Abstract
Application of acetylcholinesterase inhibitors (AChEIs; organophosphates, carbamates or quaternary ammonium compounds) at the neuromuscular junction leads to an increase in the amplitude and duration of the end-plate potential (1, 16). This effect has been considered to be a consequence of acetylcholinesterase (AChE) inhibition and of the resulting increase in concentration of acetylcholine (ACh) in the synaptic cleft (11, 12, 16). At vertebrate ganglionic cholinergic synapses (3), however, the postsynaptic response is not modified when AChE is blocked, indicating that this enzyme might not play a major role in the inactivation of released ACh. It appears that the main reason for this difference might lie in the different geometry of the endplate compared to that of a neuro-neuronal synapse: ACh can accumulate within the cleft of the neuromuscular junction, whereas at a neuro-neuronal synapse it diffuses rapidly into the intercellular space.
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