---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
PlanS_conform: '1'
_id: '22615'
abstract:
- lang: eng
  text: "Background and Objectives: \r\nAnti-immunoglobulin-like cell adhesion molecule
    5 (IgLON5) disease is a novel and poten-\r\ntially treatable entity. Therefore,
    it is important to recognize all clinical symptoms and di-\r\nagnostic clues.
    We specifically investigated neuromuscular signs and symptoms and muscle biopsy
    pathology, providing a link between IgLON5 and clinical features of myopathy.\r\nMethods:
    \r\nAll patients diagnosed with anti-IgLON5 disease in the Netherlands between
    2016 and 2023 were included. Serum and CSF samples were tested with immunohistochemistry
    on rat brain and in-house cell-based assay using live cells. Biopsies of the vastus
    lateralis muscle were performed in patients with neuromuscular signs and symptoms
    and analyzed in Vienna to-\r\ngether with 3 biopsies of non-Dutch patients sent
    to Vienna for second opinion.\r\nResults: \r\nTwenty patients with anti-IgLON5
    disease were included (10 male, 50%). The median age at onset was 61.5 years (range
    45–85), and the median time from onset to diagnosis was 30 months (range 3–280).
    Neuromuscular symptoms were present in over half of the patients (11/20), including
    proximal limb weakness (n = 11), axial weakness (n = 1), muscle atrophy (n = 6),
    and fasciculations (n = 5). All 12 muscle biopsies (9 from the Dutch cohort, 3
    external) showed mild myopathic alterations, 2 additionally presented target fibers
    and fiber type grouping (compatible with neu-\r\nrogenic myopathy), and 3 patients
    showed immune cell infiltration. We found a strong upregulation of IgLON5 expression
    in muscle fibers in all patients and also in different muscle disease controls,
    while immunoreactivity in healthy control muscle was faint/absent.\r\nDiscussion:
    \r\nOur data support that IgLON5 might play a role in muscle regeneration, which
    might result in proximal myopathy as a prominent clinical feature in anti-IgLON5
    disease. This finding broadens the clinical phenotype of anti-IgLON5 disease and
    can be an important clue for earlier diagnosis and start of immunotherapy."
acknowledgement: "One author (Manuela Paunovic) was removed from the paper due to
  personal circumstances. Her contributions were removed from the manuscript before
  final review. The authors thank all patients for their participation and all referring
  physicians. The authors thank Professor Joachim Weis at the Medical Faculty RWTH
  Aachen University for his contribution to the manuscript. The authors would like
  to thank Andrea Polt and Irene Erber at the Medical University of Vienna, and Jacqueline
  Montanaro at IST Austria, for their assistance in the laboratory. N.A.M.E. van der
  Beek participates in EURO-NMD. M.W.J. Schreurs, P.A.E. Sillevis Smitt, J.M. de Vries,
  and M.J. Titulaer are members of the European Reference Network for Rare Immunodeficiency,
  Autoinflammatory and Autoimmune Diseases–Project ID No 739543 (ERN-RITA; HCP Erasmus
  MC). IK was funded by the Austrian Science Fund (FWF, T996-B30). RS was funded by
  the Austrian Science Fund (FWF, SYNABS, I6565-B). JL was funded by German Federal
  Ministry of Education and Research (BMBF, Forschungsverbund CONNECT-GEN-\r\nERATE,
  01 GM2208B). RvS was funded by AEA Seed Grant 2023 and InterAct Grant of Alzheimer
  Nederland 2023. LS was funded by Instituto de Salud Carlos III (ISCIII, PI21/ 00165)
  and the Networking Support Scheme funded from the European Union’s Horizon 2020
  research and innovation program (EJP RD COFUND-EJP N° 825575). JdV was funded by
  AEA Seed Grant 2021. RH was funded by grants from the Austrian Science Fund (FWF,
  SYNABS, I4685-B, I6565-B), Forschungsf¨orderungsgesellschaft (FFG, IGNITE-\r\nMIND,
  FO999920011), and the Austrian Society of\r\nNeurology (\r\n¨\r\nOsterreichische
  Gesellschaft f¨ur Neurologie).\r\nMT was funded by the Dutch EpilepsieNL Foundation
  (NEF 19-08), an Interlaken Leadership award, Dioraphte (2001 0403) the Dutch Research
  Council (ZonMW, PARADE-\r\nVIMP) and E-RARE JTC 2018 (UltraAIE, 90030376505)."
article_processing_charge: Yes
article_type: original
author:
- first_name: Yvette S.
