The electrophysiological mechanism underlying afterhyperpolarization induced by the activation of the nicotinic acetylcholine receptor (nAChR) in male rat major pelvic ganglion neurons (MPG) was investigated using a gramicidin-perforated patch clamp and microscopic fluorescence measurement system. Acetylcholine (ACh) induced fast depolarization through the activation of nAChR, followed by a sustained hyperpolarization after the removal of ACh in a dose-dependent manner (10μM to 1mM). ACh increased both intracellular Ca2+ ([Ca2+]i) and Na+ concentrations ([Na+]i) in MPG neurons. The recovery of [Na+]i after the removal of ACh was markedly delayed by ouabain (100μM), an inhibitor of Na+/K+ ATPase. Pretreatment with ouabain blocked ACh-induced hyperpolarization by 67.2±5.4% (n=7). ACh-induced hyperpolarization was partially attenuated by either the chelation of [Ca2+]i with BAPTA/AM (20μM) or the blockade of small-conductance Ca2+-activated K+ channels by apamin (500nM). Taken together, the activation of nAChR increases [Na+]i and [Ca2+]i, which activates Na+/K+ ATPase and Ca2+-activated K+ channels, respectively. Consequently, hyperpolarization occurs after the activation of nAChR in the autonomic pelvic ganglia.
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