TMEM16B Calcium-Activated Chloride Channels Regulate Action Potential Firing in Lateral Septum and Aggression in Male Mice.
Ano2
Anoctamin 2
CaCC
TMEM16B
aggression
lateral septum
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN: 1529-2401
Titre abrégé: J Neurosci
Pays: United States
ID NLM: 8102140
Informations de publication
Date de publication:
04 09 2019
04 09 2019
Historique:
received:
14
12
2018
revised:
11
06
2019
accepted:
11
07
2019
pubmed:
20
7
2019
medline:
1
7
2020
entrez:
20
7
2019
Statut:
ppublish
Résumé
The lateral septum (LS) plays an important role in regulating aggression. It is well recognized that LS lesions lead to a dramatic increase in aggressive behaviors. A better understanding of LS neurophysiology and its functional output is therefore important to assess LS involvement in regulating aggression. The LS is a heterogeneous structure that maintains inputs and outputs with multiple brain regions, and is also divided into subregions that innervate one another. Thus, it is challenging to identify the exact cell type and projections for characterization. In this study, we determined the expression pattern of the calcium-activated chloride channel, TMEM16B, in the LS of both male and female mice. We then investigated the physiological contribution of the calcium-activated chloride channel to LS neuronal signaling. By performing whole-cell patch-clamp recording, we showed that TMEM16B alters neurotransmitter release at the hippocampal-LS synapse, and regulates spike frequency and spike frequency adaptation in subpopulations of LS neurons. We further demonstrated that loss of TMEM16B function promotes lengthened displays of aggressive behaviors by male mice during the resident intruder paradigm. In conclusion, our findings suggest that TMEM16B function contributes to neuronal excitability in subpopulations of LS neurons and the regulation of aggression in male mice.
Identifiants
pubmed: 31320449
pii: JNEUROSCI.3137-18.2019
doi: 10.1523/JNEUROSCI.3137-18.2019
pmc: PMC6733546
doi:
Substances chimiques
ANO2 protein, mouse
0
Anoctamins
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
7102-7117Subventions
Organisme : NIDA NIH HHS
ID : K99 DA041500
Pays : United States
Organisme : NIDA NIH HHS
ID : R00 DA041500
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS069229
Pays : United States
Organisme : Howard Hughes Medical Institute
Pays : United States
Informations de copyright
Copyright © 2019 the authors.
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