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Intracerebroventricular d ‐galactose administration impairs memory and alters activity and expression of acetylcholinesterase in the rat
Author(s) -
Rodrigues André Felipe,
Biasibetti Helena,
Zanotto Bruna Stela,
Sanches Eduardo Farias,
Pierozan Paula,
Schmitz Felipe,
Parisi Mariana Migliorini,
BarbéTuana Florencia,
Netto Carlos Alexandre,
Wyse Angela T.S.
Publication year - 2016
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.2016.01.007
Subject(s) - galactosemia , hippocampus , galactose , acetylcholinesterase , aché , medicine , endocrinology , memory impairment , cerebral cortex , inhibitory postsynaptic potential , recognition memory , chemistry , neuroscience , psychology , cognition , biochemistry , enzyme
Tissue accumulation of galactose is a hallmark in classical galactosemia. Cognitive deficit is a symptom of this disease which is poorly understood. The aim of this study was to investigate the effects of intracerebroventricular administration of galactose on memory (inhibitory avoidance and novel object recognition tasks) of adult rats. We also investigated the effects of galactose on acetylcholinesterase (AChE) activity, immunocontent and gene expression in hippocampus and cerebral cortex. Wistar rats received a single injection of galactose (4 mM) or saline (control). For behavioral parameters, galactose was injected 1 h or 24 h previously to the testing. For biochemical assessment, animals were decapitated 1 h, 3 h or 24 h after galactose or saline injection; hippocampus and cerebral cortex were dissected. Results showed that galactose impairs the memory formation process in aversive memory (inhibitory avoidance task) and recognition memory (novel object recognition task) in rats. The activity of AChE was increased, whereas the gene expression of this enzyme was decreased in hippocampus, but not in cerebral cortex. These findings suggest that these changes in AChE may, at least in part, to lead to memory impairment caused by galactose. Taken together, our results can help understand the etiopathology of classical galactosemia.