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  • Title: Reward Inhibits Paraventricular CRH Neurons to Relieve Stress.
    Author: Yuan Y, Wu W, Chen M, Cai F, Fan C, Shen W, Sun W, Hu J.
    Journal: Curr Biol; 2019 Apr 01; 29(7):1243-1251.e4. PubMed ID: 30853436.
    Abstract:
    Chronic, uncontrollable stress can lead to various pathologies [1-6]. Adaptive behaviors, such as reward consumption, control excessive stress responses and promote positive health outcomes [3, 7-10]. Corticotrophin-releasing hormone (CRH) neurons in paraventricular nucleus (PVN) represent a key neural population organizing endocrine, autonomic, and behavioral responses to stress by initiating hormonal cascades along the hypothalamic-pituitary-adrenal (HPA) axis and orchestrating stress-related behaviors through direct projections to limbic and autonomic brain centers [11-18]. Although stress and reward have been reported to induce changes of c-Fos and CRH expression in PVN CRH neurons [19-23], it has remained unclear how these neurons respond dynamically to rewarding stimuli to mediate the stress-buffering effects of reward. Using fiber photometry of Ca2+ signals within genetically identified PVN CRH neurons in freely behaving mice [24-26], 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.
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