  full_name: Crijnen, Yvette S.
  last_name: Crijnen
- first_name: Verena
  full_name: Endmayr, Verena
  last_name: Endmayr
- first_name: Suzanne C.
  full_name: Franken, Suzanne C.
  last_name: Franken
- first_name: Nadine A.M.E.
  full_name: Van Der Beek, Nadine A.M.E.
  last_name: Van Der Beek
- first_name: Maartje
  full_name: Louter, Maartje
  last_name: Louter
- first_name: Thomas
  full_name: Ströbel, Thomas
  last_name: Ströbel
- first_name: Ellen
  full_name: Gelpi, Ellen
  last_name: Gelpi
- first_name: Inga
  full_name: Koneczny, Inga
  last_name: Koneczny
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Jan
  full_name: Lewerenz, Jan
  last_name: Lewerenz
- first_name: Birgit
  full_name: Högl, Birgit
  last_name: Högl
- first_name: Julia V.
  full_name: Wanschitz, Julia V.
  last_name: Wanschitz
- first_name: Ulrich He
  full_name: Hofstadt-Van Oy, Ulrich He
  last_name: Hofstadt-Van Oy
- first_name: Robin W.
  full_name: Van Steenhoven, Robin W.
  last_name: Van Steenhoven
- first_name: Mariska M.P.
  full_name: Nagtzaam, Mariska M.P.
  last_name: Nagtzaam
- first_name: Jeroen
  full_name: Kerstens, Jeroen
  last_name: Kerstens
- first_name: Juliette
  full_name: Brenner, Juliette
  last_name: Brenner
- first_name: Anna E.M.
  full_name: Bastiaansen, Anna E.M.
  last_name: Bastiaansen
- first_name: Robert M.
  full_name: Verdijk, Robert M.
  last_name: Verdijk
- first_name: Thierry P.P.
  full_name: Van Den Bosch, Thierry P.P.
  last_name: Van Den Bosch
- first_name: Marco
  full_name: Schreurs, Marco
  last_name: Schreurs
- first_name: Sharon
  full_name: Veenbergen, Sharon
  last_name: Veenbergen
- first_name: Marcel M.
  full_name: Verbeek, Marcel M.
  last_name: Verbeek
- first_name: Dave L.
  full_name: Roelen, Dave L.
  last_name: Roelen
- first_name: Mar
  full_name: Guasp, Mar
  last_name: Guasp
- first_name: Peter A.E.
  full_name: Sillevis Smitt, Peter A.E.
  last_name: Sillevis Smitt
- first_name: Lidia
  full_name: Sabater, Lidia
  last_name: Sabater
- first_name: Juna M.
  full_name: De Vries, Juna M.
  last_name: De Vries
- first_name: Romana
  full_name: Höftberger, Romana
  last_name: Höftberger
- first_name: Maarten J.
  full_name: Titulaer, Maarten J.
  last_name: Titulaer
citation:
  ama: Crijnen YS, Endmayr V, Franken SC, et al. Muscle regeneration failure may lead
    to clinical features of myopathy in anti-IgLON5 disease. <i>Neurology, Neuroimmunology
    &#38; Neuroinflammation</i>. 2026;13(5):e200525. doi:<a href="https://doi.org/10.1212/NXI.0000000000200525">10.1212/NXI.0000000000200525</a>
  apa: Crijnen, Y. S., Endmayr, V., Franken, S. C., Van Der Beek, N. A. M. E., Louter,
    M., Ströbel, T., … Titulaer, M. J. (2026). Muscle regeneration failure may lead
    to clinical features of myopathy in anti-IgLON5 disease. <i>Neurology, Neuroimmunology
    &#38; Neuroinflammation</i>. Wolters Kluwer. <a href="https://doi.org/10.1212/NXI.0000000000200525">https://doi.org/10.1212/NXI.0000000000200525</a>
  chicago: Crijnen, Yvette S., Verena Endmayr, Suzanne C. Franken, Nadine A.M.E. Van
    Der Beek, Maartje Louter, Thomas Ströbel, Ellen Gelpi, et al. “Muscle Regeneration
    Failure May Lead to Clinical Features of Myopathy in Anti-IgLON5 Disease.” <i>Neurology,
    Neuroimmunology &#38; Neuroinflammation</i>. Wolters Kluwer, 2026. <a href="https://doi.org/10.1212/NXI.0000000000200525">https://doi.org/10.1212/NXI.0000000000200525</a>.
