Dual effects of mastoparan on intracellular free Ca2+ concentrations in human astrocytoma cells

Abstract

The effect of mastoparan, a wasp venom toxin, on intracellular free Ca2+ concentration ([Ca2+]i) was examined in human astrocytoma cells. Mastoparan inhibited [Ca2+]i induced by carbachol (100 μm) in a concentration‐dependent manner in the absence of extracellular Ca2+, consistent with our previous results showing that mastoparan inhibits phosphoinositide hydrolysis in human astrocytoma cells. In contrast, mastoparan itself increased [Ca2+]i and augmented carbachol‐induced increase in the [Ca2+]i in the presence of extracellular Ca2+, suggesting that mastoparan elicited Ca2+ influx from the extracellular medium. The increase appeared to be maximum at extracellular Ca2+ concentrations of 0.1–0.2 mm. The higher concentrations of extracellular Ca2+ depressed the influx. Pertussis toxin did not affect mastoparan‐induced inhibition of [Ca2+]i in the absence of extracellular Ca2+, consistent with the previous results that pertussis toxin did not affect mastoparan‐induced inhibition of phosphoinositide hydrolysis. Pertussis toxin augmented mastoparan‐induced increase in [Ca2+]i in the presence of extracellular Ca2+, suggesting that pertussis toxin substrate(s) seems to be inhibitory for Ca2+ influx induced by mastoparan. Verapamil, nifedipine and diltiazem (each 10 μm), L‐type Ca2+ antagonists, did not affect mastoparan‐induced Ca2+ influx. However, verapamil (10 μm) slightly inhibited the increase in [Ca2+]i induced by carbachol in the presence of mastoparan. The results obtained in the present study indicate that mastoparan has two opposite effects on [Ca2+]i in human astrocytoma cells and possibly has at least two sites of action. 1994 British Pharmacological Society