---
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. <i>Journal of Neuroscience</i>. 2025;45(13).
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">10.1523/JNEUROSCI.1767-23.2024</a>
  apa: Stratigi, A., Soler-García, M., Krout, M., Shukla, S., de Bono, M., Richmond,
    J. E., &#38; Laurent, P. (2025). Neuroendocrine control of synaptic transmission
    by PHAC-1 in C. elegans. <i>Journal of Neuroscience</i>. Society for Neuroscience.
    <a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">https://doi.org/10.1523/JNEUROSCI.1767-23.2024</a>
  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.” <i>Journal of Neuroscience</i>. Society
    for Neuroscience, 2025. <a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">https://doi.org/10.1523/JNEUROSCI.1767-23.2024</a>.
  ieee: A. Stratigi <i>et al.</i>, “Neuroendocrine control of synaptic transmission
    by PHAC-1 in C. elegans,” <i>Journal of Neuroscience</i>, 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.” <i>Journal of Neuroscience</i>, vol. 45, no. 13, e1767232024,
    Society for Neuroscience, 2025, doi:<a href="https://doi.org/10.1523/JNEUROSCI.1767-23.2024">10.1523/JNEUROSCI.1767-23.2024</a>.
  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: 2025-09-30T11:29:28Z
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
has_accepted_license: '1'
intvolume: '        45'
isi: 1
issue: '13'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 45
year: '2025'
...
---
OA_embargo: 6 months
OA_place: publisher
OA_type: hybrid
_id: '18305'
abstract:
- lang: eng
  text: Motor circuits represent the main output of the central nervous system and
    produce dynamic behaviors ranging from relatively simple rhythmic activities like
    swimming in fish and breathing in mammals to highly sophisticated dexterous movements
    in humans. Despite decades of research, the development and function of motor
    circuits remain poorly understood. Breakthroughs in the field recently provided
    new tools and tractable model systems that set the stage to discover the molecular
    mechanisms and circuit logic underlying motor control. Here, we describe recent
    advances from both vertebrate (mouse, frog) and invertebrate (nematode, fruit
    fly) systems on cellular and molecular mechanisms that enable motor circuits to
    develop and function and highlight conserved and divergent mechanisms necessary
    for motor circuit development.
acknowledgement: Work in the authors’ labs is funded by the Helmholtz Association
  (N.Z.), National Institute of Neurological Disorders and Stroke (NINDS) R01NS116365
  (P.K.), NINDS R01NS123439 and National Science Foundation IOS-2048080 (R.C.), NINDS
  R01NS114510 (P.P.), Natural Sciences and Engineering Research Council of Canada
  RGPIN-2021-03154 (K.M.) and Horizon Europe European Research Council Starting Grant
  Number 101041551 (L.B.S.). P.P. is the Weidenthal Family Designated Professor in
  Career Development.
article_number: e1238242024
article_processing_charge: No
article_type: original
author:
- first_name: Paschalis
  full_name: Kratsios, Paschalis
  last_name: Kratsios
- first_name: Niccolò
  full_name: Zampieri, Niccolò
  last_name: Zampieri
- first_name: Robert
  full_name: Carrillo, Robert
  last_name: Carrillo
- first_name: Kota
  full_name: Mizumoto, Kota
  last_name: Mizumoto
- first_name: Lora Beatrice Jaeger
  full_name: Sweeney, Lora Beatrice Jaeger
  id: 56BE8254-C4F0-11E9-8E45-0B23E6697425
  last_name: Sweeney
  orcid: 0000-0001-9242-5601
- first_name: Polyxeni
  full_name: Philippidou, Polyxeni
  last_name: Philippidou
citation:
  ama: Kratsios P, Zampieri N, Carrillo R, Mizumoto K, Sweeney LB, Philippidou P.
    Molecular and cellular mechanisms of motor circuit development. <i>The Journal
    of Neuroscience</i>. 2024;44(40). doi:<a href="https://doi.org/10.1523/JNEUROSCI.1238-24.2024">10.1523/JNEUROSCI.1238-24.2024</a>
  apa: Kratsios, P., Zampieri, N., Carrillo, R., Mizumoto, K., Sweeney, L. B., &#38;
    Philippidou, P. (2024). Molecular and cellular mechanisms of motor circuit development.
    <i>The Journal of Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.1238-24.2024">https://doi.org/10.1523/JNEUROSCI.1238-24.2024</a>
  chicago: Kratsios, Paschalis, Niccolò Zampieri, Robert Carrillo, Kota Mizumoto,
    Lora B. Sweeney, and Polyxeni Philippidou. “Molecular and Cellular Mechanisms
    of Motor Circuit Development.” <i>The Journal of Neuroscience</i>. Society for
    Neuroscience, 2024. <a href="https://doi.org/10.1523/JNEUROSCI.1238-24.2024">https://doi.org/10.1523/JNEUROSCI.1238-24.2024</a>.
  ieee: P. Kratsios, N. Zampieri, R. Carrillo, K. Mizumoto, L. B. Sweeney, and P.
    Philippidou, “Molecular and cellular mechanisms of motor circuit development,”
    <i>The Journal of Neuroscience</i>, vol. 44, no. 40. Society for Neuroscience,
    2024.
  ista: Kratsios P, Zampieri N, Carrillo R, Mizumoto K, Sweeney LB, Philippidou P.
