Neuroligin3 splice isoforms shape inhibitory synaptic function in the mouse hippocampus.
Animals
CA1 Region, Hippocampal
/ metabolism
Cell Adhesion Molecules, Neuronal
/ deficiency
Excitatory Postsynaptic Potentials
Immunohistochemistry
Inhibitory Postsynaptic Potentials
Membrane Proteins
/ deficiency
Mice
Mice, Inbred C57BL
Mice, Knockout
Nerve Tissue Proteins
/ deficiency
Patch-Clamp Techniques
Protein Isoforms
/ genetics
RNA Splicing
Synapses
/ physiology
CA1 pyramidal neuron
GABA receptor
excitatory and inhibitory balance
glutamate receptor
hippocampus
neurobiology
neuroligin 3 (NLGN3)
neuron
neurotransmitter receptor
splice variants
synapse
synaptic transmission
trans-synaptic cell adhesion
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
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
8589-8595Subventions
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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