Neuroligin3 splice isoforms shape inhibitory synaptic function in the mouse hippocampus.


Journal

The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R

Informations de publication

Date de publication:
19 06 2020
Historique:
received: 22 01 2020
revised: 01 05 2020
pubmed: 10 5 2020
medline: 6 1 2021
entrez: 9 5 2020
Statut: ppublish

Résumé

Synapse formation is a dynamic process essential for the development and maturation of the neuronal circuitry in the brain. At the synaptic cleft, trans-synaptic protein-protein interactions are major biological determinants of proper synapse efficacy. The balance of excitatory and inhibitory synaptic transmission (E-I balance) stabilizes synaptic activity, and dysregulation of the E-I balance has been implicated in neurodevelopmental disorders, including autism spectrum disorders. However, the molecular mechanisms underlying the E-I balance remain to be elucidated. Here, using single-cell transcriptomics, immunohistochemistry, and electrophysiology approaches to murine CA1 pyramidal neurons obtained from organotypic hippocampal slice cultures, we investigate neuroligin (

Identifiants

pubmed: 32381505
pii: S0021-9258(17)49251-9
doi: 10.1074/jbc.AC120.012571
pmc: PMC7307194
doi:

Substances chimiques

Cell Adhesion Molecules, Neuronal 0
Membrane Proteins 0
Nerve Tissue Proteins 0
Protein Isoforms 0
neuroligin 3 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

8589-8595

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS085215
Pays : United States
Organisme : NIGMS NIH HHS
ID : T32 GM107000
Pays : United States

Informations de copyright

© 2020 Uchigashima et al.

Déclaration de conflit d'intérêts

Conflict of interest—The authors declare that they have no conflicts of interest with the contents of this article.

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Auteurs

Motokazu Uchigashima (M)

Brudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan.

Ming Leung (M)

Department of Biochemistry and Molecular Biology and Institute for Personalized Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.

Takuya Watanabe (T)

Brudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.

Amy Cheung (A)

Brudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.

Timmy Le (T)

Brudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.

Sabine Pallat (S)

Brudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.

Alexandre Luis Marques Dinis (ALM)

Brudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.

Masahiko Watanabe (M)

Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo, Hokkaido, Japan.

Yuka Imamura Kawasawa (YI)

Department of Biochemistry and Molecular Biology and Institute for Personalized Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA yimamura@pennstatehealth.psu.edu Kensuke.Futai@umassmed.edu.
Department of Pharmacology, Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.

Kensuke Futai (K)

Brudnick Neuropsychiatric Research Institute, Department of Neurobiology, University of Massachusetts Medical School, Worcester, Massachusetts, USA yimamura@pennstatehealth.psu.edu Kensuke.Futai@umassmed.edu.

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