A neural basis for tonic suppression of sodium appetite.,Nature Neuroscience

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A neural basis for tonic suppression of sodium appetite.
Nature Neuroscience ( IF 21.2 ) Pub Date : 2020-01-20 , DOI: 10.1038/s41593-019-0573-2
Seahyung Park ₁ , Kevin W Williams ₂ , Chen Liu _{2,

3} , Jong-Woo Sohn ₁

Affiliation

Sodium appetite is a powerful form of motivation that can drive ingestion of high, yet aversive concentrations of sodium in animals that are depleted of sodium. However, in normal conditions, sodium appetite is suppressed to prevent homeostatic deviations. Although molecular and neural mechanisms underlying the stimulation of sodium appetite have received much attention recently, mechanisms that inhibit sodium appetite remain largely obscure. Here we report that serotonin 2c receptor (Htr2c)-expressing neurons in the lateral parabrachial nucleus (LPBNHtr2c 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. Notably, the physiological role of Htr2c expressed by LPBN neurons is to disinhibit sodium appetite. Our results suggest that LPBNHtr2c neurons act as a brake against sodium appetite and that their alleviation is required for the full manifestation of sodium appetite.

中文翻译：

补品抑制钠食欲的神经基础。

钠食欲是一种强大的动机形式，可以促使缺钠动物摄入高浓度但令人厌恶的钠。然而，在正常情况下，钠食欲会受到抑制，以防止稳态偏差。尽管刺激钠食欲的分子和神经机制最近受到了广泛关注，但抑制钠食欲的机制仍然很大程度上不清楚。在这里，我们报道了外侧臂旁核中表达血清素 2c 受体 (Htr2c) 的神经元（LPBNHtr2c 神经元）抑制钠食欲。这些神经元的活动受体内钠含量的调节，它们的激活可以迅速抑制钠的摄入。相反，即使在血容量正常的情况下，抑制这些神经元也会特异性地促进钠食欲。值得注意的是，LPBN 神经元表达的 Htr2c 的生理作用是抑制钠食欲。我们的结果表明，LPBNHtr2c 神经元对钠食欲起到抑制作用，并且其缓解是钠食欲充分表现所必需的。

更新日期：2020-01-20

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