    2024. Molecular and cellular mechanisms of motor circuit development. The Journal
    of Neuroscience. 44(40), e1238242024.
  mla: Kratsios, Paschalis, et al. “Molecular and Cellular Mechanisms of Motor Circuit
    Development.” <i>The Journal of Neuroscience</i>, vol. 44, no. 40, e1238242024,
    Society for Neuroscience, 2024, doi:<a href="https://doi.org/10.1523/JNEUROSCI.1238-24.2024">10.1523/JNEUROSCI.1238-24.2024</a>.
  short: P. Kratsios, N. Zampieri, R. Carrillo, K. Mizumoto, L.B. Sweeney, P. Philippidou,
    The Journal of Neuroscience 44 (2024).
date_created: 2024-10-13T22:01:49Z
date_published: 2024-10-02T00:00:00Z
date_updated: 2026-01-05T14:01:26Z
day: '02'
ddc:
- '570'
department:
- _id: LoSw
doi: 10.1523/JNEUROSCI.1238-24.2024
external_id:
  isi:
  - '001335212200016'
  pmid:
  - '39358025'
has_accepted_license: '1'
intvolume: '        44'
isi: 1
issue: '40'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1523/JNEUROSCI.1238-24.2024
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: ebb66355-77a9-11ec-83b8-b8ac210a4dae
  grant_number: '101041551'
  name: Development and Evolution of Tetrapod Motor Circuits
publication: The Journal of Neuroscience
publication_identifier:
  eissn:
  - 1529-2401
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular and cellular mechanisms of motor circuit development
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 44
year: '2024'
...
---
_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. <i>Journal of Neuroscience</i>. 2024;44(21).
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.0846-23.2024">10.1523/JNEUROSCI.0846-23.2024</a>
  apa: Delamare, G., Feitosa Tomé, D., &#38; Clopath, C. (2024). Intrinsic neural
    excitability biases allocation and overlap of memory engrams. <i>Journal of Neuroscience</i>.
    Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.0846-23.2024">https://doi.org/10.1523/JNEUROSCI.0846-23.2024</a>
  chicago: Delamare, Geoffroy, Douglas Feitosa Tomé, and Claudia Clopath. “Intrinsic
    Neural Excitability Biases Allocation and Overlap of Memory Engrams.” <i>Journal
    of Neuroscience</i>. Society for Neuroscience, 2024. <a href="https://doi.org/10.1523/JNEUROSCI.0846-23.2024">https://doi.org/10.1523/JNEUROSCI.0846-23.2024</a>.
  ieee: G. Delamare, D. Feitosa Tomé, and C. Clopath, “Intrinsic neural excitability
    biases allocation and overlap of memory engrams,” <i>Journal of Neuroscience</i>,
    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.” <i>Journal of Neuroscience</i>, vol. 44, no. 21,
    e0846232024, Society for Neuroscience, 2024, doi:<a href="https://doi.org/10.1523/JNEUROSCI.0846-23.2024">10.1523/JNEUROSCI.0846-23.2024</a>.
  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
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. <i>The Journal of Neuroscience</i>.
    2023;43(23):4197-4216. doi:<a href="https://doi.org/10.1523/JNEUROSCI.1514-22.2023">10.1523/JNEUROSCI.1514-22.2023</a>
  apa: Eguchi, K., Le Monnier, E., &#38; Shigemoto, R. (2023). Nanoscale phosphoinositide
    distribution on cell membranes of mouse cerebellar neurons. <i>The Journal of
    Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.1514-22.2023">https://doi.org/10.1523/JNEUROSCI.1514-22.2023</a>
  chicago: Eguchi, Kohgaku, Elodie Le Monnier, and Ryuichi Shigemoto. “Nanoscale Phosphoinositide
    Distribution on Cell Membranes of Mouse Cerebellar Neurons.” <i>The Journal of
    Neuroscience</i>. Society for Neuroscience, 2023. <a href="https://doi.org/10.1523/JNEUROSCI.1514-22.2023">https://doi.org/10.1523/JNEUROSCI.1514-22.2023</a>.
  ieee: K. Eguchi, E. Le Monnier, and R. Shigemoto, “Nanoscale phosphoinositide distribution
    on cell membranes of mouse cerebellar neurons,” <i>The Journal of Neuroscience</i>,
    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.” <i>The Journal of Neuroscience</i>, vol. 43, no.
    23, Society for Neuroscience, 2023, pp. 4197–216, doi:<a href="https://doi.org/10.1523/JNEUROSCI.1514-22.2023">10.1523/JNEUROSCI.1514-22.2023</a>.
  short: K. Eguchi, E. Le Monnier, R. Shigemoto, The Journal of Neuroscience 43 (2023)
    4197–4216.
