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Intrastriatal hypoxanthine administration affects Na + ,K + ‐ATPase, acetylcholinesterase and catalase activities in striatum, hippocampus and cerebral cortex of rats
Author(s) -
Bavaresco Caren Serra,
Chiarani Fabria,
Wajner Moacir,
Netto Carlos Alexandre,
Souza Wyse Angela Terezinha
Publication year - 2006
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2006.08.007
Subject(s) - striatum , hippocampus , cerebral cortex , hypoxanthine , acetylcholinesterase , catalase , chemistry , cortex (anatomy) , neuroscience , medicine , biology , biochemistry , enzyme , dopamine
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.