Department of Pharmacology and Physiology, Oklahoma State University-Center for Health Sciences, 1111 West 17th St, Tulsa, OK, 74107-1898, USA.
J Physiol Sci. 2013 Jan;63(1):39-46. doi: 10.1007/s12576-012-0229-4. Epub 2012 Sep 4.
Serotonin (5-HT) has been implicated in centrally mediated compensatory responses to volume loss in rats. Accordingly, we hypothesized that slowly developing, non-hypotensive hypovolemia increases serotonin in the hindbrain nucleus of the solitary tract (NTS). We produced volume loss in adult male rats by administering hyperoncotic polyethylene glycol (PEG) and then assessed 5-HT levels in the NTS using measurements of tissue 5-HT content or 5-HT immunohistochemistry. The results show selective increases of 5-HT in the caudal NTS after PEG treatment, but no change in the primary 5-HT metabolite, 5-HIAA. Moreover, the intensity of 5-HT immunolabeled fibers in the caudal NTS was increased after PEG treatment. These findings suggest that, after PEG-induced hypovolemia, 5-HT accumulates in neural elements in the caudal NTS. We propose that this accumulation is attributable to an initial release of 5-HT that then acts at presynaptic autoreceptors to inhibit subsequent 5-HT release.
血清素(5-HT)被认为参与了大鼠容量损失引起的中枢介导的代偿反应。因此,我们假设缓慢发展的、非低血压性低血容量会增加孤束核(NTS)中的血清素。我们通过给成年雄性大鼠施用高渗聚乙二醇(PEG)来产生容量损失,然后使用组织 5-HT 含量或 5-HT 免疫组织化学测量来评估 NTS 中的 5-HT 水平。结果表明,PEG 处理后,尾侧 NTS 中的 5-HT 选择性增加,但 5-HT 的主要代谢产物 5-HIAA 没有变化。此外,PEG 处理后,尾侧 NTS 中 5-HT 免疫标记纤维的强度增加。这些发现表明,在 PEG 诱导的低血容量后,5-HT 在尾侧 NTS 的神经元件中积累。我们提出,这种积累归因于 5-HT 的初始释放,然后在突触前自身受体上作用以抑制随后的 5-HT 释放。