corr_author: '1'
date_created: 2023-07-09T22:01:12Z
date_published: 2023-06-07T00:00:00Z
date_updated: 2025-04-14T07:27:15Z
day: '07'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1523/JNEUROSCI.1514-22.2023
ec_funded: 1
external_id:
  isi:
  - '001020132100005'
  pmid:
  - '37160366'
file:
- access_level: open_access
  checksum: 70b2141870e0bf1c94fd343e18fdbc32
  content_type: application/pdf
  creator: alisjak
  date_created: 2023-07-10T09:04:58Z
  date_updated: 2023-07-10T09:04:58Z
  file_id: '13205'
  file_name: 2023_JN_Eguchi.pdf
  file_size: 7794425
  relation: main_file
  success: 1
file_date_updated: 2023-07-10T09:04:58Z
has_accepted_license: '1'
intvolume: '        43'
isi: 1
issue: '23'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: 4197-4216
pmid: 1
project:
- _id: 2659CC84-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '793482'
  name: 'Ultrastructural analysis of phosphoinositides in nerve terminals: distribution,
    dynamics and physiological roles in synaptic transmission'
- _id: 25CA28EA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '694539'
  name: 'In situ analysis of single channel subunit composition in neurons: physiological
    implication in synaptic plasticity and behaviour'
publication: The Journal of Neuroscience
publication_identifier:
  eissn:
  - 1529-2401
  issn:
  - 0270-6474
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: Nanoscale phosphoinositide distribution on cell membranes of mouse cerebellar
  neurons
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 43
year: '2023'
...
---
_id: '14656'
abstract:
- lang: eng
  text: Although much is known about how single neurons in the hippocampus represent
    an animal's position, how circuit interactions contribute to spatial coding is
    less well understood. Using a novel statistical estimator and theoretical modeling,
    both developed in the framework of maximum entropy models, we reveal highly structured
    CA1 cell-cell interactions in male rats during open field exploration. The statistics
    of these interactions depend on whether the animal is in a familiar or novel environment.
    In both conditions the circuit interactions optimize the encoding of spatial information,
    but for regimes that differ in the informativeness of their spatial inputs. This
    structure facilitates linear decodability, making the information easy to read
    out by downstream circuits. Overall, our findings suggest that the efficient coding
    hypothesis is not only applicable to individual neuron properties in the sensory
    periphery, but also to neural interactions in the central brain.
acknowledgement: M.N. was supported by the European Union Horizon 2020 Grant 665385.
  J.C. was supported by the European Research Council Consolidator Grant 281511. G.T.
  was supported by the Austrian Science Fund (FWF) Grant P34015. C.S. was supported
  by an Institute of Science and Technology fellow award and by the National Science
  Foundation (NSF) Award No. 1922658. We thank Peter Baracskay, Karola Kaefer, and
  Hugo Malagon-Vina for the acquisition of the data. We also thank Federico Stella,
  Wiktor Młynarski, Dori Derdikman, Colin Bredenberg, Roman Huszar, Heloisa Chiossi,
  Lorenzo Posani, and Mohamady El-Gaby for comments on an earlier version of the manuscript.
article_processing_charge: Yes (in subscription journal)
article_type: original
author:
- first_name: Michele
  full_name: Nardin, Michele
  id: 30BD0376-F248-11E8-B48F-1D18A9856A87
  last_name: Nardin
  orcid: 0000-0001-8849-6570
- 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: Gašper
  full_name: Tkačik, Gašper
  id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
  last_name: Tkačik
  orcid: 0000-0002-6699-1455
- first_name: Cristina
  full_name: Savin, Cristina
  id: 3933349E-F248-11E8-B48F-1D18A9856A87
  last_name: Savin
citation:
  ama: Nardin M, Csicsvari JL, Tkačik G, Savin C. The structure of hippocampal CA1
    interactions optimizes spatial coding across experience. <i>The Journal of Neuroscience</i>.
    2023;43(48):8140-8156. doi:<a href="https://doi.org/10.1523/JNEUROSCI.0194-23.2023">10.1523/JNEUROSCI.0194-23.2023</a>
  apa: Nardin, M., Csicsvari, J. L., Tkačik, G., &#38; Savin, C. (2023). The structure
    of hippocampal CA1 interactions optimizes spatial coding across experience. <i>The
    Journal of Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.0194-23.2023">https://doi.org/10.1523/JNEUROSCI.0194-23.2023</a>
  chicago: Nardin, Michele, Jozsef L Csicsvari, Gašper Tkačik, and Cristina Savin.
    “The Structure of Hippocampal CA1 Interactions Optimizes Spatial Coding across
    Experience.” <i>The Journal of Neuroscience</i>. Society for Neuroscience, 2023.
    <a href="https://doi.org/10.1523/JNEUROSCI.0194-23.2023">https://doi.org/10.1523/JNEUROSCI.0194-23.2023</a>.
  ieee: M. Nardin, J. L. Csicsvari, G. Tkačik, and C. Savin, “The structure of hippocampal
    CA1 interactions optimizes spatial coding across experience,” <i>The Journal of
    Neuroscience</i>, vol. 43, no. 48. Society for Neuroscience, pp. 8140–8156, 2023.
  ista: Nardin M, Csicsvari JL, Tkačik G, Savin C. 2023. The structure of hippocampal
    CA1 interactions optimizes spatial coding across experience. The Journal of Neuroscience.
