Takeshige C, Nakamura A, Asamoto S, Arai T
Department of Physiology, Showa University School of Medicine, Tokyo, Japan.
Brain Res Bull. 1992 Jul;29(1):37-44. doi: 10.1016/0361-9230(92)90006-j.
Potentials in the final sector of the afferent pathway from the acupuncture point (AP) were enhanced by intraperitoneal 0.5 mg/kg morphine without changing the threshold of AP stimulation and greatly decreased by hypophysectomy. The decreased potentials were restored to the control level by morphine (0.5 mg/kg, IP). Potentials evoked in the final sector of the afferent pathway from the nonacupuncture point (NAP) by NAP stimulation after lesion of the analgesia inhibitory system were greatly enhanced by corticotropin (ACTH) (0.25 mg/kg, IP) and greatly decreased by hypophysectomy. Diminished potentials were restored to the control level by ACTH (0.25 mg/kg, IP). Both morphine (0.5 mg/kg, IP) and ACTH (0.25 mg/kg, IP) produced analgesia, but morphine did not affect acupuncture analgesia (AA) and ACTH did not affect nonacupuncture point stimulation-produced analgesia (NAA). All analgesia, that due to 0.5 mg/kg morphine or 0.25 mg/kg ACTH, AA, and NAA were abolished by hypophysectomy. The abolished AA and NAA were restored by 0.5 mg/kg morphine and 0.25 mg/kg ACTH, respectively. Hence, beta-E and ACTH liberated from the pituitary gland by stimulation of an AP and NAP may act as positive feedback on the AA and NAA afferent pathways, respectively.
腹腔注射0.5mg/kg吗啡可增强穴位传入通路终末节段的电位,而不改变穴位刺激阈值,垂体切除则使其大幅降低。降低的电位可通过吗啡(0.5mg/kg,腹腔注射)恢复至对照水平。损毁镇痛抑制系统后,非穴位刺激在非穴位传入通路终末节段诱发的电位,在注射促肾上腺皮质激素(ACTH)(0.25mg/kg,腹腔注射)后大幅增强,垂体切除则使其大幅降低。降低的电位可通过ACTH(0.25mg/kg,腹腔注射)恢复至对照水平。吗啡(0.5mg/kg,腹腔注射)和ACTH(0.25mg/kg,腹腔注射)均可产生镇痛作用,但吗啡不影响针刺镇痛(AA),ACTH不影响非穴位刺激产生的镇痛(NAA)。垂体切除可消除所有镇痛作用,包括0.5mg/kg吗啡或0.25mg/kg ACTH所致的镇痛、AA和NAA。被消除的AA和NAA分别可通过0.5mg/kg吗啡和0.25mg/kg ACTH恢复。因此,刺激穴位和非穴位从垂体释放的β-内啡肽和ACTH可能分别对AA和NAA的传入通路起正反馈作用。