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Related Experiment Videos

Regulatory volume decrease in nematocytes isolated from acontia of Aiptasia diaphana.

G La Spada1, T Biundo, R Nardella

  • 1Institute of General Physiology, University of Messina, Italy. glaspada@imeuniv.unime.it

Cellular and Molecular Biology (Noisy-Le-Grand, France)
|May 7, 1999
PubMed
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Marine cnidarian cells, Aiptasia diaphana nematocytes, regulate volume during hypoosmotic shock. This regulatory volume decrease (RVD) involves calcium influx, potassium and chloride ion channels, and calmodulin.

Area of Science:

  • Cellular Physiology
  • Marine Biology
  • Biophysics

Background:

  • Cnidarians like Aiptasia diaphana inhabit environments with fluctuating salinity.
  • Nematocytes, specialized stinging cells, must maintain osmotic balance.
  • Understanding volume regulation is crucial for cnidarian survival in variable marine conditions.

Purpose of the Study:

  • To investigate regulatory volume decrease (RVD) in Aiptasia diaphana nematocytes.
  • To elucidate the ion transport mechanisms and signaling pathways involved in RVD.
  • To determine the role of calcium and calmodulin in hypoosmotic shock response.

Main Methods:

  • Isolation of microbasic mastigophore nematocytes from Aiptasia diaphana acontia.
  • Exposure to hypoosmotic shock (35% decrease).

Related Experiment Videos

  • Pharmacological manipulation using Ca2+-free medium, Gd3+, trifluoperazine (TFP), quinine, gramicidine, and DIDS to block specific ion channels and pathways.

    • Main Results:

    • Hypoosmotic shock induced cell swelling followed by rapid RVD.
    • RVD was inhibited by blocking Ca2+ influx (Ca2+-free medium, Gd3+).
    • Calmodulin inhibition (TFP) and quinine treatment blocked RVD, while DIDS partially inhibited it, suggesting involvement of K+ and Cl- channels and Ca2+-dependent pathways.

    Conclusions:

    • Aiptasia diaphana nematocytes effectively regulate cell volume under hypoosmotic stress.
    • RVD mechanisms primarily involve increased K+ and Cl- conductance, with some H+/K+-Cl-/HCO3- exchange.
    • Ionic fluxes are initiated by elevated intracellular calcium ([Ca2+]i), potentially involving calmodulin.