Acetylcholine induces hyperpolarization mediated by activation of K (Ca) channels in cultured chick myoblasts

Doyun Lee, Jaehee Han, Jae-Yong Park

Research output: Contribution to journalArticle

Abstract

Our previous report demonstrated that chick myoblasts are equipped with Ca 2+ -permeable stretch-activated channels and Ca 2+ -activated potassium channels (K Ca ), and that hyperpolarization-induced by K Ca channels provides driving force for Ca 2+ influx through the stretch-activated channels into the cells. Here, we showed that acetylcholine (ACh) also hyperpolarized the membrane of cultured chick myoblasts, suggesting that nicotinic acetylcholine receptor (nAChR) may be another pathway for Ca 2+ influx. Under cell-attatched patch configuration, ACh increased the open probability of K Ca channels from 0.007 to 0.055 only when extracellular Ca 2+ was present. Nicotine, a nAChR agonist, increased the open probability of K Ca channels from 0.008 to 0.023, whereas muscarine failed to do so. Since the activity of K Ca channel is sensitive to intracellular Ca 2+ level, nAChR seems to be capable of inducing Ca 2+ influx. Using the Ca 2+ imaging analysis, we were able to provide direct evidence that ACh induced Ca 2+ influx from extracellular solution, which was dramatically increased by valinomycin-mediated hyperpolarization. In addition, ACh hyperpolarized the membrane potential from -12.5±3 to -31.2±5 mV by generating the outward current through K Ca channels. These results suggest that activation of nAChR increases Ca 2+ influx, which activates K Ca channels, thereby hyperpolarizing the membrane potential in chick myoblasts.

Original languageEnglish
Pages (from-to)37-43
Number of pages7
JournalKorean Journal of Physiology and Pharmacology
Volume9
Issue number1
Publication statusPublished - 2005 Feb 1
Externally publishedYes

Fingerprint

Myoblasts
Nicotinic Receptors
Acetylcholine
Membrane Potentials
Muscarine
Valinomycin
Cholinergic Agonists
Potassium Channels
Nicotine
Membranes

Keywords

  • Acetylcholine
  • Ca infulx
  • Hyperpolarization
  • K channel
  • Nicotinic acetylcholine receptor

ASJC Scopus subject areas

  • Physiology
  • Pharmacology

Cite this

Acetylcholine induces hyperpolarization mediated by activation of K (Ca) channels in cultured chick myoblasts . / Lee, Doyun; Han, Jaehee; Park, Jae-Yong.

In: Korean Journal of Physiology and Pharmacology, Vol. 9, No. 1, 01.02.2005, p. 37-43.

Research output: Contribution to journalArticle

@article{2106b8cca8a74215abed86495e4b7a19,
title = "Acetylcholine induces hyperpolarization mediated by activation of K (Ca) channels in cultured chick myoblasts",
abstract = "Our previous report demonstrated that chick myoblasts are equipped with Ca 2+ -permeable stretch-activated channels and Ca 2+ -activated potassium channels (K Ca ), and that hyperpolarization-induced by K Ca channels provides driving force for Ca 2+ influx through the stretch-activated channels into the cells. Here, we showed that acetylcholine (ACh) also hyperpolarized the membrane of cultured chick myoblasts, suggesting that nicotinic acetylcholine receptor (nAChR) may be another pathway for Ca 2+ influx. Under cell-attatched patch configuration, ACh increased the open probability of K Ca channels from 0.007 to 0.055 only when extracellular Ca 2+ was present. Nicotine, a nAChR agonist, increased the open probability of K Ca channels from 0.008 to 0.023, whereas muscarine failed to do so. Since the activity of K Ca channel is sensitive to intracellular Ca 2+ level, nAChR seems to be capable of inducing Ca 2+ influx. Using the Ca 2+ imaging analysis, we were able to provide direct evidence that ACh induced Ca 2+ influx from extracellular solution, which was dramatically increased by valinomycin-mediated hyperpolarization. In addition, ACh hyperpolarized the membrane potential from -12.5±3 to -31.2±5 mV by generating the outward current through K Ca channels. These results suggest that activation of nAChR increases Ca 2+ influx, which activates K Ca channels, thereby hyperpolarizing the membrane potential in chick myoblasts.",
keywords = "Acetylcholine, Ca infulx, Hyperpolarization, K channel, Nicotinic acetylcholine receptor",
author = "Doyun Lee and Jaehee Han and Jae-Yong Park",
year = "2005",
month = "2",
day = "1",
language = "English",
volume = "9",
pages = "37--43",
journal = "Korean Journal of Physiology and Pharmacology",
issn = "1226-4512",
publisher = "Korean Physiological Soc. and Korean Soc. of Pharmacology",
number = "1",

