论文部分内容阅读
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。
The hypothalamic arcuate nucleus (ARC) is a major nucleus in the brain that concentrates the β-END endoplasmic reticulum. Neonatal injection of monosodium glutamate (MSG) can selectively damage neuronal soma in ARC without involving the passing fibers, and is a good model for studying neuronal physiological functions in ARC. This experiment uses this experimental model to study the analgesic effect of stimulating ARC. As a result, it was found that in such MSG-treated rats, there was no apparent analgesic effect stimulated by ARC (as measured by electrical stimulation of rat tail-cries). Intracerebroventricular administration of β-END (5 μg / 10 μl) restored the analgesic effect of stimulating ARC. However, intracerebroventricular injection of dopamine (5 μg / 10 μl) not only failed to recover, but attenuated the analgesic effect of normal ARC on ARC effect. The experimental results suggest that there is no obvious analgesic effect in MSG-treated rats, which may be due to the loss of β-END neurons in ARC and DA neurons play no role in them.