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A neural basis for tonic suppression of sodium appetite
Sodium appetite is a powerful form of motivation that can drive ingestion of high, yet aversive concentrations of sodium in animals depleted of sodium. However, in normal conditions sodium appetite is suppressed to prevent homeostatic deviations. While molecular and neural mechanisms underlying the...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7065971/ https://www.ncbi.nlm.nih.gov/pubmed/31959933 http://dx.doi.org/10.1038/s41593-019-0573-2 |
Sumario: | Sodium appetite is a powerful form of motivation that can drive ingestion of high, yet aversive concentrations of sodium in animals depleted of sodium. However, in normal conditions sodium appetite is suppressed to prevent homeostatic deviations. While molecular and neural mechanisms underlying the stimulation of sodium appetite received much attention recently, those that inhibit sodium appetite remain largely obscure. Here, we report that serotonin 2c receptor (Htr2c)-expressing neurons in the lateral parabrachial nucleus (LPBN(Htr2c) neurons) inhibit sodium appetite. Activity of these neurons is regulated by bodily sodium content and their activation can rapidly suppress sodium intake. Conversely, inhibition of these neurons specifically drives sodium appetite, even during euvolemic conditions. Importantly, the physiological role of Htr2c expressed by LPBN neurons is to disinhibit sodium appetite. Our results suggest that LPBN(Htr2c) neurons act as a brake against sodium appetite and that its alleviation is required for the full manifestation of sodium appetite. |
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