Nature Neuroscience · 2017 · 117 citations · 41 references
Life SciencesNeurosciencePhysiologyBehavioral NeuroscienceNeuroendocrinologyNeurophysiologyAppetite RegulationDehydration PhysiologyNeuroendocrine PhysiologyNeuromodulatory CircuitsOxytocin PhysiologyWater Balance PhysiologyCentral Oxytocinergic PathwaysChemogenetic NeuromodulationFluid Balance HomeostasisHypothalamic Oxytocin NeuronsOxytocin Receptor SignalingParabrachial NucleusParaventricular NucleusPhysiological Homeostasis
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 (OxtrPBN neurons) are key regulators of fluid satiation. Chemogenetic activation of OxtrPBN 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, OxtrPBN neurons were activated by fluid satiation and hypertonic saline injection. OxtrPBN neurons were directly innervated by oxytocin neurons in the paraventricular hypothalamus (OxtPVH neurons), which mildly attenuated fluid intake. Activation of neurons in the nucleus of the solitary tract substantially suppressed fluid intake and activated OxtrPBN neurons. Our results suggest that OxtrPBN 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. The authors show that oxytocin-receptor-expressing neurons in the parabrachial nucleus are key regulators of fluid homeostasis that suppress fluid intake when activated, but do not decrease food intake after fasting or salt intake after salt depletion.
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Fay Wang, John J. Flanagan, Nan Su et al. · Journal of Molecular Diagnostics · 2011 · 2.7K citations · Full text
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Medicine, Neurobiology, Neuroscience +14