff, M.A. Jösch, J. Nakai, A. Borst,
Journal of Neuroscience 25 (2005) 4766–4778.
date_created: 2018-12-11T11:51:13Z
date_published: 2005-03-11T00:00:00Z
date_updated: 2026-08-14T10:30:59Z
day: '11'
doi: 10.1523/JNEUROSCI.4900-04.2005
extern: '1'
external_id:
pmid:
- '15888652'
fulldoi: https://doi.org/10.1523/JNEUROSCI.4900-04.2005
intvolume: ' 25'
issue: '19'
language:
- iso: eng
month: '03'
oa_version: None
page: 4766 - 4778
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '5975'
status: public
title: In vivo performance of genetically encoded indicators of neural activity in
flies
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 25
year: '2005'
...
---
OA_type: closed access
_id: '2645'
abstract:
- lang: eng
text: 'The globus pallidus (GP) is a critical component of the basal ganglia circuitry
controlling motor behavior. Dysregulation of GP activity has been implicated in
a number of psychomotor disorders, including Parkinson''s disease (PD), in which
a cardinal feature of the pathophysiology is an alteration in the pattern and
synchrony of discharge in GP neurons. Yet the determinants of this activity in
GP neurons are poorly understood. To help fill this gap, electrophysiological,
molecular, and computational approaches were used to identify and characterize
GABAergic GP neurons in tissue slices from rodents. In vitro, GABAergic GP neurons
generate a regular, autonomous, single-spike pacemaker activity. Hyperpolarization-activated,
cyclic nucleotide-gated cation (HCN) channels make an important contribution to
this process: their blockade with ZD7288 significantly slowed discharge rate and
decreased its regularity. HCN currents evoked by somatic voltage clamp had fast
and slow components. Single-cell RT-PCR and immunohistochemical approaches revealed
robust expression of HCN2 subunits as well as significant levels of HCN1 subunits
in GABAergic GP neurons. Transient activation of striatal GABAergic input to GP
neurons led to a resetting of rhythmic discharge that was dependent on HCN currents.
Simulations suggested that the ability of transient striatal GABAergic input to
reset pacemaking was dependent on dendritic HCN2/HCN1 channels. Together, these
studies show that HCN channels in GABAergic GP neurons are key determinants of
the regularity and rate of pacemaking as well as striatal resetting of this activity,
implicating HCN channels in the emergence of synchrony in PD.'
article_processing_charge: No
article_type: original
author:
- first_name: Savio
full_name: Chan, Savio
last_name: Chan
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Jeff
full_name: Mercer, Jeff
last_name: Mercer
- first_name: James
full_name: Surmeier, James
last_name: Surmeier
citation:
ama: Chan S, Shigemoto R, Mercer J, Surmeier J. HCN2 and HCN1 channels govern the
regularity of autonomous pacemaking and synaptic resetting in globus pallidus
neurons. Journal of Neuroscience. 2004;24(44):9921-9932. doi:10.1523/JNEUROSCI.2162-04.2004
apa: Chan, S., Shigemoto, R., Mercer, J., & Surmeier, J. (2004). HCN2 and HCN1
channels govern the regularity of autonomous pacemaking and synaptic resetting
in globus pallidus neurons. Journal of Neuroscience. Society for Neuroscience.
https://doi.org/10.1523/JNEUROSCI.2162-04.2004
chicago: Chan, Savio, Ryuichi Shigemoto, Jeff Mercer, and James Surmeier. “HCN2
and HCN1 Channels Govern the Regularity of Autonomous Pacemaking and Synaptic
Resetting in Globus Pallidus Neurons.” Journal of Neuroscience. Society
for Neuroscience, 2004. https://doi.org/10.1523/JNEUROSCI.2162-04.2004.
ieee: S. Chan, R. Shigemoto, J. Mercer, and J. Surmeier, “HCN2 and HCN1 channels
govern the regularity of autonomous pacemaking and synaptic resetting in globus
pallidus neurons,” Journal of Neuroscience, vol. 24, no. 44. Society for
Neuroscience, pp. 9921–9932, 2004.
ista: Chan S, Shigemoto R, Mercer J, Surmeier J. 2004. HCN2 and HCN1 channels govern
the regularity of autonomous pacemaking and synaptic resetting in globus pallidus
neurons. Journal of Neuroscience. 24(44), 9921–9932.
mla: Chan, Savio, et al. “HCN2 and HCN1 Channels Govern the Regularity of Autonomous
Pacemaking and Synaptic Resetting in Globus Pallidus Neurons.” Journal of Neuroscience,
vol. 24, no. 44, Society for Neuroscience, 2004, pp. 9921–32, doi:10.1523/JNEUROSCI.2162-04.2004.
short: S. Chan, R. Shigemoto, J. Mercer, J. Surmeier, Journal of Neuroscience 24
(2004) 9921–9932.
date_created: 2018-12-11T11:58:51Z
date_published: 2004-11-03T00:00:00Z
date_updated: 2026-09-22T13:15:36Z
day: '03'
doi: 10.1523/JNEUROSCI.2162-04.2004
extern: '1'
external_id:
pmid:
- '15525777'
fulldoi: https://doi.org/10.1523/JNEUROSCI.2162-04.2004
intvolume: ' 24'
issue: '44'
language:
- iso: eng
month: '11'
oa_version: None
page: 9921 - 9932
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '4252'
status: public
title: HCN2 and HCN1 channels govern the regularity of autonomous pacemaking and synaptic
resetting in globus pallidus neurons
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 24
year: '2004'
...
