Bernasconi R, Bencze W, Hauser K, Klein M, Martin P, Schmutz M
Neurosci Lett. 1984 Jun 29;47(3):339-44. doi: 10.1016/0304-3940(84)90536-6.
GABA level and the activity of L-glutamate-1-decarboxylase (GAD) (EC 4.1.1.15) were studied in brains of mice treated with beta-vinyllactic acid, a new, selective and pyridoxal phosphate-independent GAD inhibitor. Valproate and diazepam protected mice against convulsions caused by beta-vinyllactic acid although both anti-epileptic drugs antagonized neither the decrease in GABA concentrations nor the inhibition of GAD observed after treatment with beta-vinyllactic acid alone. Assuming that the anticonvulsant effect measured with both antiepileptics is GABA mediated, these results support the hypothesis of a postsynaptic enhancement of GABAergic transmission by diazepam and valproate.
研究了新型、选择性且不依赖磷酸吡哆醛的谷氨酸脱羧酶（GAD）（EC 4.1.1.15）抑制剂β-乙烯基乳酸处理的小鼠大脑中的γ-氨基丁酸（GABA）水平及GAD活性。丙戊酸盐和地西泮可保护小鼠免受β-乙烯基乳酸引起的惊厥，尽管这两种抗癫痫药物均未拮抗单独使用β-乙烯基乳酸处理后观察到的GABA浓度降低或GAD抑制。假设这两种抗癫痫药物测得的抗惊厥作用是由GABA介导的，这些结果支持了地西泮和丙戊酸盐对GABA能传递进行突触后增强的假说。