    43(48), 8140–8156.
  mla: Nardin, Michele, et al. “The Structure of Hippocampal CA1 Interactions Optimizes
    Spatial Coding across Experience.” <i>The Journal of Neuroscience</i>, vol. 43,
    no. 48, Society for Neuroscience, 2023, pp. 8140–56, doi:<a href="https://doi.org/10.1523/JNEUROSCI.0194-23.2023">10.1523/JNEUROSCI.0194-23.2023</a>.
  short: M. Nardin, J.L. Csicsvari, G. Tkačik, C. Savin, The Journal of Neuroscience
    43 (2023) 8140–8156.
date_created: 2023-12-10T23:00:58Z
date_published: 2023-11-29T00:00:00Z
date_updated: 2025-09-09T13:37:51Z
day: '29'
ddc:
- '570'
department:
- _id: JoCs
- _id: GaTk
doi: 10.1523/JNEUROSCI.0194-23.2023
ec_funded: 1
external_id:
  isi:
  - '001148071000005'
  pmid:
  - '37758476'
file:
- access_level: open_access
  checksum: e2503c8f84be1050e28f64320f1d5bd2
  content_type: application/pdf
  creator: dernst
  date_created: 2023-12-11T11:30:37Z
  date_updated: 2024-06-02T22:30:03Z
  embargo: 2024-06-01
  file_id: '14674'
  file_name: 2023_JourNeuroscience_Nardin.pdf
  file_size: 2280632
  relation: main_file
file_date_updated: 2024-06-02T22:30:03Z
has_accepted_license: '1'
intvolume: '        43'
isi: 1
issue: '48'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 8140-8156
pmid: 1
project:
- _id: 257A4776-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '281511'
  name: Memory-related information processing in neuronal circuits of the hippocampus
    and entorhinal cortex
- _id: 626c45b5-2b32-11ec-9570-e509828c1ba6
  grant_number: P34015
  name: Efficient coding with biophysical realism
- _id: 2564DBCA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '665385'
  name: International IST Doctoral Program
publication: The Journal of Neuroscience
publication_identifier:
  eissn:
  - 1529-2401
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
related_material:
  record:
  - id: '10077'
    relation: earlier_version
    status: public
scopus_import: '1'
status: public
title: The structure of hippocampal CA1 interactions optimizes spatial coding across
  experience
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: 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 Ca<sup>21</sup>
    channel topography and regulates release probability and vesicle replenishment
    at a fast central synapse. <i>Journal of Neuroscience</i>. 2021;41(37):7742-7767.
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.0586-21.2021">10.1523/JNEUROSCI.0586-21.2021</a>
  apa: Butola, T., Alvanos, T., Hintze, A., Koppensteiner, P., Kleindienst, D., Shigemoto,
    R., … Moser, T. (2021). RIM-binding protein 2 organizes Ca<sup>21</sup> channel
    topography and regulates release probability and vesicle replenishment at a fast
    central synapse. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a
    href="https://doi.org/10.1523/JNEUROSCI.0586-21.2021">https://doi.org/10.1523/JNEUROSCI.0586-21.2021</a>
  chicago: Butola, Tanvi, Theocharis Alvanos, Anika Hintze, Peter Koppensteiner, David
    Kleindienst, Ryuichi Shigemoto, Carolin Wichmann, and Tobias Moser. “RIM-Binding
    Protein 2 Organizes Ca<sup>21</sup> Channel Topography and Regulates Release Probability
    and Vesicle Replenishment at a Fast Central Synapse.” <i>Journal of Neuroscience</i>.
    Society for Neuroscience, 2021. <a href="https://doi.org/10.1523/JNEUROSCI.0586-21.2021">https://doi.org/10.1523/JNEUROSCI.0586-21.2021</a>.
  ieee: T. Butola <i>et al.</i>, “RIM-binding protein 2 organizes Ca<sup>21</sup>
    channel topography and regulates release probability and vesicle replenishment
    at a fast central synapse,” <i>Journal of Neuroscience</i>, 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 Ca<sup>21</sup> 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 Ca<sup>21</sup> Channel
    Topography and Regulates Release Probability and Vesicle Replenishment at a Fast
    Central Synapse.” <i>Journal of Neuroscience</i>, vol. 41, no. 37, Society for
    Neuroscience, 2021, pp. 7742–67, doi:<a href="https://doi.org/10.1523/JNEUROSCI.0586-21.2021">10.1523/JNEUROSCI.0586-21.2021</a>.
  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
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 Ca<sup>21</sup> 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. <i>The Journal of Neuroscience</i>. 2021;41(5):813-822.
    doi:<a href="https://doi.org/10.1523/jneurosci.1655-20.2020">10.1523/jneurosci.1655-20.2020</a>
  apa: Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N.
    V., Cardin, J. A., Voytek, B., &#38; Muotri, A. R. (2021). The logic of developing
    neocortical circuits in health and disease. <i>The Journal of Neuroscience</i>.
    Society for Neuroscience. <a href="https://doi.org/10.1523/jneurosci.1655-20.2020">https://doi.org/10.1523/jneurosci.1655-20.2020</a>
  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.” <i>The Journal
    of Neuroscience</i>. Society for Neuroscience, 2021. <a href="https://doi.org/10.1523/jneurosci.1655-20.2020">https://doi.org/10.1523/jneurosci.1655-20.2020</a>.
  ieee: I. L. Hanganu-Opatz <i>et al.</i>, “The logic of developing neocortical circuits
    in health and disease,” <i>The Journal of Neuroscience</i>, 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.” <i>The Journal of Neuroscience</i>, vol. 41, no. 5, Society
    for Neuroscience, 2021, pp. 813–22, doi:<a href="https://doi.org/10.1523/jneurosci.1655-20.2020">10.1523/jneurosci.1655-20.2020</a>.
