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.
|Number of pages||7|
|Journal||Korean Journal of Physiology and Pharmacology|
|Publication status||Published - 2005 Feb 1|
- Ca infulx
- K channel
- Nicotinic acetylcholine receptor
ASJC Scopus subject areas