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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6 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)167-171
Number of pages5
JournalNeuroscience Letters
Issue number2
Publication statusPublished - 2010 Sept

Bibliographical note

Funding Information:
This study was supported by a grant from the Myung Sun Kim Memorial Foundation (2009), the Korea Health 21 R&D Project, Ministry of Health & Welfare ( 03-PJI-PG10-21300-0012 ), and the Korean Ministry of Science of Information and Communication ( IMT-2000-C3-C5 ).

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)


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