  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
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: '7908'
abstract:
- lang: eng
  text: Volatile anesthetics are widely used for surgery, but neuronal mechanisms
    of anesthesia remain unidentified. At the calyx of Held in brainstem slices from
    rats of either sex, isoflurane at clinical doses attenuated EPSCs by decreasing
    the release probability and the number of readily releasable vesicles. In presynaptic
    recordings of Ca2+ currents and exocytic capacitance changes, isoflurane attenuated
    exocytosis by inhibiting Ca2+ currents evoked by a short presynaptic depolarization,
    whereas it inhibited exocytosis evoked by a prolonged depolarization via directly
    blocking exocytic machinery downstream of Ca2+ influx. Since the length of presynaptic
    depolarization can simulate the frequency of synaptic inputs, isoflurane anesthesia
    is likely mediated by distinct dual mechanisms, depending on input frequencies.
    In simultaneous presynaptic and postsynaptic action potential recordings, isoflurane
    impaired the fidelity of repetitive spike transmission, more strongly at higher
    frequencies. Furthermore, in the cerebrum of adult mice, isoflurane inhibited
    monosynaptic corticocortical spike transmission, preferentially at a higher frequency.
    We conclude that dual presynaptic mechanisms operate for the anesthetic action
    of isoflurane, of which direct inhibition of exocytic machinery plays a low-pass
    filtering role in spike transmission at central excitatory synapses.
article_processing_charge: No
article_type: original
author:
- 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: Takayuki
  full_name: Yamashita, Takayuki
  last_name: Yamashita
- first_name: Tomoyuki
  full_name: Takahashi, Tomoyuki
  last_name: Takahashi
citation:
  ama: Wang HY, Eguchi K, Yamashita T, Takahashi T. Frequency-dependent block of excitatory
    neurotransmission by isoflurane via dual presynaptic mechanisms. <i>Journal of
    Neuroscience</i>. 2020;40(21):4103-4115. doi:<a href="https://doi.org/10.1523/JNEUROSCI.2946-19.2020">10.1523/JNEUROSCI.2946-19.2020</a>
  apa: Wang, H. Y., Eguchi, K., Yamashita, T., &#38; Takahashi, T. (2020). Frequency-dependent
    block of excitatory neurotransmission by isoflurane via dual presynaptic mechanisms.
    <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.2946-19.2020">https://doi.org/10.1523/JNEUROSCI.2946-19.2020</a>
  chicago: Wang, Han Ying, Kohgaku Eguchi, Takayuki Yamashita, and Tomoyuki Takahashi.
    “Frequency-Dependent Block of Excitatory Neurotransmission by Isoflurane via Dual
    Presynaptic Mechanisms.” <i>Journal of Neuroscience</i>. Society for Neuroscience,
    2020. <a href="https://doi.org/10.1523/JNEUROSCI.2946-19.2020">https://doi.org/10.1523/JNEUROSCI.2946-19.2020</a>.
  ieee: H. Y. Wang, K. Eguchi, T. Yamashita, and T. Takahashi, “Frequency-dependent
    block of excitatory neurotransmission by isoflurane via dual presynaptic mechanisms,”
    <i>Journal of Neuroscience</i>, vol. 40, no. 21. Society for Neuroscience, pp.
    4103–4115, 2020.
  ista: Wang HY, Eguchi K, Yamashita T, Takahashi T. 2020. Frequency-dependent block
    of excitatory neurotransmission by isoflurane via dual presynaptic mechanisms.
    Journal of Neuroscience. 40(21), 4103–4115.
  mla: Wang, Han Ying, et al. “Frequency-Dependent Block of Excitatory Neurotransmission
    by Isoflurane via Dual Presynaptic Mechanisms.” <i>Journal of Neuroscience</i>,
    vol. 40, no. 21, Society for Neuroscience, 2020, pp. 4103–15, doi:<a href="https://doi.org/10.1523/JNEUROSCI.2946-19.2020">10.1523/JNEUROSCI.2946-19.2020</a>.
  short: H.Y. Wang, K. Eguchi, T. Yamashita, T. Takahashi, Journal of Neuroscience
    40 (2020) 4103–4115.
date_created: 2020-05-31T22:00:48Z
date_published: 2020-05-20T00:00:00Z
date_updated: 2025-03-07T08:29:32Z
day: '20'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1523/JNEUROSCI.2946-19.2020
external_id:
  isi:
  - '000535694700004'
  pmid:
  - '32327530'
file:
- access_level: open_access
  checksum: 6571607ea9036154b67cc78e848a7f7d
  content_type: application/pdf
  creator: dernst
  date_created: 2020-06-02T09:12:16Z
  date_updated: 2020-07-14T12:48:05Z
  file_id: '7912'
  file_name: 2020_JourNeuroscience_Wang.pdf
  file_size: 3817360
  relation: main_file
file_date_updated: 2020-07-14T12:48:05Z
has_accepted_license: '1'
intvolume: '        40'
isi: 1
issue: '21'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 4103-4115
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
  eissn:
  - 1529-2401
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: Frequency-dependent block of excitatory neurotransmission by isoflurane via
  dual presynaptic mechanisms
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: 40
year: '2020'
...
---
_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.
    <i>Journal of Neuroscience</i>. 2020;40(1):171-190. doi:<a href="https://doi.org/10.1523/jneurosci.1278-19.2019">10.1523/jneurosci.1278-19.2019</a>
  apa: Lombardi, F., Gómez-Extremera, M., Bernaola-Galván, P., Vetrivelan, R., Saper,
    C. B., Scammell, T. E., &#38; 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. <i>Journal of
    Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/jneurosci.1278-19.2019">https://doi.org/10.1523/jneurosci.1278-19.2019</a>
  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.”
