CAPACITATIVE CALCIUM-ENTRY IN RAT SERTOLI CELLS

Depletion of intracellular Ca2+ stores activates an influx of Ca2+ fro m the extracellular medium. This capacitative Ca2+ entry as originally proposed by Putney in 1986 can be studied with drugs that inhibit sar co/endoplasmic reticulum ATPase. In the present study we examined the effects of depletion of internal Ca2+ stores on Ca2+ influx in rat Ser toli cells utilizing thapsigargin and cyclopiazonic acid, Both inhibit ors induced a rapid and dose-dependent rise in [Ca2+](i) that was depe ndent on an influx of Ca2+ from the extracellular medium since it was rapidly blocked by the addition of the Ca2+ chelating agent EGTA. In t he absence of external Ca2+ thapsigargin and cyclopiazonic acid still produced an increase in [Ca2+](i) that was lower than that observed in Ca2+ medium and was transient since [Ca2+](i) returned to basal level s by few minutes, In these experimental conditions readdition of Ca2induced a rapid rise in [Ca2+](i) supporting a role for Ca2+ influx. I ncrease of plasma membrane permeability to Ca2+ induced by thapsigargi n and cyclopiazonic acid were confirmed by the ability of Mn2+ to perm eate through Ca2+ channels and to quench intracellular fura-2 fluoresc ence after challenge with these inhibitors. Mn2+ induced influx was bl ocked by La3+, a well known blocker of Ca2+ channels, These results de monstrate that internal Ca2+ stores depletion induce Ca2+ influx from the extracellular medium in rat Sertoli cells providing evidence for t he existence of capacitative Ca2+ entry in these cells. (C) 1996, Edit rice Kurtis