Intrastriatal hypoxanthine administration affects Na+,K+‐ATPase, acetylcholinesterase and catalase activities in striatum, hippocampus and cerebral cortex of rats

The aim of this study was to investigate the effects of a single intrastriatal injection of hypoxanthine, the major metabolite accumulating in Lesch–Nyhan disease, on Na+,K+‐ATPase, acetylcholinesterase and catalase activities in striatum, cerebral cortex and hippocampus of rats at different post‐in...

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Veröffentlicht in:International journal of developmental neuroscience 2006-11, Vol.24 (7), p.411-417
Hauptverfasser: Bavaresco, Caren Serra, Chiarani, Fabria, Wajner, Moacir, Netto, Carlos Alexandre, Souza Wyse, Angela Terezinha
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Sprache:eng
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Zusammenfassung:The aim of this study was to investigate the effects of a single intrastriatal injection of hypoxanthine, the major metabolite accumulating in Lesch–Nyhan disease, on Na+,K+‐ATPase, acetylcholinesterase and catalase activities in striatum, cerebral cortex and hippocampus of rats at different post‐infusion periods. Adult Wistar rats were divided in two groups: (1) vehicle‐injected group (control) and (2) hypoxanthine‐injected group. For Na+,K+‐ATPase activity determination, the animals were sacrificed 3 h, 24 h and 7 days after drug infusion. For the evaluation of acetylcholinesterase and catalase activities, the animals were sacrificed 30 min, 3 h, 24 h and 7 days after hypoxanthine infusion. Results show regional and time dependent effects of hypoxanthine on Na+,K+‐ATPase, acetylcholinesterase and catalase activities. The in vitro effect of hypoxanthine on the same enzymes in striatum was also investigated. Results showed that hypoxanthine inhibited Na+,K+‐ATPase, but not the activities of acetylcholinesterase and catalase in rat striatum. We suggest that these modification on cerebral biochemical parameters (Na+,K+‐ATPase, acetylcholinesterase and catalase activities) induced by intrastriatal administration of hypoxanthine in all cerebral structures studied, striatum, hippocampus and cerebral cortex, could be involved in the pathophysiology of Lesch–Nyhan disease.
ISSN:0736-5748
1873-474X
DOI:10.1016/j.ijdevneu.2006.08.007