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.