A Possible Neurochemical Basis of the Central Stimulatory Effects of pp′DDT

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Abstract
Striatal neurochemical changes induced by p,p''-DDT (600 mg/kg) in mice were: increased concentration of free ammonia, decreased level of GABA [.gamma.-aminobenzoic acid] and a reduction in the level of acetylcholine. These changes were maximal 5 h after treatment with p,p''-DDT, when the animals [mice] developed severe convulsions. Convulsions and striatal neurochemical changes were modified to different degrees by barbiturates. Phenobarbitone protected all animals from p,p''-DDT-induced convulsions. Levels of striatal acetylcholine and GABA in these animals were within normal limits. Prominal reduced the severity of convulsions in p,p''-DDT-treated animals. Levels of striatal acetylcholine and GABA were significantly lower than control values in these animals. Primidone did not modify convulsions or striatal neurochemical changes in p,p''-DDT-treated animals. Increased concentration of free ammonia in p,p''-DDT-treated animals was not modified by barbiturates. Aminooxyacetic acid raised the GABA level above normal and abolished convulsions in p,p''-DDT-treated animals; the level of acetylcholine was within normal limits in these animals. Hydroxylamine produced a similar but less marked effect. Pyridoxine had no effect on convulsions or striatal neurochemical changes induced by p,p''-DDT. Increased concentration of free ammonia in p,p''-DDT-treated animals was not modified by these agents. It was likely that p,p''-DDT produced stimulatory effects by increasing the concentration of free ammonia which may be involved in reducing the level of GABA, while changes in the level of acetylcholine may be an effect of p,p''-DDT-induced convulsions.