Litvinova S V, Kalyuzhnyi L V, Shulgovskii V V, Aristova V V, Salieva R M
Department of Higher Nervous Activity, Moscow State University.
Biomed Sci. 1990;1(5):471-4.
Intravenous injection of beta-endorphin antiserum (AS) with antibody titres of 1:1,600, 1:3,200, 1:12,800, and 1:20,000 decreased the voltage threshold in the tail-shock test (electrocutaneous nociceptive stimulus) in rats for 2 days, after which time control levels were regained. In the case of AS of titres 1:12,800 and 1:20,000 this threshold then increased to above control levels for about 40 and 100 days, respectively. This effect was abolished by naloxone. In the same rats, an injection of AS of titre 1:1,600 did not alter the latency of the tail-flick test (thermal nociceptive stimulus) but AS of titres 1:3,200, 1:12,800, and 1:20,000 decreased it for 1-4 h, the actual length of time being titre-dependent. After control levels had been regained, there was no further change in latency in the tail-flick test in the subsequent 42 days. Injection with preimmune serum did not change either voltage threshold or latency in the two tail-stimulation tests in control rats. Thus the hyperalgesic short-term effect seen in response to treatment with beta-endorphin AS was more pronounced in response to an electrocutaneous stimulus than to a thermal one, and the long-term selective analgesic effect was present in response to rats given electrocutaneous stimulation but not to thermal stimulation. It is proposed that beta-endorphin AS has a two-stage selective effect: a reduction in beta-endorphin release followed by a 'rebound' increase.
静脉注射抗体效价分别为1:1600、1:3200、1:12800和1:20000的β-内啡肽抗血清(AS),可使大鼠在尾电击试验(电皮肤伤害性刺激)中的电压阈值降低2天,之后恢复到对照水平。对于效价为1:12800和1:20000的AS,该阈值随后分别在约40天和100天内升高至对照水平以上。这种效应可被纳洛酮消除。在同一批大鼠中,注射效价为1:1600的AS并未改变甩尾试验(热伤害性刺激)的潜伏期,但效价为1:3200、1:12800和1:20000的AS可使其潜伏期缩短1 - 4小时,实际缩短时间取决于效价。恢复到对照水平后,在随后的42天内甩尾试验的潜伏期没有进一步变化。给对照大鼠注射免疫前血清在两种尾部刺激试验中均未改变电压阈值或潜伏期。因此,β-内啡肽AS治疗所产生的短期痛觉过敏效应在电皮肤刺激时比热刺激时更明显,而长期选择性镇痛效应则出现在接受电皮肤刺激的大鼠中,而非热刺激的大鼠中。有人提出,β-内啡肽AS具有两阶段的选择性效应:先是β-内啡肽释放减少,随后出现“反弹”增加。