Abstract
It has been said that toxopyrimidine (TXP) or isonicotinic acid hydrazide (INAH) causes a decreas of the glutamic decarboxylase activity and consequently the reaction product, γ-aminobutyric acid (ABA) or γ-amino-β-hydroxybutyric acid (OABA) is formed. If OABA may be the central nervous depressing substance, the decrease of OABA formation may be the direct cause of the occurrence of convulsions produced by the administration of TXP or INAH. Studies were made on convulsion-depressing and death-preventing actions of ABA, OABA or vitamin B_6 injected into the cisterna magna of a dog in which convulsions had been produced by the administration of TXP or INAH. Although vitamin B_6 exerted a remarkable depressing action on the convulsions, effects of ABA and OABA were not significant. It was, therefore, concluded that OABA might be not a depressor for the central nervous system.