---
OA_type: closed access
_id: '2641'
abstract:
- lang: eng
text: The Na+-K+ pump current (Ip) and the h-current (Ih) flowing through hyperpolarization-activated
channels (h-channels) participate in generating the resting potential. These two
currents are thought to be produced independently. We show here bidirectional
interactions between Na+-K+ pumps and h-channels in mesencephalic trigeminal neurons.
Activation of Ih leads to the generation of two types of ouabain-sensitive Ip
with temporal profiles similar to those of instantaneous and slow components of
I h, presumably reflecting Na+ transients in a restricted cellular space. Moreover,
the Ip activated by instantaneous I h can facilitate the subsequent activation
of slow Ih. Such counteractive and cooperative interactions were also disclosed
by replacing extracellular Na+ with Li+, which is permeant through h-channels
but does not stimulate the Na+-K+ pump as strongly as Na+ ions. These observations
indicate that the interactions are bidirectional and mediated by Na+ ions. Also
after substitution of extracellular Na+ with Li+, the tail Ih was reduced markedly
despite an enhancement of Ih itself, attributable to a negative shift of the reversal
potential for I h presumably caused by intracellular accumulation of Li+ ions.
This suggests the presence of a microdomain where the interactions can take place.
Thus, the bidirectional interactions between Na+-K + pumps and h-channels are
likely to be mediated by Na+ microdomain. Consistent with these findings, hyperpolarization-activated
and cyclic nucleotide-modulated subunits (HCN1/2) and the Na+-K + pump α3 isoform
were colocalized in plasma membrane of mesencephalic trigeminal neurons having
numerous spines.
article_processing_charge: No
article_type: original
author:
- first_name: Youngnam
full_name: Kang, Youngnam
last_name: Kang
- first_name: Takuya
full_name: Notomi, Takuya
last_name: Notomi
- first_name: Mitsuru
full_name: Saito, Mitsuru
last_name: Saito
- first_name: Wei
full_name: Zhang, Wei
last_name: Zhang
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Kang Y, Notomi T, Saito M, Zhang W, Shigemoto R. Bidirectional interactions
between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons. Journal
of Neuroscience. 2004;24(14):3694-3702. doi:10.1523/JNEUROSCI.5641-03.2004
apa: Kang, Y., Notomi, T., Saito, M., Zhang, W., & Shigemoto, R. (2004). Bidirectional
interactions between H-channels and Na+-K + pumps in mesencephalic trigeminal
neurons. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.5641-03.2004
chicago: Kang, Youngnam, Takuya Notomi, Mitsuru Saito, Wei Zhang, and Ryuichi Shigemoto.
“Bidirectional Interactions between H-Channels and Na+-K + Pumps in Mesencephalic
Trigeminal Neurons.” Journal of Neuroscience. Society for Neuroscience,
2004. https://doi.org/10.1523/JNEUROSCI.5641-03.2004.
ieee: Y. Kang, T. Notomi, M. Saito, W. Zhang, and R. Shigemoto, “Bidirectional interactions
between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons,” Journal
of Neuroscience, vol. 24, no. 14. Society for Neuroscience, pp. 3694–3702,
2004.
ista: Kang Y, Notomi T, Saito M, Zhang W, Shigemoto R. 2004. Bidirectional interactions
between H-channels and Na+-K + pumps in mesencephalic trigeminal neurons. Journal
of Neuroscience. 24(14), 3694–3702.
mla: Kang, Youngnam, et al. “Bidirectional Interactions between H-Channels and Na+-K
+ Pumps in Mesencephalic Trigeminal Neurons.” Journal of Neuroscience,
vol. 24, no. 14, Society for Neuroscience, 2004, pp. 3694–702, doi:10.1523/JNEUROSCI.5641-03.2004.
short: Y. Kang, T. Notomi, M. Saito, W. Zhang, R. Shigemoto, Journal of Neuroscience
24 (2004) 3694–3702.
date_created: 2018-12-11T11:58:49Z
date_published: 2004-04-07T00:00:00Z
date_updated: 2026-09-22T13:22:20Z
day: '07'
doi: 10.1523/JNEUROSCI.5641-03.2004
extern: '1'
external_id:
pmid:
- '15071118'
fulldoi: https://doi.org/10.1523/JNEUROSCI.5641-03.2004
intvolume: ' 24'
issue: '14'
language:
- iso: eng
month: '04'
oa_version: None
page: 3694 - 3702
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '4257'
status: public
title: Bidirectional interactions between H-channels and Na+-K + pumps in mesencephalic
trigeminal neurons
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 24
year: '2004'
...