  ieee: Y. S. Crijnen <i>et al.</i>, “Muscle regeneration failure may lead to clinical
    features of myopathy in anti-IgLON5 disease,” <i>Neurology, Neuroimmunology &#38;
    Neuroinflammation</i>, vol. 13, no. 5. Wolters Kluwer, p. e200525, 2026.
  ista: Crijnen YS, Endmayr V, Franken SC, Van Der Beek NAME, Louter M, Ströbel T,
    Gelpi E, Koneczny I, Shigemoto R, Lewerenz J, Högl B, Wanschitz JV, Hofstadt-Van
    Oy UH, Van Steenhoven RW, Nagtzaam MMP, Kerstens J, Brenner J, Bastiaansen AEM,
    Verdijk RM, Van Den Bosch TPP, Schreurs M, Veenbergen S, Verbeek MM, Roelen DL,
    Guasp M, Sillevis Smitt PAE, Sabater L, De Vries JM, Höftberger R, Titulaer MJ.
    2026. Muscle regeneration failure may lead to clinical features of myopathy in
    anti-IgLON5 disease. Neurology, Neuroimmunology &#38; Neuroinflammation. 13(5),
    e200525.
  mla: Crijnen, Yvette S., et al. “Muscle Regeneration Failure May Lead to Clinical
    Features of Myopathy in Anti-IgLON5 Disease.” <i>Neurology, Neuroimmunology &#38;
    Neuroinflammation</i>, vol. 13, no. 5, Wolters Kluwer, 2026, p. e200525, doi:<a
    href="https://doi.org/10.1212/NXI.0000000000200525">10.1212/NXI.0000000000200525</a>.
  short: Y.S. Crijnen, V. Endmayr, S.C. Franken, N.A.M.E. Van Der Beek, M. Louter,
    T. Ströbel, E. Gelpi, I. Koneczny, R. Shigemoto, J. Lewerenz, B. Högl, J.V. Wanschitz,
    U.H. Hofstadt-Van Oy, R.W. Van Steenhoven, M.M.P. Nagtzaam, J. Kerstens, J. Brenner,
    A.E.M. Bastiaansen, R.M. Verdijk, T.P.P. Van Den Bosch, M. Schreurs, S. Veenbergen,
    M.M. Verbeek, D.L. Roelen, M. Guasp, P.A.E. Sillevis Smitt, L. Sabater, J.M. De
    Vries, R. Höftberger, M.J. Titulaer, Neurology, Neuroimmunology &#38; Neuroinflammation
    13 (2026) e200525.
das_tickbox: '1'
dataavailabilitystatement: Any data not published within this article are available
  at Erasmus MC, Rotterdam, and Medical University of Vienna. Data will be shared
  on reasonable request from any qualified investigator, ascertaining anonymization
  of the individual patients, in line with European privacy regulations.
date_created: 2026-08-02T22:01:52Z
date_published: 2026-09-01T00:00:00Z
date_updated: 2026-08-03T08:16:04Z
day: '01'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1212/NXI.0000000000200525
external_id:
  pmid:
  - '42441930'
file:
- access_level: open_access
  checksum: 7cc4c4c180a2cf65603a02bef7b75784
  content_type: application/pdf
  creator: dernst
  date_created: 2026-08-03T08:06:16Z
  date_updated: 2026-08-03T08:06:16Z
  file_id: '22631'
  file_name: 2026_Neurology_Crijnen.pdf
  file_size: 1122644
  relation: main_file
  success: 1
file_date_updated: 2026-08-03T08:06:16Z
fulldoi: https://doi.org/10.1212/NXI.0000000000200525
has_accepted_license: '1'
intvolume: '        13'
issue: '5'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: e200525
pmid: 1
project:
- _id: 05970B30-7A3F-11EA-A408-12923DDC885E
  grant_number: I04638
  name: LGI1 antibody-induced pathophysiology in synapses
publication: Neurology, Neuroimmunology & Neuroinflammation
publication_identifier:
  eissn:
  - 2332-7812
publication_status: published
publisher: Wolters Kluwer
quality_controlled: '1'
researchdata_availability: upon request
scopus_import: '1'
status: public
supplementarymaterial: no
title: Muscle regeneration failure may lead to clinical features of myopathy in anti-IgLON5
  disease
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: 13
year: '2026'
...
