Abstract
Depolymerization of the actin cytoskeleton may liberate Ca 2+ from InsP 3-sensitive stores in some cell types, including starfish oocytes, while inhibiting Ca 2+ influx in others. However, no information is available on the modulation of membrane potential ( V m) by actin. The present study was aimed to ascertain whether the widely employed actin depolymerizing drug, latrunculin A (Lat A), affects V m in mature oocytes of the starfish Astropecten aranciacus. Lat A induced a membrane depolarization which was mimicked by cytochalasin D, another popular actin disruptor, and prevented by jasplakinolide, a stabilizer of the actin network. Lat A-elicited depolarization consisted in a positive shift in V m which reached the threshold of activation of voltage-gated Ca 2+ channels (VGCC), thus triggering an action potential. Lat A-promoted depolarization lacked the action potential in Ca 2+-free sea water, while it was abolished upon removal of external Na +. Moreover, membrane depolarization was prevented by pre-injection of BAPTA and heparin, but not ryanodine. These data indicate that Lat A induces a membrane depolarization by releasing Ca 2+ from InsP 3Rs. The Ca 2+ signal in turn activates a Ca 2+-dependent Na + entry, which causes the positive shift in V m and stimulates the VGCC.
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