作者
Yuan Yuan,Wéi Wú,Ming Chen,Fang Cai,Chengyu Fan,Wei L. Shen,Wenzhi Sun,Ji Hu
摘要
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Curry D.C. de Waal F.B. Young L.J. Oxytocin-dependent consolation behavior in rodents.Science. 2016; 351: 375-378Crossref PubMed Scopus (332) Google Scholar], we find that PVN CRH neurons are rapidly and strongly inhibited by reward consumption. Reward decreases anxiety-like behavior and stress-hormone surge induced by direct acute activation of PVN CRH neurons or repeated stress challenge. Repeated stress upregulates glutamatergic transmission and induces an N-methyl-D-aspartate receptor (NMDAR)-dependent burst-firing pattern in these neurons, whereas reward consumption rebalances the synaptic homeostasis and abolishes the burst firing. Anatomically, PVN CRH neurons integrate widespread information from both stress- and reward-related brain areas in the forebrain and midbrain, including multiple direct long-range GABAergic afferents. Together, these findings reveal a hypothalamic circuit that organizes adaptive stress response by complementarily integrating reward and stress signals and suggest that intervention in this circuit could provide novel methods to treat stress-related disorders.