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作 者:龚珊[1] 矫勇益[1] 殷伟平[1] 印其章[1]
机构地区:[1]苏州医学院神经生物学研究室
出 处:《神经科学》1994年第1期7-11,共5页Chinese Journal of Neuroscience
基 金:国家自然科学基金
摘 要:下丘脑弓状核(ARC)是脑内β-内啡肽(β-END)能神经元胞体集中的一个主要核团。新生期注射谷氨酸单钠(MSG)能选择性地损毁ARC中的神经元胞体而不累及路过纤维,是研究ARC中神经元生理功能的一个良好模型。本实验利用这个实验模型研究刺激ARC的镇痛效应。结果发现在这种MSG处理的大鼠,刺激ARC不再出现明显的镇痛效应(用电刺激鼠尾-嘶叫法测定)。这时脑室内注射β-END(5μg/10μl)能使刺激ARC的镇痛效应恢复;若脑室注射多巴胺(DA,5μg/10μl)不仅没有恢复作用,反而能削弱正常大鼠刺激ARC的镇痛效应。实验结果提示,经MSG处理的大鼠之所以不出现明显的镇痛效应,可能是由于ARC中丧失了β-END能神经元的结果,DA能神经元在其中不起重要作用。Hypothalamic arcuate nucleus(ARC) is the principal nucleus contaiaing β-endorphinergic (β-END) neurons in the brain. Neuronal cell bodies in ARC can be destroyed, hut sparing the fibers of passage, by neonatal administration of monosodium glutamate(MSG) in rats, which is a valuable model for studying the function of neurons in ARC. In the present experiment this model(MSG-treated rats) was used to investigate the analgesic effect of ARC stimulation by tail stimulation-vocalization test. It was found that no significant analgesic effect was observed after ARC stimulation in MSG-treated rats. The analgesic effect of ARC stimulation in MSG-treated rats could he recovered after intracerebroveotricular injection of β-END (5μg/ 10μl), hut not of dopamine(5μg/ 10μl), which on the contrary, could attenuate the analgesic effect of ARC stimulation in normal rats. Experimeotal results suggest that the disappearance of analgesic effect of ARC stimulation in MSG-treated rats might be the result of damage of β-END neurons in ARC, and no significant role could be attributed to dopaminergic neurons.
分 类 号:R338.3[医药卫生—人体生理学]
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