}

TY - JOUR

T1 - Acetylcholine induces hyperpolarization mediated by activation of K (Ca) channels in cultured chick myoblasts

AU - Lee, Doyun

AU - Han, Jaehee

AU - Park, Jae-Yong

PY - 2005/2/1

Y1 - 2005/2/1

N2 - Our previous report demonstrated that chick myoblasts are equipped with Ca 2+ -permeable stretch-activated channels and Ca 2+ -activated potassium channels (K Ca ), and that hyperpolarization-induced by K Ca channels provides driving force for Ca 2+ influx through the stretch-activated channels into the cells. Here, we showed that acetylcholine (ACh) also hyperpolarized the membrane of cultured chick myoblasts, suggesting that nicotinic acetylcholine receptor (nAChR) may be another pathway for Ca 2+ influx. Under cell-attatched patch configuration, ACh increased the open probability of K Ca channels from 0.007 to 0.055 only when extracellular Ca 2+ was present. Nicotine, a nAChR agonist, increased the open probability of K Ca channels from 0.008 to 0.023, whereas muscarine failed to do so. Since the activity of K Ca channel is sensitive to intracellular Ca 2+ level, nAChR seems to be capable of inducing Ca 2+ influx. Using the Ca 2+ imaging analysis, we were able to provide direct evidence that ACh induced Ca 2+ influx from extracellular solution, which was dramatically increased by valinomycin-mediated hyperpolarization. In addition, ACh hyperpolarized the membrane potential from -12.5±3 to -31.2±5 mV by generating the outward current through K Ca channels. These results suggest that activation of nAChR increases Ca 2+ influx, which activates K Ca channels, thereby hyperpolarizing the membrane potential in chick myoblasts.

AB - Our previous report demonstrated that chick myoblasts are equipped with Ca 2+ -permeable stretch-activated channels and Ca 2+ -activated potassium channels (K Ca ), and that hyperpolarization-induced by K Ca channels provides driving force for Ca 2+ influx through the stretch-activated channels into the cells. Here, we showed that acetylcholine (ACh) also hyperpolarized the membrane of cultured chick myoblasts, suggesting that nicotinic acetylcholine receptor (nAChR) may be another pathway for Ca 2+ influx. Under cell-attatched patch configuration, ACh increased the open probability of K Ca channels from 0.007 to 0.055 only when extracellular Ca 2+ was present. Nicotine, a nAChR agonist, increased the open probability of K Ca channels from 0.008 to 0.023, whereas muscarine failed to do so. Since the activity of K Ca channel is sensitive to intracellular Ca 2+ level, nAChR seems to be capable of inducing Ca 2+ influx. Using the Ca 2+ imaging analysis, we were able to provide direct evidence that ACh induced Ca 2+ influx from extracellular solution, which was dramatically increased by valinomycin-mediated hyperpolarization. In addition, ACh hyperpolarized the membrane potential from -12.5±3 to -31.2±5 mV by generating the outward current through K Ca channels. These results suggest that activation of nAChR increases Ca 2+ influx, which activates K Ca channels, thereby hyperpolarizing the membrane potential in chick myoblasts.

KW - Acetylcholine

KW - Ca infulx

KW - Hyperpolarization

KW - K channel

KW - Nicotinic acetylcholine receptor

UR - http://www.scopus.com/inward/record.url?scp=14944384741&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=14944384741&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:14944384741

VL - 9

SP - 37

EP - 43

JO - Korean Journal of Physiology and Pharmacology

JF - Korean Journal of Physiology and Pharmacology

SN - 1226-4512

IS - 1

ER -