Inhibitory effects of (1R,9S)-beta-Hydrastine on calcium transport in PC12 cells

Abstract

(1R,9S)-beta-Hydrastine (BHS), at 100 microM, has been shown to mainly reduce the K+-induced dopamine release and Ca2+ influx by blocking the L-type Ca2+ channel and inhibit the caffeine activated store-operated Ca2+ channels, but not those activated by thapsigargin, in PC12 cells. In this study, the effects of BHS on Ca2+ transport from Ca2+ stores in the absence of external Ca2+ were investigated in PC12 cells. BHS decreased the basal intracellular Ca2+ concentration ([Ca2+]i) in the absence of external Ca2+ in PC12 cells. In the absence of external Ca2+, pretreating PC12 cells with 100 microM BHS reduced the rapid increase in the [Ca2+]i elicited by 20 mM caffeine, but not that by 1 microM thapsigargin. In addition, BHS inhibited the increase in the [Ca2+]i elicited by restoration of 2 mM CaCl2 after the Ca2+ stores had been depleted by 20 mM caffeine, but not those depleted by 1 microM thapsigargin, in the absence of external Ca2+. These results suggested that BHS mainly inhibited Ca2+ leakage from the Ca2+ stores and the caffeine-stimulated release of Ca2+ from the caffeine-sensitive Ca2+ stores in PC12 cells.