Role of Calcr expressing neurons in the medial amygdala in social contact among females.

Autor: Fukumitsu K; Laboratory for Affiliative Social Behavior, RIKEN Center for Brain Science, Hirosawa 2-1, Wakoshi, Saitama, 351-0198, Japan. kansai.fukumitsu@riken.jp., Huang AJ; Laboratory for Circuit and Behavioral Physiology, RIKEN Center for Brain Science, Wakoshi, Saitama, 351-0198, Japan., McHugh TJ; Laboratory for Circuit and Behavioral Physiology, RIKEN Center for Brain Science, Wakoshi, Saitama, 351-0198, Japan., Kuroda KO; Laboratory for Affiliative Social Behavior, RIKEN Center for Brain Science, Hirosawa 2-1, Wakoshi, Saitama, 351-0198, Japan.
Jazyk: angličtina
Zdroj: Molecular brain [Mol Brain] 2023 Jan 19; Vol. 16 (1), pp. 10. Date of Electronic Publication: 2023 Jan 19.
DOI: 10.1186/s13041-023-00993-4
Abstrakt: Social animals become stressed upon social isolation, proactively engaging in affiliative contacts among conspecifics after resocialization. We have previously reported that calcitonin receptor (Calcr) expressing neurons in the central part of the medial preoptic area (cMPOA) mediate contact-seeking behaviors in female mice. Calcr neurons in the posterodorsal part of the medial amygdala (MeApd) are also activated by resocialization, however their role in social affiliation is still unclear. Here we first investigated the functional characteristics of MeApd Calcr + cells; these neurons are GABAergic and show female-biased Calcr expression. Next, using an adeno-associated virus vector expressing a short hairpin RNA targeting Calcr we aimed to identify its molecular role in the MeApd. Inhibiting Calcr expression in the MeApd increased social contacts during resocialization without affecting locomotor activity, suggesting that the endogenous Calcr signaling in the MeApd suppresses social contacts. These results demonstrate the distinct roles of Calcr in the cMPOA and MeApd for regulating social affiliation.
(© 2023. The Author(s).)
Databáze: MEDLINE
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