Abstract
Brain glutamic acid decarboxylase activity during the running fit induced by injection of a pyrimidine derivative, 2,5-dimethyl-4-aminopyrimidine, and carbonyl reagents (hydroxylamine, semicarbazide, thiosemicarbazide, isonicotinic hydrazide, benzoic hydrazide) in the white rat was compared to that found during convulsions induced by other convulsive agents (strychnine, cardiazol, ammonium chloride). The brain glutamic acid decarboxylase was reduced in the running fit induced animals and moreover, this inhibition was already present prior to the convulsion. It is suggested that inhibition of this enzyme is characteristic of the running fit and that the nucleus lenticularis and nucleus caudatus of the brain stem are the sites of origin of the running fit.
