Bernasconi R, Klein M, Martin P, Portet C, Maître L, Jones R S, Baltzer V, Schmutz M
J Neural Transm. 1985;63(2):169-89. doi: 10.1007/BF01252616.
Amino acid concentrations were measured in the cortex, cerebellum and hippocampus of the mouse brain before and during seizures induced by isoniazid (250 mg/kg i.p.), an inhibitor of L-glutamate-1-decarboxylase (EC 4.1.1.15: GAD). Valproate sodium and diazepam dose-dependently delay the onset of convulsive fits caused by isoniazid. However, neither diazepam nor valproate prevented the decrease in GABA concentrations produced by isoniazid alone. Also, these antiepileptic drugs did not modify the rate of GABA depletion elicited by isoniazid. These results, observed in four different brain structures, strengthen those first obtained with beta-vinyllactic acid, another inhibitor of GAD.
在通过腹腔注射异烟肼（250mg/kg）诱发癫痫发作之前及期间，测量了小鼠大脑皮层、小脑和海马体中的氨基酸浓度。异烟肼是L-谷氨酸脱羧酶（EC 4.1.1.15：GAD）的抑制剂。丙戊酸钠和地西泮可剂量依赖性地延迟异烟肼引起的惊厥发作的起始。然而，地西泮和丙戊酸钠均不能阻止异烟肼单独引起的GABA浓度降低。此外，这些抗癫痫药物并未改变异烟肼引起的GABA消耗速率。在四种不同脑结构中观察到的这些结果，强化了最初用另一种GAD抑制剂β-乙烯基乳酸获得的结果。
