Muscarinic hyperstimulation

Muscarinic hyperstimulation leads to a clinical presentation of miosis, lacrimation, salivation, bradyarrhythmias, urinary incontinence, and intestinal hypermotility (Levy-Khademi et al, 2007). Nicotinic hyperstimulation leads to fasciculations, weakness, and paralysis of skeletal muscles. CNS effects include depression and agitation with coma and... 

These compounds inhibit the hydrolysis of the neurotransmitter acetylcholine by the enzyme acetylcholinesterase within the mammalian nervous system (Zwiener and Ginsburg, 1988). This inhibition causes acetylcholine levels to rise, thus causing cholinergic hyperstimulation at muscarinic and nicotinic receptors. There are important differences in the way carbamates and OPs bind to acetylcholinesterase as well as their abililty to affect the CNS. Carbamates are reversible inhibitors of cholinesterase enzymes. Carbamates create a reversible bond to the cholinesterase enzyme through carbamylation which can spontaneously hydrolyze, reversing toxicity. Carbamate poisoning produces toxicity similar to that of OPs however, the toxicity is usually of a shorter duration and less severe in nature (Lifshitz et al, 1994). In contrast, OPs inhibit cholinesterase via an irreversible bond of phosphate radicals... 

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