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用４％水合氯醛麻醉大鼠，在下丘脑室旁核（ＰＶＮ）、中缝大核（ＮＲＭ）埋藏双极刺激电极或不锈钢管，以便刺激、电解损毁或微电泳兴奋剂或激动剂。并暴露脊髓背角，利用玻璃微电极记录脊髓背角神经元对伤害刺激坐骨神经的反应，信号经计算机处理。实验结果表明：电刺激ＰＶＮ可抑制脊髓背角神经元伤害反应，其作用时间持续１５～２５ｍｉｎ，刺激ＰＶＮ后３ｍｉｎ抑制作用最强（Ｐ＜０．０１）。电解损毁ＮＲＭ后，刺激ＰＶＮ抑制脊髓背角神经元伤害反应仍然存在，并符合ＰＶＮ抑制伤害反应的林点，实验结果提示：ＰＶＮ参与脊髓背角神经元伤害反应的调制过程，其作用可通过内源性镇痛系统（ＰＡＧ－ＮＲＭ）途径，但也可通过ＰＶＮ－脊髓背角间的直接神经投射途径。
Rats were anesthetized with 4% chloral hydrate and bipolar stimulation electrodes or stainless steel tubes were buried in the hypothalamic paraventricular nucleus (PVN), mesenchymal nucleus (NRM) for stimulation, electrolytic destruction or micro-electrophoresis of agonists or agonists. The dorsal horn of the spinal cord was exposed. The response of the dorsal horn neurons to the injured sciatic nerve was recorded by glass microelectrode. The signals were processed by computer. The experimental results showed that electrical stimulation of PVN could inhibit the neuronal injury in spinal dorsal horn. The duration of action was 15-25 minutes, and the inhibition was the strongest at 3 minutes after PVN stimulation (P <0.01). Electrolytic damage NRM, PVN inhibition of spinal dorsal horn neuronal damage still exists, and consistent with PVN inhibition of injury point Lin point, the experimental results suggest that: PVN involved in spinal dorsal horn neuronal injury in the modulation process, its role can be within Source analgesic system (PAG-NRM) pathway, but also through the direct neuro-projection route between the PVN-spinal dorsal horn.