---
DOAJ_listed: '1'
OA_place: publisher
OA_type: gold
_id: '17457'
abstract:
- lang: eng
  text: "Autoantibodies against the protein leucine-rich glioma inactivated 1 (LGI1)
    cause the most\r\ncommon subtype of autoimmune encephalitis with predominant involvement
    of the limbic\r\nsystem, associated with seizures and memory deficits. LGI1 and
    its receptor ADAM22 are part\r\nof a transsynaptic protein complex that includes
    several proteins involved in presynaptic\r\nneurotransmitter release and postsynaptic
    glutamate sensing. Autoantibodies against LGI1\r\nincrease excitatory synaptic
    strength, but studies that genetically disrupt the LGI1-ADAM22\r\ncomplex report
    a reduction in postsynaptic glutamate receptor-mediated responses. Thus, the\r\nmechanisms
    underlying the increased synaptic strength induced by LGI1 autoantibodies remain
    elusive, and the contributions of presynaptic molecules to the LGI1-transsynaptic
    complex remain unclear. We therefore investigated the presynaptic mechanisms that
    mediate\r\nautoantibody-induced synaptic strengthening."
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
acknowledgement: 'The authors thank Claudia Sommer for expert technical assistance,
  the Electron Microscopy Facility of IST-Austria for resources, and Tereza Belinova
  in the Imaging and Optics Facility of IST-Austria for 3D reconstruction. '
article_processing_charge: Yes
article_type: original
author:
- first_name: Andreas
  full_name: Ritzau-Jost, Andreas
  last_name: Ritzau-Jost
- first_name: Felix
  full_name: Gsell, Felix
  last_name: Gsell
- first_name: Josefine
  full_name: Sell, Josefine
  last_name: Sell
- first_name: Stefan
  full_name: Sachs, Stefan
  last_name: Sachs
- first_name: Jacqueline-Claire
  full_name: Montanaro-Punzengruber, Jacqueline-Claire
  id: 3786AB44-F248-11E8-B48F-1D18A9856A87
  last_name: Montanaro-Punzengruber
- first_name: Toni
  full_name: Kirmann, Toni
  last_name: Kirmann
- first_name: Sebastian
  full_name: Maaß, Sebastian
  last_name: Maaß
- first_name: Sarosh R.
  full_name: Irani, Sarosh R.
  last_name: Irani
- first_name: Christian
  full_name: Werner, Christian
  last_name: Werner
- first_name: Christian
  full_name: Geis, Christian
  last_name: Geis
- first_name: Markus
  full_name: Sauer, Markus
  last_name: Sauer
- first_name: Ryuichi
  full_name: Shigemoto, Ryuichi
  id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
  last_name: Shigemoto
  orcid: 0000-0001-8761-9444
- first_name: Stefan
  full_name: Hallermann, Stefan
  last_name: Hallermann
citation:
  ama: Ritzau-Jost A, Gsell F, Sell J, et al. LGI1 autoantibodies enhance synaptic
    transmission by presynaptic Kv1 loss and increased action potential broadening.
    <i>Neurology, Neuroimmunology &#38; Neuroinflammation</i>. 2024;11(5):e200284.
    doi:<a href="https://doi.org/10.1212/NXI.0000000000200284">10.1212/NXI.0000000000200284</a>
  apa: Ritzau-Jost, A., Gsell, F., Sell, J., Sachs, S., Montanaro-Punzengruber, J.-C.,
    Kirmann, T., … Hallermann, S. (2024). LGI1 autoantibodies enhance synaptic transmission
    by presynaptic Kv1 loss and increased action potential broadening. <i>Neurology,
    Neuroimmunology &#38; Neuroinflammation</i>. Wolters Kluwer. <a href="https://doi.org/10.1212/NXI.0000000000200284">https://doi.org/10.1212/NXI.0000000000200284</a>
  chicago: Ritzau-Jost, Andreas, Felix Gsell, Josefine Sell, Stefan Sachs, Jacqueline-Claire
    Montanaro-Punzengruber, Toni Kirmann, Sebastian Maaß, et al. “LGI1 Autoantibodies
    Enhance Synaptic Transmission by Presynaptic Kv1 Loss and Increased Action Potential
    Broadening.” <i>Neurology, Neuroimmunology &#38; Neuroinflammation</i>. Wolters
    Kluwer, 2024. <a href="https://doi.org/10.1212/NXI.0000000000200284">https://doi.org/10.1212/NXI.0000000000200284</a>.
  ieee: A. Ritzau-Jost <i>et al.</i>, “LGI1 autoantibodies enhance synaptic transmission
    by presynaptic Kv1 loss and increased action potential broadening,” <i>Neurology,
    Neuroimmunology &#38; Neuroinflammation</i>, vol. 11, no. 5. Wolters Kluwer, p.
    e200284, 2024.
  ista: Ritzau-Jost A, Gsell F, Sell J, Sachs S, Montanaro-Punzengruber J-C, Kirmann
    T, Maaß S, Irani SR, Werner C, Geis C, Sauer M, Shigemoto R, Hallermann S. 2024.
    LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and
    increased action potential broadening. Neurology, Neuroimmunology &#38; Neuroinflammation.
    11(5), e200284.
  mla: Ritzau-Jost, Andreas, et al. “LGI1 Autoantibodies Enhance Synaptic Transmission
    by Presynaptic Kv1 Loss and Increased Action Potential Broadening.” <i>Neurology,
    Neuroimmunology &#38; Neuroinflammation</i>, vol. 11, no. 5, Wolters Kluwer, 2024,
    p. e200284, doi:<a href="https://doi.org/10.1212/NXI.0000000000200284">10.1212/NXI.0000000000200284</a>.
  short: A. Ritzau-Jost, F. Gsell, J. Sell, S. Sachs, J.-C. Montanaro-Punzengruber,
    T. Kirmann, S. Maaß, S.R. Irani, C. Werner, C. Geis, M. Sauer, R. Shigemoto, S.
    Hallermann, Neurology, Neuroimmunology &#38; Neuroinflammation 11 (2024) e200284.
das_tickbox: '1'
dataavailabilitystatement: Data that support the findings of this study are available
  from the corresponding author on reasonable request.
date_created: 2024-08-25T22:01:07Z
date_published: 2024-09-01T00:00:00Z
date_updated: 2026-09-17T11:27:41Z
day: '01'
ddc:
- '570'
department:
- _id: RySh
doi: 10.1212/NXI.0000000000200284
external_id:
  isi:
  - '001291908600001'
  pmid:
  - '39141878'
file:
- access_level: open_access
  checksum: 1e6d1230e0387f72752e3268f5330c9e
  content_type: application/pdf
  creator: dernst
  date_created: 2025-01-09T13:42:42Z
  date_updated: 2025-01-09T13:42:42Z
  file_id: '18815'
  file_name: 2024_NeurologyNeuroimmNeuroinflamm_RitzauJost.pdf
  file_size: 855818
  relation: main_file
  success: 1
file_date_updated: 2025-01-09T13:42:42Z
fulldoi: https://doi.org/10.1212/NXI.0000000000200284
has_accepted_license: '1'
intvolume: '        11'
isi: 1
issue: '5'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: e200284
pmid: 1
project:
- _id: 05970B30-7A3F-11EA-A408-12923DDC885E
  grant_number: I04638
  name: LGI1 antibody-induced pathophysiology in synapses
publication: Neurology, Neuroimmunology & Neuroinflammation
publication_identifier:
  eissn:
  - 2332-7812
publication_status: published
publisher: Wolters Kluwer
quality_controlled: '1'
related_material:
  link:
  - relation: earlier_version
    url: https://doi.org/10.1101/2023.10.04.560631
researchdata_availability: upon request
scopus_import: '1'
status: public
supplementarymaterial: yes
title: LGI1 autoantibodies enhance synaptic transmission by presynaptic Kv1 loss and
  increased action potential broadening
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 11
year: '2024'
...
---
_id: '10890'
abstract:
- lang: eng
  text: Upon the arrival of action potentials at nerve terminals, neurotransmitters
    are released from synaptic vesicles (SVs) by exocytosis. CaV2.1, 2.2, and 2.3
    are the major subunits of the voltage-gated calcium channel (VGCC) responsible
    for increasing intraterminal calcium levels and triggering SV exocytosis in the
    central nervous system (CNS) synapses. The two-dimensional analysis of CaV2 distributions
    using sodium dodecyl sulfate (SDS)-digested freeze-fracture replica labeling (SDS-FRL)
    has revealed their numbers, densities, and nanoscale clustering patterns in individual
    presynaptic active zones. The variation in these properties affects the coupling
    of VGCCs with calcium sensors on SVs, synaptic efficacy, and temporal precision
    of transmission. In this study, we summarize how the morphological parameters
    of CaV2 distribution obtained using SDS-FRL differ depending on the different
    types of synapses and could correspond to functional properties in synaptic transmission.
acknowledgement: "This work was supported by the European Research Council advanced
  grant No. 694539 and the joint German-Austrian DFG and FWF project SYNABS (FWF:
  I-4638-B) to RS.\r\nThe authors thank Walter Kaufmann for his critical comments
  on the manuscript."
article_number: '846615'
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: Jacqueline-Claire
  full_name: Montanaro-Punzengruber, Jacqueline-Claire
  id: 3786AB44-F248-11E8-B48F-1D18A9856A87
  last_name: Montanaro-Punzengruber
- 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, Montanaro-Punzengruber J-C, Le Monnier E, Shigemoto R. The number
    and distinct clustering patterns of voltage-gated Calcium channels in nerve terminals.
