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Adolescent CB1 receptor antagonism influences subsequent social interactions and neural activity in female rats
Author(s) -
Simone Jonathan J.,
Baumbach Jennet L.,
McPherson Jennifer,
McCormick Cheryl M.
Publication year - 2020
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1002/jdn.10028
Subject(s) - am251 , nucleus accumbens , prefrontal cortex , endocannabinoid system , cannabinoid receptor , cannabinoid , psychology , medicine , endocrinology , agonist , dentate gyrus , neuroscience , hippocampus , receptor , central nervous system , biology , cognition
We previously demonstrated that repeated exposure to the CB1 receptor antagonist/inverse agonist AM251 in adolescence (PND 30–44) increased social interactions in female rats when tested 48 h after the final exposure to the antagonist. Here, we investigated whether the increased sociality would be present after a longer drug washout period (5 days) in both male and female rats (experiment 1), and sought to identify candidate brain regions that may explain the observed differences in social behaviours between AM251 and vehicle‐treated female rats (experiment 2). While drug‐free, adolescent AM251 treatment increased social interactions in females and not in males. AM251 female rats had increased neural activity (as measured by the expression of early growth response protein‐1; EGR‐1) in the nucleus accumbens shell and cingulate gyrus of the medial prefrontal cortex, with no observed differences in EGR‐1 expression in the dorsal hippocampus, nucleus accumbens core, or prelimbic and infralimbic subdivisions of the medial prefrontal cortex relative to vehicle rats. Together, these results demonstrate a sex‐specific role of adolescent endocannabinoid signalling in the normative development of social behaviours and provide further support for adolescence as a vulnerable period for the effects of altered endocannabinoid signalling.