Gralewicz_1997_Med.Pr_48_469

Organophosphorus pesticides (OP) inhibit irreversibly acetylcholinesterase (AChE). The known function of AChE is hydrolysis of the neurotransmitter, acetylcholine (ACh). Therefore, the consequences of OP intoxication are usually perceived as results of transient excess of ACh in cholinergic synapses of the central and peripheral nervous system as well as in cholinergically innervated organs and tissues. Since a long time it has been known, however, that in the nervous system the localization pattern of AChE does not overlap the localization of cholinergic neurons, and several recent findings show that apart from being the ACh hydrolyzing enzyme, AChE is also a neuromodulator participating in the phenomenon of neuronal plasticity i.e. induction of longterm changes in synaptic efficacy. It is likely then, that out of the known effects of OP poisoning regarded as results of cholinergic hyperactivity some are due to the loss of the nonenzymatic, neuromodulatory role of AChE. They may include the longterm alterations of cognitive function which may follow longterm occupational OP exposure or OP poisoning.