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游泳应激增强下丘脑室旁核中还原型辅酶II-黄递酶组织化学染色。

Swim stress enhances the NADPH-diaphorase histochemical staining in the paraventricular nucleus of the hypothalamus.

作者信息

Sánchez F, Moreno M N, Vacas P, Carretero J, Vázquez R

机构信息

Department of Human Anatomy and Histology, Faculty of Medicine, University of Salamanca, Campus Unamuno, 37007, Salamanca, Spain.

出版信息

Brain Res. 1999 May 15;828(1-2):159-62. doi: 10.1016/s0006-8993(99)01295-0.

DOI:10.1016/s0006-8993(99)01295-0
PMID:10320736
Abstract

Regulatory control of the hypothalamic-pituitary-adrenocortical axis (HPA) originates principally from the paraventricular nucleus (PVN), which contains an important population of nitric oxide synthesizing (NOS) neurons. In the present study, the effect of swim stress upon these neurons was investigated by means of the NADPH-diaphorase (ND) histochemical technique. A significant increase in the number of ND-neurons was observed following forced swim, especially after 30 min. These data confirm the involvement of NOS-neurons of the PVN in the response to different types of acute stressors.

摘要

下丘脑-垂体-肾上腺皮质轴(HPA)的调节控制主要源于室旁核(PVN),该核包含大量重要的一氧化氮合成(NOS)神经元。在本研究中,通过NADPH黄递酶(ND)组织化学技术研究了游泳应激对这些神经元的影响。强迫游泳后,尤其是30分钟后,观察到ND神经元数量显著增加。这些数据证实了PVN的NOS神经元参与了对不同类型急性应激源的反应。

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