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Study of the biochemical processing of the biowarning information through the hypothalamu

下丘脑生物预警信息生化处理的研究

基本信息

批准号：
04670095
负责人：
SHIMIZU Nobuaki
金额：
$ 1.34万
依托单位：
Kanazawa University (1993)Kyushu University (1992)
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

项目摘要

This study was designed to study the dynamic changes in serotonin (5HT) and noradrenaline (NA) levels during the stressful stimuli, and have reached the following conclusions in rats. (1) Immobilization-stress caused anorexia in conjunction with an immediate increase in thehypothalamic 5HT release. Injection of 5HT receptor antagonist significantly reduced the immobilization-induced anorexia, suggesting that the hypothalamic serotonergic ystem is activated during stress and 5HT is an inhibitory transmitter in feeding behavior. (2) Immobilization elevated NA levels in the medial prefrontal cortex (PFC). Pre-injection of a benzodiazepine receptor agonist, diazepam, significantly attenuated the immobilization-induced NA release, while the injection of an anxiogenic compound, FG7142, facilitated it in non-stressed condition. Thus the stressfull stimuli activate the NA system in the medial PFC which may be modulated by an activation of the benzodiazepine receptors in the brain. (3) Immobilization-stress rapidly increased NA levels of spleen in conjunction with the suppression of natural killer (NK) cytotoxicity. Both theincreased levelsof NA ad he suppresion of NK cytotoxicity were significantly attenuated after surgical denervation of the splenic sympathetic nerve, indicating that immobilization-induced suppression of splenic N/K cytotoxicity was mediated predominantly through enhanced activity of the splenic sympathetic nerve..These results suggest that both 5HT and NA may act asneurotransmitters and/or neuromodlators which regulate biowarning processes in the living body.

本研究旨在研究应激刺激对大鼠5-羟色胺（5-HT）和去甲肾上腺素（NA）水平的动态变化，并得出以下结论。(1)制动应激引起食欲减退，并立即增加下丘脑5-HT的释放。注射5-HT受体拮抗剂可明显减轻束缚引起的厌食，提示应激时下丘脑多巴胺能神经元被激活，5-HT是摄食行为的抑制性递质。(2)制动升高NA水平的内侧前额叶皮层（PFC）。预先注射苯二氮卓类受体激动剂地西泮，显着衰减固定诱导的NA释放，而注射的抗焦虑化合物，FG 7142，促进它在非应激条件下。因此，应激刺激激活内侧PFC中的NA系统，这可能是由大脑中的苯二氮卓类受体的激活来调节的。(3)制动应力迅速增加NA水平的脾脏结合自然杀伤细胞（NK）的细胞毒性的抑制。去脾交感神经后，NA水平的升高和NK细胞毒性的抑制均显著减弱，表明制动诱导的脾N/K细胞毒性抑制主要通过增强脾交感神经的活性来介导。这些结果表明，5-HT和NA可能都是生物体内生物预警过程的神经递质和/或神经调节剂。