Na+,K(+)-ATPase activities are increased in brain in both congenital and acquired hyperammonemic syndromes.
Activities of Na+,K(+)-ATPase were measured in brain regions of experimental 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 hyperammonemia, 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 striatum (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). Stimulation of Na+,K(+)-ATPase and the subsequent alteration of neuronal excitability could contribute to the CNS dysfunction characteristic of chronic hyperammonemic syndromes.
Ratnakumari
L
L
Neuroscience Research Unit, Hospital Saint-Luc (University of Montreal, Quebec, Canada.
Audet
R
R
Qureshi
I A
IA
Butterworth
R F
RF
D000641:Ammonia / Q000097:blood*; D000818:Animals; D001921:Brain / Q000201:enzymology*; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D018377:Neurotransmitter Agents / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D009435:Synaptic Transmission / Q000502:physiology*; D013577:Syndrome
D018377:Neurotransmitter Agents; D000641:Ammonia; D000254:Sodium-Potassium-Exchanging ATPase