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Latrunculin A depolarizes starfish oocytes.

F Moccia1

  • 1Department of Structural and Functional Biology, University of Naples Federico II, viale Cinthia, 80126 Naples, Italy. moccia1972@hotmail.it

Comparative Biochemistry and Physiology. Part A, Molecular & Integrative Physiology
|September 28, 2007
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Summary

Actin depolymerization with latrunculin A causes membrane depolarization in starfish oocytes by releasing calcium and activating sodium channels. This process triggers an action potential via voltage-gated calcium channels.

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Area of Science:

  • Cell Biology
  • Neuroscience
  • Biophysics

Background:

  • The actin cytoskeleton's role in membrane potential regulation is not fully understood.
  • Actin depolymerization can affect intracellular calcium levels and calcium influx.
  • Previous studies lack information on actin's direct impact on membrane potential.

Purpose of the Study:

  • To investigate the effect of the actin depolymerizing drug latrunculin A (Lat A) on the membrane potential (V(m)) of starfish oocytes.
  • To elucidate the mechanisms underlying actin-mediated V(m) modulation.

Main Methods:

  • Treatment of starfish oocytes with actin-disrupting agents (Lat A, cytochalasin D) and stabilizers (jasplakinolide).
  • Electrophysiological recordings to measure membrane potential changes.
  • Experiments in Ca2+-free seawater and Na+-free conditions.
  • Intracellular calcium measurements using BAPTA and heparin, and testing ryanodine.

Main Results:

  • Lat A induced membrane depolarization, mimicked by cytochalasin D and blocked by jasplakinolide.
  • Lat A-promoted depolarization activated voltage-gated calcium channels (VGCCs) and triggered action potentials.
  • Depolarization was dependent on extracellular calcium and sodium, and involved calcium release from InsP3 receptors.
  • Pre-injection of BAPTA and heparin prevented depolarization, while ryanodine had no effect.

Conclusions:

  • Latrunculin A induces membrane depolarization in starfish oocytes by releasing Ca2+ from InsP3 receptors.
  • The released Ca2+ activates a Ca2+-dependent Na+ influx, leading to V(m) depolarization.
  • This depolarization stimulates VGCCs, initiating an action potential.