Hexamethonium infusion (intravenous) does not alter the concentrations of brain catecholamines, ammonia, and amino acids in rats under normal conditions. However, it decreases the concentration of blood adrenaline (A) and nonadrenaline (NA) significantly without affecting blood ammonia and amino acids. Injection of α-methyl-p-tyrosine (α-MPT) (intraperitoneal) decreases brain catecholamines without affecting the concentration of ammonia and amino acids in the brain or catecholamines, ammonia, and amino acids in the blood. In normal, hexamethonium-, and α-MPT-treated rats convulsed by exposure to oxygen at high pressure (OHP), the concentration of ammonia and glutamine plus aspargine increased and glutamate and γ-aminobutyric acid (GABA) (brain only) decreased significantly in both blood and brain. After convulsion, hexamethonium and α-MPT effect the same degree of concentration change for ammonia and amino acids in both blood and brain. When hexamethonium-treated rats are convulsed by OHP, the concentrations of A and NA in blood increased sigificantly. However, the postconvulsive concentration of A in these rats is significantly less than the preconvulsive control values of normal, undrugged rats. Hexamethonium also prolongs the latency period before convulsions induced by exposure of rats to OHP. This protective action of hexamethonium against oxygen toxicity is probably due to (a) some direct effect of low circulating catecholamines, or (b) delay in the production of toxic levels of ammonia from oxidative deamination of catecholamines, as initial low catecholamine concentration would hinder accumulation of ammonia from such deamination. α-MPT treatment was ineffective in producing an increased latency period before convulsion occurred despite the prevailing low brain catecholamines initially produced by α-MPT treatment. However, the concentration of brain A, NA, and total catecholamines decreased sigificantly after α-MPT-treated rats were convulsed by OHP exposure. The response of blood catecholamines to OHP-induced convulsions in these α-MPT-treated rats is the same as in normal rats. As α-MPT blocks the synthesis of catecholamines, a further decrease in brain catecholamine values after oxygen-induced convulsions in drugged animals suggests that brain catecholamines are oxidatively deaminated to produce ammonia. These observations suggest that, contrary to earlier reports, brain catecholamines do play an important role in producing ammonia during oxygen toxicity, which in turn, induces convulsions.