Afterhyperpolarization induced by the activation of nicotinic acetylcholine receptors in pelvic ganglion neurons of male rats
- Kyu-Sang Park; Seung-Kuy Cha; Min-Jeong Kim; Na-Hyun Kim; Joong-Woo Lee; Seong-Woo Jeong; In Deok Kong
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- Nicotinic acetylcholine receptor; Autonomic ganglia; Afterhyperpolarization; Sodium/potassium ATPase; Ca2+-activated K+ channel
- 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 (10 μM to 1 mM). 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 (100 μM), 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 (20 μM) or the blockade of small-conductance Ca2+-activated K+ channels by apamin (500 nM). 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.
MPG, major pelvic ganglion;
nAChR, nicotinic acetylcholine receptor;
[Ca2+]i, intracellular calcium ion concentration;
[Na+]i, intracellular sodium ion concentration
Nicotinic acetylcholine receptor;
Ca2+-activated K+ channel
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