Citation:

Dvergsten, C. AND R. Meeker. MUSCARINIC CHOLINERGIC RECEPTOR REGULATION AND ACETYLCHOLINESTERASE INHIBITION IN RESPONSE TO INSECTICIDE EXPOSURE DURING DEVELOPMENT. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-94/515 (NTIS PB95148771), 1994.

Description:

Daily injections of low doses of the organophosphorus pesticide, parathion, into neonatal rats during the rapid phase of cholinergic system development (postnatal days 8-20), resulted in an average 67% inhibition of acetylcholinesterase and a 23% down regulation of muscarinic cholinergic receptors on postnatal day 21. orrelation of 0.7, was found between the level of acetylcholinesterase inhibition and the decrease of muscarinic receptors. egional analyses of receptor autoradiograms indicated that muscarinic receptors in the cortex and hippocampus were most sensitive to the effects of acetylcholinesterase inhibition. he anterior thalamus was notable in having a high density of cholinergic receptors which were relatively unaffected by parathion treatment. o changes were found in the affinity of [3H]QNB for the receptor or the binding of acetylcholine. ndernourished rats yoked to the body weight gain of the parathion treated rats exhibited no changes in muscarinic cholinergic receptor density or affinity. ourteen days after the last parathion injection (postnatal day 36), acetylcholinesterase activity and muscarinic receptor density had returned to normal. hese results indicate that cholinoreceptive cells in neonatal rats respond to chronic acetylcholinesterase inhibition in a manner similar to the response observed in adults. eceptor densities and acetylcholinesterase levels returned to normal values after a 2 week recovery period in spite of the-perturbation of cholinergic function during development of cholinergic synapses and receptors.

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