    <i>Journal of Neuroscience</i>. Society for Neuroscience, 2020. <a href="https://doi.org/10.1523/jneurosci.1278-19.2019">https://doi.org/10.1523/jneurosci.1278-19.2019</a>.
  ieee: F. Lombardi <i>et al.</i>, “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,” <i>Journal of Neuroscience</i>,
    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.” <i>Journal of Neuroscience</i>,
    vol. 40, no. 1, Society for Neuroscience, 2020, pp. 171–90, doi:<a href="https://doi.org/10.1523/jneurosci.1278-19.2019">10.1523/jneurosci.1278-19.2019</a>.
  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
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: '8126'
abstract:
- lang: eng
  text: Cortical areas comprise multiple types of inhibitory interneurons with stereotypical
    connectivity motifs, but their combined effect on postsynaptic dynamics has been
    largely unexplored. Here, we analyse the response of a single postsynaptic model
    neuron receiving tuned excitatory connections alongside inhibition from two plastic
    populations. Depending on the inhibitory plasticity rule, synapses remain unspecific
    (flat), become anti-correlated to, or mirror excitatory synapses. Crucially, the
    neuron’s receptive field, i.e., its response to presynaptic stimuli, depends on
    the modulatory state of inhibition. When both inhibitory populations are active,
    inhibition balances excitation, resulting in uncorrelated postsynaptic responses
    regardless of the inhibitory tuning profiles. Modulating the activity of a given
    inhibitory population produces strong correlations to either preferred or non-preferred
    inputs, in line with recent experimental findings showing dramatic context-dependent
    changes of neurons’ receptive fields. We thus confirm that a neuron’s receptive
    field doesn’t follow directly from the weight profiles of its presynaptic afferents.
article_processing_charge: No
article_type: original
author:
- first_name: Everton J.
  full_name: Agnes, Everton J.
  last_name: Agnes
  orcid: 0000-0001-7184-7311
- first_name: Andrea I.
  full_name: Luppi, Andrea I.
  last_name: Luppi
- first_name: Tim P
  full_name: Vogels, Tim P
  id: CB6FF8D2-008F-11EA-8E08-2637E6697425
  last_name: Vogels
  orcid: 0000-0003-3295-6181
citation:
  ama: Agnes EJ, Luppi AI, Vogels TP. Complementary inhibitory weight profiles emerge
    from plasticity and allow attentional switching of receptive fields. <i>The Journal
    of Neuroscience</i>. 2020;40(50):9634-9649. doi:<a href="https://doi.org/10.1523/JNEUROSCI.0276-20.2020">10.1523/JNEUROSCI.0276-20.2020</a>
  apa: Agnes, E. J., Luppi, A. I., &#38; Vogels, T. P. (2020). Complementary inhibitory
    weight profiles emerge from plasticity and allow attentional switching of receptive
    fields. <i>The Journal of Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.0276-20.2020">https://doi.org/10.1523/JNEUROSCI.0276-20.2020</a>
  chicago: Agnes, Everton J., Andrea I. Luppi, and Tim P Vogels. “Complementary Inhibitory
    Weight Profiles Emerge from Plasticity and Allow Attentional Switching of Receptive
    Fields.” <i>The Journal of Neuroscience</i>. Society for Neuroscience, 2020. <a
    href="https://doi.org/10.1523/JNEUROSCI.0276-20.2020">https://doi.org/10.1523/JNEUROSCI.0276-20.2020</a>.
  ieee: E. J. Agnes, A. I. Luppi, and T. P. Vogels, “Complementary inhibitory weight
    profiles emerge from plasticity and allow attentional switching of receptive fields,”
    <i>The Journal of Neuroscience</i>, vol. 40, no. 50. Society for Neuroscience,
    pp. 9634–9649, 2020.
  ista: Agnes EJ, Luppi AI, Vogels TP. 2020. Complementary inhibitory weight profiles
    emerge from plasticity and allow attentional switching of receptive fields. The
    Journal of Neuroscience. 40(50), 9634–9649.
  mla: Agnes, Everton J., et al. “Complementary Inhibitory Weight Profiles Emerge
    from Plasticity and Allow Attentional Switching of Receptive Fields.” <i>The Journal
    of Neuroscience</i>, vol. 40, no. 50, Society for Neuroscience, 2020, pp. 9634–49,
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.0276-20.2020">10.1523/JNEUROSCI.0276-20.2020</a>.
  short: E.J. Agnes, A.I. Luppi, T.P. Vogels, The Journal of Neuroscience 40 (2020)
    9634–9649.
