Acetylcholine Increases Intracellular Ca in Taste Cells Via Activation of Muscarinic Receptors

Ogura, Tatsuya. Acetylcholine increases intracellular Ca in taste cells via activation of muscarinic receptors. J Neurophysiol 87: 2643–2649, 2002; 10.1152/jn.00610.2001. Previous studies suggest that acetylcholine (ACh) is a transmitter released from taste cells as well as a transmitter in cholinergic efferent neurons innervating taste buds. However, the physiological effects on taste cells have not been established. I examined effects of ACh on taste-receptor cells by monitoring [Ca ]i. ACh increased [Ca 2 ]i in both rat and mudpuppy taste cells. Atropine blocked the ACh response, but D-tubocurarine did not. U73122, a phospholipase C inhibitor, and thapsigargin, a Ca ATPase inhibitor that depletes intracellular Ca stores, blocked the ACh response. These results suggest that ACh binds to M1/M3/M5like subtypes of muscarinic ACh receptors, causing an increase in inositol 1,4,5-trisphosphate and subsequent release of Ca from the intracellular stores. A long incubation with ACh induced a transient response followed by a sustained phase of [Ca ]i increase. In Ca 2 free solution, the sustained phases disappeared, suggesting that Ca influx is involved in the sustained phase. Depletion of Ca stores by thapsigargin alone induced Ca influx. These findings suggest that Ca store-operated channels may be present in taste cells and that they may participate in the sustained phase of [Ca ]i increase. Immunocytochemical experiments indicated that the M1 subtype of muscarinic receptors is present in both rat and mudpuppy taste cells.