Latrunculin A depolarizes starfish oocytes

Depolymerization of the actin cytoskeleton may liberate Ca²⁺ from InsP₃-sensitive stores in some cell types, including starfish oocytes, while inhibiting Ca²⁺ 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 Ca²⁺ channels (VGCC), thus triggering an action potential. Lat A-promoted depolarization lacked the action potential in Ca²⁺-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 Ca²⁺ from InsP₃Rs. The Ca²⁺ signal in turn activates a Ca²⁺-dependent Na⁺ entry, which causes the positive shift in V_m and stimulates the VGCC.