[논문]Acetylcholine Induces Hyperpolarization Mediated by Activation of <tex>$K_{(ca)}$</tex> Channels in Cultured Chick Myoblasts

Lee, Do-Yun; Han, Jae-Hee; Park, Jae-Yong

Acetylcholine Induces Hyperpolarization Mediated by Activation of $K_{(ca)}$ Channels in Cultured Chick Myoblasts 원문보기

The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, v.9 no.1, 2005년, pp.37 - 43

Lee, Do-Yun (Department of Physiology and Biophysics, Seoul National University College of Medicine) , Han, Jae-Hee (Department of Physiology Institute of Health Science, Gyeongsang National University College of Medicine) , Park, Jae-Yong (Department of Physiology Institute of Health Science, Gyeongsang National University College of Medicine)

Abstract ▼ AI-Helper

Our previous report demonstrated that chick myoblasts are equipped with $Ca^{2+}$-permeable stretchactivated 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 $-12.5{\pm}3$ to $-31.2{\pm}5$ 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.

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