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首页> 外文期刊>American Journal of Physiology >Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst.
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Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst.

机译：钠的消耗与口渴无关，可激活NTS中的醛固酮敏感神经元。

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Thirst and sodium appetite are both critical for restoring blood volume. Because these two behavioral drives can arise under similar physiological conditions, some of the brain sensory sites that stimulate thirst may also drive sodium appetite. However, the physiological and temporal dynamics of these two appetites exhibit clear differences, suggesting that they involve separate brain circuits. Unlike thirst-associated sensory neurons in the hypothalamus, the 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2) neurons in the rat nucleus tractus solitarius (NTS) are activated in close association with sodium appetite (16). Here, we tested whether the HSD2 neurons are also activated in response to either of the two physiological stimuli for thirst: hyperosmolarity and hypovolemia. Hyperosmolarity, produced by intraperitoneal injection of hypertonic saline, stimulated a large increase in water intake and a substantial increase in immunoreactivity for the neuronal activity marker c-Fos within the medial NTS, but not in the HSD2 neurons. Hypovolemia, produced by subcutaneous injection of hyperoncotic polyethylene glycol (PEG), stimulated an increase in water intake within 1-4 h without elevating c-Fos expression in the HSD2 neurons. The HSD2 neurons were, however, activated by prolonged hypovolemia, which also stimulated sodium appetite. Twelve hours after PEG was injected in rats that had been sodium deprived for 4 days, the HSD2 neurons showed a consistent increase in c-Fos immunoreactivity. In summary, the HSD2 neurons are activated specifically in association with sodium appetite and appear not to function in thirst.
机译：口渴和食欲不振对恢复血容量均至关重要。因为这两种行为驱动可能在相似的生理条件下发生，所以刺激口渴的某些大脑感觉部位也可能驱动钠的食欲。然而，这两种食欲的生理和时间动力学表现出明显的差异，表明它们涉及分开的脑回路。与下丘脑中与口渴相关的感觉神经元不同，大鼠孤束核（NTS）中的11-β-羟基类固醇脱氢酶2型（HSD2）神经元与食欲密切相关（16）。在这里，我们测试了HSD2神经元是否也响应口渴的两种生理刺激之一：高渗和血容量不足而被激活。腹膜内注射高渗盐水产生的高渗性刺激了水的摄入量的大量增加以及内侧NTS内神经元活动标记c-Fos的免疫反应性的实质性增加，但在HSD2神经元中却没有。皮下注射高渗聚乙二醇（PEG）引起的血容量不足，可在1-4小时内刺激饮水量的增加，而不会提高HSD2神经元中的c-Fos表达。然而，长时间的血容量不足会激活HSD2神经元，这也会刺激食欲。在将缺钠4天的大鼠中注射PEG后12小时，HSD2神经元显示c-Fos免疫反应性持续增加。总之，HSD2神经元与食欲钠特别相关地被激活，并且似乎在口渴时不起作用。

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