Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst
Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst
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DOI：
10.1152/ajpregu.00391.2006
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发表时间：
2007-03-01
影响因子：
2.8
通讯作者：
Loewy, Arthur D.
中科院分区：
文献类型：
--
作者：
Geerling, Joel C.;Loewy, Arthur D.
口渴和对钠的需求对恢复血容量都至关重要。由于这两种行为驱动可以在类似的生理条件下产生，因此刺激口渴的一些大脑感觉部位也可能会驱动钠的食欲。然而，这两种欲望的生理和时间动力学表现出明显的差异，表明它们涉及不同的大脑回路。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（HSD 2）神经元与钠食欲密切相关（16）。在这里，我们测试了HSD 2神经元是否也响应于口渴的两种生理刺激中的任一种而被激活：高渗和低血容量。高渗，通过腹腔注射高渗盐水，刺激了大量增加的水摄入量和大量增加的免疫反应性的神经元活动标记c-Fos内的内侧NTS，但不是在HSD 2神经元。通过皮下注射高渗聚乙二醇（PEG）产生的低血容量在1 - 4 h内刺激了水摄入量的增加，而没有升高HSD 2神经元中的c-Fos表达。然而，HSD 2神经元被长时间的低血容量激活，这也刺激了钠食欲。在钠剥夺4天的大鼠中注射PEG后12小时，HSD 2神经元显示出c-Fos免疫反应性的一致增加。总之，HSD 2神经元被激活，特别是与钠的食欲，似乎没有功能的口渴。
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.