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中缝背核整合了由缺钠诱导摄钠所引发的应激信息。

Dorsal raphe nuclei integrate allostatic information evoked by depletion-induced sodium ingestion.

作者信息

Badauê-Passos Daniel, Godino Andrea, Johnson Alan Kim, Vivas Laura, Antunes-Rodrigues José

机构信息

Departmento de Fisiologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Brazil.

出版信息

Exp Neurol. 2007 Jul;206(1):86-94. doi: 10.1016/j.expneurol.2007.04.008. Epub 2007 Apr 27.

Abstract

Structures of the lamina terminalis (LT) sense and integrate information reflecting the state of body water and sodium content. Output from the LT projects into a neural network that regulates body fluid balance. Serotonin (5-HT) and the dorsal raphe nuclei (DRN) have been implicated in the inhibitory control of salt intake (i.e., sodium appetite). Signals arriving from the LT evoked by fluid depletion-induced sodium ingestion interact with this inhibitory serotonergic system. We investigated the role of neurons along the LT that directly project to the DRN. We analyzed the pattern of immunoreactivity (ir) of LT cells double-labeled for Fos (a marker of neural activity) and Fluorogold (FG; a retrograde tracer) following sodium depletion-induced sodium intake. Seven days after injection of FG into the DRN, sodium appetite was induced by furosemide injection and overnight access to only a low sodium diet (Furo-LSD) and distilled water. Twenty-four hours later, access to 0.3 M NaCl was given to depleted or sham-depleted rats and sodium intake was measured over the following 60 min. Ninety minutes after the termination of the intake test, the animals were perfused and their brains were processed for immunohistochemical detection of Fos and FG. Compared to sham-depleted animals there was a significantly greater number of Fos-/FG-ir double-labeled cells in the subfornical organ, the organum vasculosum of the lamina terminalis and the median preoptic nucleus in rats that ingested NaCl. Projections from the LT cells may contribute to inhibitory mechanisms involving 5-HT neurons in the DRN that limit the intake of sodium and prevent excess volume expansion.

摘要

终板(LT)的结构感知并整合反映机体水和钠含量状态的信息。LT的输出投射到调节体液平衡的神经网络中。血清素(5-HT)和中缝背核(DRN)与盐摄入(即钠食欲)的抑制性控制有关。由液体耗竭诱导的钠摄入所引发的来自LT的信号与这种抑制性血清素能系统相互作用。我们研究了沿LT直接投射到DRN的神经元的作用。我们分析了在钠耗竭诱导的钠摄入后,Fos(神经活动标记物)和荧光金(FG;逆行示踪剂)双标的LT细胞的免疫反应性(ir)模式。在将FG注射到DRN七天后,通过注射速尿并让动物过夜仅摄入低钠饮食(速尿-低钠饮食)和蒸馏水来诱导钠食欲。二十四小时后,给耗竭或假耗竭的大鼠提供0.3 M NaCl,并在接下来的60分钟内测量钠摄入量。在摄入测试结束后九十分钟,对动物进行灌注,并对其大脑进行处理以进行Fos和FG的免疫组织化学检测。与假耗竭动物相比,摄入NaCl的大鼠的穹窿下器官、终板血管器官和视前正中核中Fos-/FG-ir双标细胞的数量明显更多。LT细胞的投射可能有助于涉及DRN中5-HT神经元的抑制机制,该机制限制钠的摄入并防止过量液体潴留。

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