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Oxytocin-receptor-expressing neurons in the parabrachial nucleus regulate fluid intake

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...

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Detalles Bibliográficos
Autores principales: Ryan, Philip J., Ross, Silvano I., Campos, Carlos A., Derkach, Victor A., Palmiter, Richard D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group US 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705772/
https://www.ncbi.nlm.nih.gov/pubmed/29184212
http://dx.doi.org/10.1038/s41593-017-0014-z
Descripción
Sumario: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.