date_created: 2020-07-16T12:25:04Z
date_published: 2020-12-09T00:00:00Z
date_updated: 2023-08-22T07:54:26Z
day: '09'
ddc:
- '570'
department:
- _id: TiVo
doi: 10.1523/JNEUROSCI.0276-20.2020
external_id:
  isi:
  - '000606706400009'
  pmid:
  - '33168622'
file:
- access_level: open_access
  checksum: 7977e4dd6b89357d1a5cc88babac56da
  content_type: application/pdf
  creator: dernst
  date_created: 2020-12-28T08:31:47Z
  date_updated: 2020-12-28T08:31:47Z
  file_id: '8977'
  file_name: 2020_JourNeuroscience_Agnes.pdf
  file_size: 2750920
  relation: main_file
  success: 1
file_date_updated: 2020-12-28T08:31:47Z
has_accepted_license: '1'
intvolume: '        40'
isi: 1
issue: '50'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 9634-9649
pmid: 1
publication: The Journal of Neuroscience
publication_identifier:
  eissn:
  - 1529-2401
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: Complementary inhibitory weight profiles emerge from plasticity and allow attentional
  switching of receptive fields
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: 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. <i>Journal of neuroscience</i>. 2020;40(1):131-142. doi:<a
    href="https://doi.org/10.1523/JNEUROSCI.1571-19.2019">10.1523/JNEUROSCI.1571-19.2019</a>
  apa: Piriya Ananda Babu, L., Wang, H. Y., Eguchi, K., Guillaud, L., &#38; Takahashi,
    T. (2020). Microtubule and actin differentially regulate synaptic vesicle cycling
    to maintain high-frequency neurotransmission. <i>Journal of Neuroscience</i>.
    Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.1571-19.2019">https://doi.org/10.1523/JNEUROSCI.1571-19.2019</a>
  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.” <i>Journal of Neuroscience</i>.
    Society for Neuroscience, 2020. <a href="https://doi.org/10.1523/JNEUROSCI.1571-19.2019">https://doi.org/10.1523/JNEUROSCI.1571-19.2019</a>.
  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,” <i>Journal of neuroscience</i>, 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.” <i>Journal
    of Neuroscience</i>, vol. 40, no. 1, Society for Neuroscience, 2020, pp. 131–42,
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.1571-19.2019">10.1523/JNEUROSCI.1571-19.2019</a>.
  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
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: '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. <i>Journal of Neuroscience</i>. 2014;34(47):15779-15792.
    doi:<a href="https://doi.org/10.1523/JNEUROSCI.1141-14.2014">10.1523/JNEUROSCI.1141-14.2014</a>
  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. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a
    href="https://doi.org/10.1523/JNEUROSCI.1141-14.2014">https://doi.org/10.1523/JNEUROSCI.1141-14.2014</a>
  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.” <i>Journal of Neuroscience</i>. Society
    for Neuroscience, 2014. <a href="https://doi.org/10.1523/JNEUROSCI.1141-14.2014">https://doi.org/10.1523/JNEUROSCI.1141-14.2014</a>.
  ieee: H. Matsukawa <i>et al.</i>, “Netrin-G/NGL complexes encode functional synaptic
    diversification,” <i>Journal of Neuroscience</i>, 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.” <i>Journal of Neuroscience</i>, vol. 34, no. 47, Society for
    Neuroscience, 2014, pp. 15779–92, doi:<a href="https://doi.org/10.1523/JNEUROSCI.1141-14.2014">10.1523/JNEUROSCI.1141-14.2014</a>.
  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
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'
...
---
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. <i>The Journal of Neuroscience</i>.
    2008;28(48):12956-12968. doi:<a href="https://doi.org/10.1523/JNEUROSCI.2890-08.2008">10.1523/JNEUROSCI.2890-08.2008</a>
  apa: Doischer, D., Hosp, J., Yanagawa, Y., Obata, K., Jonas, P. M., Vida, I., &#38;
    Bartos, M. (2008). Postnatal differentiation of basket cells from slow to fast
    signaling devices. <i>The Journal of Neuroscience</i>. Society for Neuroscience.
    <a href="https://doi.org/10.1523/JNEUROSCI.2890-08.2008">https://doi.org/10.1523/JNEUROSCI.2890-08.2008</a>
  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.” <i>The Journal of Neuroscience</i>. Society
    for Neuroscience, 2008. <a href="https://doi.org/10.1523/JNEUROSCI.2890-08.2008">https://doi.org/10.1523/JNEUROSCI.2890-08.2008</a>.
  ieee: D. Doischer <i>et al.</i>, “Postnatal differentiation of basket cells from
    slow to fast signaling devices,” <i>The Journal of Neuroscience</i>, 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.” <i>The Journal of Neuroscience</i>, vol. 28, no. 48,
    Society for Neuroscience, 2008, pp. 12956–68, doi:<a href="https://doi.org/10.1523/JNEUROSCI.2890-08.2008">10.1523/JNEUROSCI.2890-08.2008</a>.
  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'
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: '3804'
abstract:
- lang: eng
  text: Kv3 channels are thought to be essential for the fast-spiking (FS) phenotype
    in GABAergic interneurons, but how these channels confer the ability to generate
    action potentials (APs) at high frequency is unknown. To address this question,
    we developed a fast dynamic-clamp system (approximately 50 kHz) that allowed us
    to add a Kv3 model conductance to CA1 oriens alveus (OA) interneurons in hippocampal
    slices. Selective pharmacological block of Kv3 channels by 0.3 mm 4-aminopyridine
    or 1 mm tetraethylammonium ions led to a marked broadening of APs during trains
    of short stimuli and a reduction in AP frequency during 1 sec stimuli. The addition
    of artificial Kv3 conductance restored the original AP pattern. Subtraction of
    Kv3 conductance by dynamic clamp mimicked the effects of the blockers. Application
    of artificial Kv3 conductance also led to FS in OA interneurons after complete
    K+ channel block and even induced FS in hippocampal pyramidal neurons in the absence
    of blockers. Adding artificial Kv3 conductance with altered deactivation kinetics
    revealed a nonmonotonic relationship between mean AP frequency and deactivation
    rate, with a maximum slightly above the original value. Insertion of artificial
    Kv3 conductance with either lowered activation threshold or inactivation also
    led to a reduction in the mean AP frequency. However, the mechanisms were distinct.
