An α3β4 subunit combination acts as a major functional nicotinic acetylcholine receptor in male rat pelvic ganglion neurons

Kyu Sang Park, Seung Kyu Cha, Min Jeong Kim, Dae Ran Kim, Seong Woo Jeong, Joong Woo Lee, In Deok Kong

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

We identified major subunits of the nicotinic acetylcholine receptor (nAChR) involved in excitatory postsynaptic potential and intracellular Ca 2+ ([Ca2+]i) increase in the major pelvic ganglion (MPG) neurons of the male rat. ACh elicited fast inward currents in both sympathetic and parasympathetic MPG neurons. Mecamylamine, a selective antagonist for α3β4 nAChR, potently inhibited the ACh-induced currents in sympathetic and parasympathetic neurons (IC50; 0.53 and 0.22 μM, respectively). Furthermore, α-conotoxin AuIB (10 μM), a new selective antagonist for α3β4 nAChR, blocked more than 80% of the ACh-induced currents in MPG neurons. Conversely, α-bungarotoxin, α-methyllycaconitine, and dihydro-β-erythroidine, known as blockers of the α7 or α4β2, did not show selective blocking effects on MPG neurons. ACh transiently increased [Ca2+]i which was subsequently abolished in the extracellular Ca2+-free environment. Simultaneous recording of [Ca2+]i and ionic currents revealed that ACh increased [Ca2+]i under the conditions of the voltage-clamped (at -80 mV) state, and this resulted from the influx through nAChR itself. ACh-induced [Ca2+]i increase was blocked by mecamylamine (10 μM), but was not affected by atropine (1 μM). RT-PCR analysis showed that, among subunits of nAChR, α3 and β4 were predominantly expressed in MPG. We suggest that activation of α3 and β4 nAChR subunits in MPG neurons induce fast inward currents and [Ca 2+]i increase, possibly mediating a major role in pelvic autonomic synaptic transmission.

Original languageEnglish
Pages (from-to)775-783
Number of pages9
JournalPflugers Archiv European Journal of Physiology
Volume452
Issue number6
DOIs
Publication statusPublished - 2006 Sep 1

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

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