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在大鼠腰脊髓背角泳入辣根过氧化酶（ＨＲＰ），下丘脑室旁核（ＰＶＮ）找到逆行标记细胞；在ＰＶＮ泳入ＨＲＰ，脊髓内均有顺行标记纤维和终末分布于脊髓背角第Ⅰ、Ⅱ、和Ⅳ、Ⅴ板层。可见大鼠ＰＶＮ－脊髓背角间存在直接纤维联系。用行为测痛法观察到电刺激ＰＶＮ或注射谷氨酸钠、盐酸吗啡，痛阈均显著升高。纳络酮可翻转盐酸吗啡的作用。电刺激ＰＶＮ的同时，电针双侧“足三里”痛阈升高更显著，说明刺激ＰＶＮ可使痛阈升高，电针“足三里”有协同作用。用微电极记录脊髓背角神经元伤害单位活动，其反应可被电刺激ＰＶＮ所抑制。分别电解中脑导水管周围灰质（ＰＡＧ）和中缝大核（ＮＲＭ）后，ＰＶＮ对脊髓背角神经元伤害反应的抑制仍存在。实验结果表明，ＰＶＮ参与了痛觉下行的调制过程。
HRP and PVN were found in rat lumbar dorsal horn. Retrogradely labeled cells were found in the PVN. In the PVN, HRP was labeled with antegrade fibers and terminals in the spinal cord Spinal dorsal horn Ⅰ, Ⅱ, and Ⅳ, Ⅴ plate layer. Visible PVN - spinal dorsal horn exists between the direct fiber connection. Pain was observed by behavioral testing of electrical stimulation of PVN or sodium glutamate, morphine hydrochloride, pain threshold were significantly increased. Naloxone reverses the effect of morphine hydrochloride. Electrical stimulation of PVN at the same time, electroacupuncture “Zusanli” pain threshold increased more significantly, indicating that stimulation of PVN can increase the pain threshold, EA “Zusanli” has a synergistic effect. Microelectrodes were used to record the neuronal injury unit activity in the dorsal horn of the spinal cord, and their responses could be suppressed by electrical stimulation of PVN. Inhibition of PVN injury to neurons in the dorsal horn of the spinal cord still existed after electrolysis of the periaqueductal gray (PAG) and the midnucleus ramen (NRM), respectively. The experimental results show that PVN participates in the pain modulation process.