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脑室微量注射青霉素(11.9 mg·ml~(-1),15μI)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 GABA_A和 GABA_B 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 GABA_A 受体亲和力显著减弱,而海马、下丘脑 GABA_A 受体亲和力无变化;青霉素惊厥使四个脑区中 GABA_B 受体均显著下降。提示,除了海马和下丘脑的 GABA_A 受体以外,四个脑区的 GABA_A和 GABA_B 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 GABA_A 和 GABA_B 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。
Ventricular microinjection of penicillin (11.9 mg · ml -1, 15μI) made mouse convulsion model; and using isotope tracer method to study the cerebral cortex, cerebellum, hippocampus, hypothalamic brain regions GABA_A and GABA_B receptor affinity Variety. The results showed that penicillin convulsions in the cerebral cortex and cerebellum GABA_A receptor affinity decreased significantly, while the hippocampus, hypothalamus GABA_A receptor affinity did not change; penicillin convulsion so that the four brain regions of GABA_B receptor were significantly decreased. Tip, in addition to the hippocampus and hypothalamus GABA_A receptor, the four brain regions of GABA_A and GABA_B receptors are involved in penicillin-induced convulsions. Penicillin may block the GABA-mediated presynaptic and postsynaptic inhibitory effects and increase the release of excitatory neurotransmitters by competing with the binding of endogenous GABA to the GABA A and GABA B receptors, demonstrating the seizure effect.