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.