期刊
NATURE NEUROSCIENCE
卷 20, 期 12, 页码 1722-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41593-017-0014-z
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资金
- Australian American Fellowship
- National Health and Medical Council of Australia
- Hope Funds for Cancer Research
- US National Institutes of Health [R01-DA24908]
- DECODE grant program
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.
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