    <i>Frontiers in Neuroanatomy</i>. 2022;16. doi:<a href="https://doi.org/10.3389/fnana.2022.846615">10.3389/fnana.2022.846615</a>
  apa: Eguchi, K., Montanaro-Punzengruber, J.-C., Le Monnier, E., &#38; Shigemoto,
    R. (2022). The number and distinct clustering patterns of voltage-gated Calcium
    channels in nerve terminals. <i>Frontiers in Neuroanatomy</i>. Frontiers. <a href="https://doi.org/10.3389/fnana.2022.846615">https://doi.org/10.3389/fnana.2022.846615</a>
  chicago: Eguchi, Kohgaku, Jacqueline-Claire Montanaro-Punzengruber, Elodie Le Monnier,
    and Ryuichi Shigemoto. “The Number and Distinct Clustering Patterns of Voltage-Gated
    Calcium Channels in Nerve Terminals.” <i>Frontiers in Neuroanatomy</i>. Frontiers,
    2022. <a href="https://doi.org/10.3389/fnana.2022.846615">https://doi.org/10.3389/fnana.2022.846615</a>.
  ieee: K. Eguchi, J.-C. Montanaro-Punzengruber, E. Le Monnier, and R. Shigemoto,
    “The number and distinct clustering patterns of voltage-gated Calcium channels
    in nerve terminals,” <i>Frontiers in Neuroanatomy</i>, vol. 16. Frontiers, 2022.
  ista: Eguchi K, Montanaro-Punzengruber J-C, Le Monnier E, Shigemoto R. 2022. The
    number and distinct clustering patterns of voltage-gated Calcium channels in nerve
    terminals. Frontiers in Neuroanatomy. 16, 846615.
  mla: Eguchi, Kohgaku, et al. “The Number and Distinct Clustering Patterns of Voltage-Gated
    Calcium Channels in Nerve Terminals.” <i>Frontiers in Neuroanatomy</i>, vol. 16,
    846615, Frontiers, 2022, doi:<a href="https://doi.org/10.3389/fnana.2022.846615">10.3389/fnana.2022.846615</a>.
  short: K. Eguchi, J.-C. Montanaro-Punzengruber, E. Le Monnier, R. Shigemoto, Frontiers
    in Neuroanatomy 16 (2022).
corr_author: '1'
date_created: 2022-03-20T23:01:39Z
date_published: 2022-02-24T00:00:00Z
date_updated: 2026-04-16T08:18:54Z
day: '24'
ddc:
- '570'
department:
- _id: RySh
doi: 10.3389/fnana.2022.846615
ec_funded: 1
external_id:
  isi:
  - '000766662700001'
  pmid:
  - '35280978'
file:
- access_level: open_access
  checksum: 51ec9b90e7da919e22c01a15489eaacd
  content_type: application/pdf
  creator: dernst
  date_created: 2022-03-21T09:41:19Z
  date_updated: 2022-03-21T09:41:19Z
  file_id: '10911'
  file_name: 2022_FrontiersNeuroanatomy_Eguchi.pdf
  file_size: 2416395
  relation: main_file
  success: 1
file_date_updated: 2022-03-21T09:41:19Z
fulldoi: https://doi.org/10.3389/fnana.2022.846615
has_accepted_license: '1'
intvolume: '        16'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 25CA28EA-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '694539'
  name: 'In situ analysis of single channel subunit composition in neurons: physiological
    implication in synaptic plasticity and behaviour'
- _id: 05970B30-7A3F-11EA-A408-12923DDC885E
  grant_number: I04638
  name: LGI1 antibody-induced pathophysiology in synapses
publication: Frontiers in Neuroanatomy
publication_identifier:
  eissn:
  - 1662-5129
publication_status: published
publisher: Frontiers
quality_controlled: '1'
scopus_import: '1'
status: public
title: The number and distinct clustering patterns of voltage-gated Calcium channels
  in nerve terminals
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: 16
year: '2022'
...