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Altered Cholinergic Metabolism in Rat CNS Following Aluminum Exposure: Implications on Learning Performance
Author(s) -
Julka Deepinder,
Sandhir Rajat,
Gill Kiran Dip
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.65052157.x
Subject(s) - cholinergic , muscarinic acetylcholine receptor , acetylcholine , acetylcholinesterase , choline acetyltransferase , endocrinology , choline , medicine , neurotransmitter , muscarinic acetylcholine receptor m4 , chemistry , cholinesterase , hippocampus , biology , receptor , central nervous system , biochemistry , enzyme
The effects of Al on the central cholinergic system have been studied. Al, at a dose of 10 mg/kg of body weight/day for 4 weeks, had a deleterious effect on the activities of biosynthetic (choline acetyltransferase) and hydrolytic (acetylcholinesterase) enzymes of the neurotransmitter acetylcholine. The levels of acetylcholine were also significantly lowered in different brain regions at the end of the dose regimen. There was a significant decrease in high‐affinity choline uptake following Al exposure. Muscarinic acetylcholine receptor binding studies revealed a decreased number of binding sites ( B max ), with the maximum effects being manifested in the hippocampus. Exogenous addition of 10 µ M desferrioxamine restored the muscarinic receptor binding completely. The impaired cholinergic functioning had severe effects on cognitive functions. Neurobehavioral deficits were manifested in terms of decreased active (52%) and passive (73.30%) avoidance tests. The results suggest that Al exerts its toxic effects by altering cholinergic transmission, which is ultimately reflected in neurobehavioral deficits.