    Shifting the activation threshold induced adaptation, whereas adding inactivation
    caused frequency-dependent AP broadening. In conclusion, Kv3 channels are necessary
    for the FS phenotype of OA interneurons, and several of their gating properties
    appear to be optimized for high-frequency repetitive activity.
article_processing_charge: No
article_type: original
author:
- first_name: Cheng
  full_name: Lien, Cheng
  last_name: Lien
- first_name: Peter M
  full_name: Jonas, Peter M
  id: 353C1B58-F248-11E8-B48F-1D18A9856A87
  last_name: Jonas
  orcid: 0000-0001-5001-4804
citation:
  ama: Lien C, Jonas PM. Kv3 potassium conductance is necessary and kinetically optimized
    for high-frequency action potential generation in hippocampal interneurons. <i>Journal
    of Neuroscience</i>. 2003;23(6):2058-2068. doi:<a href="https://doi.org/10.1523/JNEUROSCI.23-06-02058.2003">10.1523/JNEUROSCI.23-06-02058.2003</a>
  apa: Lien, C., &#38; Jonas, P. M. (2003). Kv3 potassium conductance is necessary
    and kinetically optimized for high-frequency action potential generation in hippocampal
    interneurons. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.23-06-02058.2003">https://doi.org/10.1523/JNEUROSCI.23-06-02058.2003</a>
  chicago: Lien, Cheng, and Peter M Jonas. “Kv3 Potassium Conductance Is Necessary
    and Kinetically Optimized for High-Frequency Action Potential Generation in Hippocampal
    Interneurons.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2003.
    <a href="https://doi.org/10.1523/JNEUROSCI.23-06-02058.2003">https://doi.org/10.1523/JNEUROSCI.23-06-02058.2003</a>.
  ieee: C. Lien and P. M. Jonas, “Kv3 potassium conductance is necessary and kinetically
    optimized for high-frequency action potential generation in hippocampal interneurons,”
    <i>Journal of Neuroscience</i>, vol. 23, no. 6. Society for Neuroscience, pp.
    2058–68, 2003.
  ista: Lien C, Jonas PM. 2003. Kv3 potassium conductance is necessary and kinetically
    optimized for high-frequency action potential generation in hippocampal interneurons.
    Journal of Neuroscience. 23(6), 2058–68.
  mla: Lien, Cheng, and Peter M. Jonas. “Kv3 Potassium Conductance Is Necessary and
    Kinetically Optimized for High-Frequency Action Potential Generation in Hippocampal
    Interneurons.” <i>Journal of Neuroscience</i>, vol. 23, no. 6, Society for Neuroscience,
    2003, pp. 2058–68, doi:<a href="https://doi.org/10.1523/JNEUROSCI.23-06-02058.2003">10.1523/JNEUROSCI.23-06-02058.2003</a>.
  short: C. Lien, P.M. Jonas, Journal of Neuroscience 23 (2003) 2058–68.
date_created: 2018-12-11T12:05:16Z
date_published: 2003-03-15T00:00:00Z
date_updated: 2026-05-08T09:38:20Z
day: '15'
doi: 10.1523/JNEUROSCI.23-06-02058.2003
extern: '1'
external_id:
  pmid:
  - '12657664'
intvolume: '        23'
issue: '6'
keyword:
- Kv3 channels
- dynamic clamp
- fast spiking
- deactivation kinetics
- OA interneurons
- hippocampal slices
- two electrode current clamp
language:
- iso: eng
month: '03'
oa_version: None
page: 2058 - 68
pmid: 1
publication: Journal of Neuroscience
publication_identifier:
  eissn:
  - 1529-2401
  issn:
  - 0270-6474
publication_status: published
publisher: Society for Neuroscience
publist_id: '2406'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Kv3 potassium conductance is necessary and kinetically optimized for high-frequency
  action potential generation in hippocampal interneurons
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 23
year: '2003'
...
---
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. <i>Journal of Neuroscience</i>.
    2003;23(35):11026-11035. doi:<a href="https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003">10.1523/JNEUROSCI.23-35-11026.2003</a>
  apa: Kulik, Á., Vida, I., Luján, R., Haas, C., López Bendito, G., Shigemoto, R.,
    &#38; Frotscher, M. (2003). Subcellular Localization of Metabotropic GABAB Receptor
    Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus. <i>Journal of Neuroscience</i>.
    Society for Neuroscience. <a href="https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003">https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003</a>
  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.” <i>Journal
    of Neuroscience</i>. Society for Neuroscience, 2003. <a href="https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003">https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003</a>.
  ieee: Á. Kulik <i>et al.</i>, “Subcellular Localization of Metabotropic GABAB Receptor
    Subunits GABAB1a/b and GABAB2 in the Rat Hippocampus,” <i>Journal of Neuroscience</i>,
    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.” <i>Journal of Neuroscience</i>,
    vol. 23, no. 35, Society for Neuroscience, 2003, pp. 11026–35, doi:<a href="https://doi.org/10.1523/JNEUROSCI.23-35-11026.2003">10.1523/JNEUROSCI.23-35-11026.2003</a>.
  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'
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'
...
