Takeshige C, Zhao W H, Guo S Y
Department of Physiology, Showa University School of Medicine, Tokyo, Japan.
Brain Res Bull. 1991 May;26(5):771-8. doi: 10.1016/0361-9230(91)90174-i.
Lesion of the preoptic area (POA) or medial arcuate nucleus (M-HARN) abolished acupuncture analgesia (AA). Potentials in the median eminence (ME) evoked by stimulation of the acupuncture point (AP) were not affected by lesion of either the POA or M-HARN alone, but were abolished by concurrent lesion of both. No analgesia was produced by stimulation of the POA. Analgesia produced by stimulation of the M-HARN was abolished by lesion of the POA, and the abolished analgesia was restored by concurrent stimulation of the POA and M-HARN, hence POA and M-HARN outputs might converge in the ME to produce AA. Similar convergence from the anterior arcuate nucleus (A-HARN) and POA to the ME was observed in analgesia (NAA) produced by stimulation of a nonacupuncture point (NAP). Two pathways diverged from the lateral hypothalamus in the AA afferent pathway and two from the lateral periaqueductal central gray (L-PAG) in the NAA afferent pathway. POA potentials evoked by stimulation of the AP were reversed by naloxone, and those evoked by stimulation of the AP were reversed by dexamethasone. ACTH sensitive sites were found in both the L-PAG and the anterior hypothalamus.
视前区(POA)或内侧弓状核(M-HARN)损伤可消除针刺镇痛(AA)。针刺穴位(AP)所诱发的正中隆起(ME)电位,单独损伤POA或M-HARN均不受影响,但两者同时损伤则该电位消失。刺激POA不产生镇痛作用。刺激M-HARN所产生的镇痛作用,经POA损伤后消失,而同时刺激POA和M-HARN可恢复已消失的镇痛作用,因此POA和M-HARN的输出可能在ME汇聚以产生AA。在刺激非穴位(NAP)所产生的镇痛(NAA)中,观察到从前弓状核(A-HARN)和POA到ME有类似的汇聚。在AA传入通路中有两条通路从外侧下丘脑发出,在NAA传入通路中有两条通路从外侧导水管周围中央灰质(L-PAG)发出。刺激AP所诱发的POA电位可被纳洛酮逆转,刺激AP所诱发的电位可被地塞米松逆转。在L-PAG和下丘脑前部均发现了促肾上腺皮质激素敏感位点。