青霉素惊厥与脑中GABA_A和GABA_B受体亲和力的关系

脑室微量注射青霉素（１１．９ｍｇ·ｍｌ－１，１５μｌ）制作小白鼠惊厥模型；并以同位素示踪法研究大脑皮层、小脑、海马、下丘脑四个脑区ＧＡＢＡＡ和ＧＡＢＡＢ受体亲和力的变化。结果显示，青霉素惊厥时大脑皮层和小脑ＧＡＢＡＡ受体亲和力显著减弱，而海马、下丘脑ＧＡＢＡＡ受体亲和力无变化；青霉素惊厥使四个脑区中ＧＡＢＡＢ受体均显著下降。提示，除了海马和下丘脑的ＧＡＢＡＡ受体以外，四个脑区的ＧＡＢＡＡ和ＧＡＢＡＢ受体均参与了青霉素的致惊厥过程。青霉素可能通过竞争内源性ＧＡＢＡ与ＧＡＢＡＡ和ＧＡＢＡＢ受体的结合，阻断了ＧＡＢＡ介导的突触前和突触后抑制效应并增加了兴奋性递质的释放，显示了惊厥效应。

Relationship Between Penicilline Seizure and Affinity of GABA A and GABA B Receptors of Brain in Mice

We studied the effects of penicilline seizure with intracerebroventricular microinjection penicilline on the affinity of GABA A and GABA B receptors in four brain areas: cerebral cortex, cerebellum, hippocampus, hypothalamus in mice. The results showed that the affinity of GABA A receptor in both cerebral cortex and cerebellam was markedly weakened when penicilline seizure was developed, whereas the affinity of GABA A receptor in hippocampus and hypothalamus had no change. The penicilline seizure significantly decreased the affinity of GABA B receptor in all of four brain areas. These results suggested that besides GABA A receptor in hippocampus and hypothalamus, all of other GABA A and GABA B receptors in the four brain areas participated in the development of penicilline seizure. Probably the penicilline blockeded the presynaptic and postsynaptic inhibition which was mediated by GABA through competing the GABA binding sites on GABA A and GABA B receptors with endogenous GABA, and increased the release of excitatory neurotransmitters from presynaptic membranes, thereby evoking the seizure.