Abstract
Nicotinic acetylcholine receptor-channels (AChR) are believed to be the target site of cartap. In order to clarify the mechanisms of the cartap interaction with nicotinic AChRs, single-channel patch clamp experiments were performed using rat clonal phaeochromocytoma (PC12) cells. Cartap increased the short closures occurring during single-channel openings induced by acetylcholine (ACh). Thus, when co-applied with acetylcholine, cartap markedly shortened the open time associated with bursts. These effects were voltage-dependent, being more prominent at negative voltages. These results strongly suggest that cartap acts as an open channel blocker at the neuronal nicotinic AChR.
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