Brain regions that regulate fluid satiation are not well characterized, yet are essential for understanding fluid homeostasis. We found that oxytocin-receptor-expressing neurons in the parabrachial nucleus of mice (Oxtr^PBN neurons) are key regulators of fluid satiation. Chemogenetic activation of Oxtr^PBN neurons robustly suppressed noncaloric fluid intake, but did not decrease food intake after fasting or salt intake following salt depletion; inactivation increased saline intake after dehydration and hypertonic saline injection. Under physiological conditions, Oxtr^PBN neurons were activated by fluid satiation and hypertonic saline injection. Oxtr^PBN neurons were directly innervated by oxytocin neurons in the paraventricular hypothalamus (Oxt^PVH neurons), which mildly attenuated fluid intake. Activation of neurons in the nucleus of the solitary tract substantially suppressed fluid intake and activated Oxtr^PBN neurons. Our results suggest that Oxtr^PBN neurons act as a key node in the fluid satiation neurocircuitry, which acts to decrease water and/or saline intake to prevent or attenuate hypervolemia and hypernatremia.

中文翻译：

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臂旁核中表达催产素受体的神经元调节体液摄入

调节体液饱合度的大脑区域尚未很好地表征，但对于理解体液稳态是必不可少的。我们发现，小鼠臂旁核中的催产素受体表达神经元（Oxtr ^PBN神经元）是体液饱和的关键调节因子。Oxtr ^PBN神经元的化学遗传学激活强烈抑制了非卡路里液体的摄入，但禁食后的食物摄入量或盐分耗尽后的盐摄入量并未减少。失活增加脱水和注射高渗盐水后的盐摄入量。在生理条件下，Oxtr ^PBN神经元通过液体饱和和高渗盐水注射而被激活。Oxtr ^PBN丘脑下丘脑旁的催产素神经元直接刺激神经元（Oxt ^PVH 神经元），从而轻度减少了液体摄入。孤立道细胞核中神经元的激活基本上抑制了液体的摄入并激活了Oxtr ^PBN神经元。我们的结果表明，Oxtr ^PBN神经元在体液充血神经回路中起着关键节点的作用，其作用是减少水和/或盐的摄入量，以预防或减轻高血容量和高钠血症。