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Herein, we investigated the role for the corticotropin-releasing factor receptor 1 (CRF\n                    <jats:sub>1<\/jats:sub>\n                    ) in the acute sociability deficits induced by morphine and the related activity of oxytocin (OXY)- and arginine-vasopressin (AVP)-expressing neurons of the paraventricular nucleus of the hypothalamus (PVN). For this purpose, we used both the CRF\n                    <jats:sub>1<\/jats:sub>\n                    receptor-preferring antagonist compound antalarmin and the genetic mouse model of CRF\n                    <jats:sub>1<\/jats:sub>\n                    receptor-deficiency. Antalarmin completely abolished sociability deficits induced by morphine in male, but not in female, C57BL\/6J mice. Accordingly, genetic CRF\n                    <jats:sub>1<\/jats:sub>\n                    receptor-deficiency eliminated morphine-induced sociability deficits in male mice. Ex vivo electrophysiology studies showed that antalarmin also eliminated morphine-induced firing of PVN neurons in male, but not in female, C57BL\/6J mice. Likewise, genetic CRF\n                    <jats:sub>1<\/jats:sub>\n                    receptor-deficiency reduced morphine-induced firing of PVN neurons in a CRF\n                    <jats:sub>1<\/jats:sub>\n                    gene expression-dependent manner. The electrophysiology results consistently mirrored the behavioral results, indicating a link between morphine-induced PVN activity and sociability deficits. Interestingly, in male mice antalarmin abolished morphine-induced firing in neurons co-expressing OXY and AVP, but not in neurons expressing only AVP. In contrast, in female mice antalarmin did not affect morphine-induced firing of neurons co-expressing OXY and AVP or only OXY, indicating a selective sex-specific role for the CRF\n                    <jats:sub>1<\/jats:sub>\n                    receptor in opiate-induced PVN OXY activity. The present findings demonstrate a major, sex-linked, role for the CRF\n                    <jats:sub>1<\/jats:sub>\n                    receptor in sociability deficits and related brain alterations induced by morphine, suggesting new therapeutic strategy for opiate use disorders.\n                  <\/jats:p>","DOI":"10.7554\/elife.100849","type":"journal-article","created":{"date-parts":[[2024,9,25]],"date-time":"2024-09-25T17:02:11Z","timestamp":1727283731000},"update-policy":"https:\/\/doi.org\/10.7554\/elife.100849","source":"Crossref","is-referenced-by-count":0,"title":["Disruption of the CRF1 receptor eliminates morphine-induced sociability deficits and firing of oxytocinergic neurons in male 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