---
OA_type: closed access
_id: '2635'
abstract:
- lang: eng
text: Metabotropic GABAB receptors mediate slow inhibitory effects presynaptically
and postsynaptically. Using preembedding immunohistochemical methods combined
with quantitative analysis of GABAB receptor subunit immunoreactivity, this study
provides a detailed description of the cellular and subcellular localization of
GABAB1a/b and GABA B2 in the rat hippocampus. At the light microscopic level,
an overlapping distribution of GABAB1a/b and GABAB2 was revealed in the dendritic
layers of the hippocampus. In addition, expression of the GABAB1a/b subunit was
found in somata of CA1 pyramidal cells and of a subset of GABAergic interneurons.
At the electron microscopic level, immunoreactivity for both subunits was observed
on presynaptic and, more abundantly, on postsynaptic elements. Presynaptically,
subunits were mainly detected in the extrasynaptic membrane and occasionally over
the presynaptic membrane specialization of putative glutamatergic and, to a lesser
extent, GABAergic axon terminals. Postsynaptically, the majority of GABAB receptor
subunits were localized to the extrasynaptic plasma membrane of spines and dendritic
shafts of principal cells and shafts of interneuron dendrites. Quantitative analysis
revealed enrichment of GABAB1a/b around putative glutamatergic synapses on spines
and an even distribution on dendritic shafts of pyramidal cells contacted by GABAergic
boutons. The association of GABAB receptors with glutamatergic synapses at both
presynaptic and postsynaptic sides indicates their intimate involvement in the
modulation of glutamatergic neurotransmission. The dominant extrasynaptic localization
of GABAB receptor subunits suggests that their activation is dependent on spillover
of GABA requiring simultaneous activity of populations of GABAergic cells as it
occurs during population oscillations or epileptic seizures.
article_processing_charge: No
article_type: original
author:
- first_name: Ákos
full_name: Kulik, Ákos
last_name: Kulik
- first_name: Imre
full_name: Vida, Imre
last_name: Vida
- first_name: Rafael
full_name: Luján, Rafael
last_name: Luján
- first_name: Carola
full_name: Haas, Carola
last_name: Haas
- first_name: Guillermina
full_name: López Bendito, Guillermina
last_name: López Bendito
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Michael
full_name: Frotscher, Michael
last_name: Frotscher
citation:
ama: Kulik Á, Vida I, Luján R, et al. Subcellular Localization of Metabotropic GABAB
Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus. Journal of Neuroscience.
2003;23(35):11026-11035. doi:10.1523/JNEUROSCI.23-35-11026.2003
apa: Kulik, Á., Vida, I., Luján, R., Haas, C., López Bendito, G., Shigemoto, R.,
& Frotscher, M. (2003). Subcellular Localization of Metabotropic GABAB Receptor
Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus. Journal of Neuroscience.
Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003
chicago: Kulik, Ákos, Imre Vida, Rafael Luján, Carola Haas, Guillermina López Bendito,
Ryuichi Shigemoto, and Michael Frotscher. “Subcellular Localization of Metabotropic
GABAB Receptor Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus.” Journal
of Neuroscience. Society for Neuroscience, 2003. https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003.
ieee: Á. Kulik et al., “Subcellular Localization of Metabotropic GABAB Receptor
Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus,” Journal of Neuroscience,
vol. 23, no. 35. Society for Neuroscience, pp. 11026–11035, 2003.
ista: Kulik Á, Vida I, Luján R, Haas C, López Bendito G, Shigemoto R, Frotscher
M. 2003. Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b
and GABAB2 in the Rat Hippocampus. Journal of Neuroscience. 23(35), 11026–11035.
mla: Kulik, Ákos, et al. “Subcellular Localization of Metabotropic GABAB Receptor
Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus.” Journal of Neuroscience,
vol. 23, no. 35, Society for Neuroscience, 2003, pp. 11026–35, doi:10.1523/JNEUROSCI.23-35-11026.2003.
short: Á. Kulik, I. Vida, R. Luján, C. Haas, G. López Bendito, R. Shigemoto, M.
Frotscher, Journal of Neuroscience 23 (2003) 11026–11035.
date_created: 2018-12-11T11:58:47Z
date_published: 2003-12-03T00:00:00Z
date_updated: 2026-05-22T09:50:16Z
day: '03'
doi: 10.1523/JNEUROSCI.23-35-11026.2003
extern: '1'
external_id:
pmid:
- '14657159'
fulldoi: https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003
intvolume: ' 23'
issue: '35'
language:
- iso: eng
month: '12'
oa_version: None
page: 11026 - 11035
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '4263'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Subcellular Localization of Metabotropic GABAB Receptor Subunits GABAB1a/b
and GABAB2 in the Rat Hippocampus
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 23
year: '2003'
...