title: Afterhyperpolarization induced by the activation of nicotinic acetylcholine receptors in pelvic ganglion neurons of male rats.
abstract: 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 microM to 1mM). ACh increased both intracellular Ca(2+) ([Ca(2+)](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 microM), 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 [Ca(2+)](i) with BAPTA/AM (20 microM) or the blockade of small-conductance Ca(2+)-activated K(+) channels by apamin (500 nM). Taken together, the activation of nAChR increases [Na(+)](i) and [Ca(2+)](i), which activates Na(+)/K(+) ATPase and Ca(2+)-activated K(+) channels, respectively. Consequently, hyperpolarization occurs after the activation of nAChR in the autonomic pelvic ganglia.
authors.affiliation: Department of Physiology and Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, Republic of Korea.
authors.forename: Kyu-Sang
authors.initials: KS
authors.lastname: Park
authors.forename: Seung-Kuy
authors.initials: SK
authors.lastname: Cha
authors.forename: Min-Jeong
authors.initials: MJ
authors.lastname: Kim
authors.forename: Na-Hyun
authors.initials: NH
authors.lastname: Kim
authors.forename: Joong-Woo
authors.initials: JW
authors.lastname: Lee
authors.forename: Seong-Woo
authors.initials: SW
authors.lastname: Jeong
authors.forename: In Deok
authors.initials: ID
authors.lastname: Kong
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D005725:Ganglia, Autonomic / Q000502:physiology*; D042541:Intracellular Space / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000502:physiology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D010042:Ouabain / Q000494:pharmacology; D010388:Pelvis / Q000294:innervation*; D051381:Rats; D011978:Receptors, Nicotinic / Q000502:physiology*; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000037:antagonists & inhibitors; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
chemical_list: D002614:Chelating Agents; D018722:Nicotinic Agonists; D011978:Receptors, Nicotinic; D051640:Small-Conductance Calcium-Activated Potassium Channels; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D001030:Apamin; D004533:Egtazic Acid; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D000109:Acetylcholine; D002118:Calcium