摘要
脑室注射外源性GABA可明显提高小鼠痛阈,其作用呈剂量一效应依赖关系。苯巴比妥钠通过抑制GABA摄取、激活GABA受体或GABA摹拟效应使痛阈显著升高,GABA与其呈协同作用;而青霉素通过抑制GABA摄取及竞争GABA受体对痛阈产生先上升后下降的双向效应,GABA与其呈拮抗作用。提示脑中GABA系统可能参与痛觉调制,其机制可能与脑中GABA含量无直接关系,而与GABA的突触过程密切相关。
Intracerebroventricular injection of extragenetic OABA significantly raised the pain threshold (PT) of mice, and this action app eared a dose-effect dependent relation. Sodium phenobarbital caused marked rises in PT by suppressing GABA uptake, activating GABA receptor and GABA-mimetic action. Whereas penicillin early produced PT rises by suppressing GABA uptake, late PT fall by competing GABA receptor. The results suggest that GABA system in brain seem to participate in the mediation of the Pain sense, the mechanizm of which may bear no relation on GABA content of brain while in close relationship with synaptic process of GABA.
出处
《苏州科技学院学报(社会科学版)》
1990年第S1期62-67,共6页
Journal of University of Science and Technology of Suzhou:Social Science