Isoflurane Reduces the Carbachol-evoked Ca2+ Influx in Neuronal Cells

Background: The authors previously reported that the isoflurane-caused reduction of the carbachol-evoked cytoplasmic Ca2+ transient increase ([Ca2+]cyt) was eliminated by K+ or caffeine-pretreatment. In this study the authors investigated whether the isoflurane-sensitive component of the carbachol-evoked [Ca2+]cyt transient involved Ca2+ influx through the plasma membrane.

Methods: Perfused attached human neuroblastoma SH-SY5Y cells were exposed to carbachol (1 mm, 2 min) in the absence and presence of isoflurane (1 mm) and in the absence and presence of extracellular Ca2+ (1.5 mm). The authors studied the effect of the nonspecific cationic channel blocker La3+ (100 [mu]m), of the L-type Ca2+ channel blocker nitrendipine (10 [mu]m), and of the N-type Ca2+ channel blocker [omega]-conotoxin GVIA (0.1 [mu]m) on isoflurane modulation of the carbachol-evoked [Ca2+]cyt transient. [Ca2+]cyt was detected with fura-2 and experiments were carried out at 37[degrees]C.

Results: Isoflurane reduced the peak and area of the carbachol-evoked [Ca2+]cyt transient in the presence but not in the absence of extracellular Ca2+. La3+ had a similar effect as the removal of extracellular Ca2+. [omega]-Conotoxin GVIA and nitrendipine did not affect the isoflurane sensitivity of the carbachol response although nitrendipine reduced the magnitude of the carbachol response.