Astroglial Cx30 sustains neuronal population bursts independently of gap-junction mediated biochemical coupling.
astrocyte
connexin 30
gap junctions
glutamate transporter
hippocampus
neuronal population bursts
Journal
Glia
ISSN: 1098-1136
Titre abrégé: Glia
Pays: United States
ID NLM: 8806785
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
27
07
2018
revised:
21
12
2018
accepted:
28
12
2018
pubmed:
23
2
2019
medline:
31
12
2019
entrez:
23
2
2019
Statut:
ppublish
Résumé
Astroglial networks mediated by gap junction channels contribute to neurotransmission and promote neuronal coordination. Connexin 30, one of the two main astroglial gap junction forming protein, alters at the behavioral level the reactivity of mice to novel environment and at the synaptic level excitatory transmission. However, the role and function of Cx30 at the neuronal network level remain unclear. We thus investigated whether Cx30 regulates neuronal population bursts and associated convulsive behavior. We found in vivo that Cx30 is upregulated by kainate-induced seizures and that it regulates in turn the severity of associated behavioral seizures. Using electrophysiology ex vivo, we report that Cx30 regulates aberrant network activity via control of astroglial glutamate clearance independently of gap-junction mediated biochemical coupling. Altogether, our results indicate that astroglial Cx30 is an important player in orchestrating neuronal network activity.
Identifiants
pubmed: 30794327
doi: 10.1002/glia.23591
pmc: PMC6519011
doi:
Substances chimiques
Connexin 30
0
Gjb6 protein, mouse
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1104-1112Informations de copyright
© 2019 The Authors. Glia published by Wiley Periodicals, Inc.
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