Short-and long-term ammonia toxicity was induced in mice by intraperitoneal injection, respectively, of single and six doses of 0.6 mM ammonium acetate per 100 g of body weight. The animals were sacrificed half an hour after either the single injection or after the last injection of six doses. Under these experimental conditions the ammonia levels were found to be elevated twofold in cerebral cortex, brain stem, and basal ganglia after the administration of a single dose of ammonium acetate. A fourfold increase in the content of ammonia was observed in cerebral cortex, brain stem, and basal ganglia after six injections. An elevation in the activity of pseudocholinesterase (enzyme localized in brain capillaries and dial cells) in all the above four regions resulted as a short-term effect of ammonia toxicity. True acetylcholinesterase was found to be elevated in all the four regions in short-term and in long-term ammonia toxicity. Gamma-glutamyltranspeptidase (GGTP), another enzyme localized in cerebral capillaries and glial cells, was found to be depressed in all the regions of the brain in both short-and long-term ammonia toxicity. The implications of these results are discussed in relation to glial cell function.