NA-ATPASE ACTIVITIES ARE INCREASED IN BRAIN IN BOTH CONGENITAL AND ACQUIRED HYPERAMMONEMIC SYNDROMES(,K+)

Activities of Na+,K+-ATPase were measured in brain regions of experime ntal animals with either congenital or acquired hyperammonemia. In the sparse-fur (spf) mutant mouse, with a genetic X-linked deficiency of ornithine transcarbamylase, an animal model of congenital hyperammonem ia, Na+,K+-ATPase was increased in frontal cortex (by 57%, P < 0.001), cerebellum (by 61%, P < 0.001), brainstem (by 71%, P < 0.001) and str iatum (by 48%, P < 0.01). Four weeks following portacaval anastomosis in the rat, Na+,K+-ATPase activities were increased in cerebellum and striatum (by 19%, P < 0.01) and in brainstem (by 28%, P < 0.01). Stimu lation of Na+,K+-ATPase and the subsequent alteration of neuronal exci tability could contribute to the CNS dysfunction characteristic of chr onic hyperammonemic syndromes.