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 hyperammonemic. In the sparse-fur (spf) mutant mouse, with a genetic X-linked deficiency of ornithine transcarbamylase, an animal model of congenital hyperammonemia, Na +,K +-ATPas...

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Bibliographic Details
Published in:Neuroscience letters 1995-09, Vol.197 (2), p.89-92
Main Authors: Ratnakumari, L., Audet, R., Qureshi, I.A., Butterworth, R.F.
Format: Article
Language:English
Subjects:
Acquired hyperammonemia
Ammonia - blood
Animals
Biological and medical sciences
Brain - enzymology
Congenital hyperammonemic
Errors of metabolism
Male
Medical sciences
Metabolic diseases
Mice
Mice, Mutant Strains
Miscellaneous hereditary metabolic disorders
Na +, K +-ATPase
Neurotransmitter Agents - physiology
Rats
Rats, Sprague-Dawley
Sodium-Potassium-Exchanging ATPase - metabolism
Sparse-fur mutant mouse
Synaptic Transmission - physiology
Syndrome
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Summary:Activities of Na +,K +-ATPase were measured in brain regions of experimental animals with either congenital or acquired hyperammonemic. 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.
ISSN:0304-3940
1872-7972
DOI:10.1016/0304-3940(95)11906-D