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Regulatory volume decrease in cultured astrocytes. I. Potassium- and chloride-activated permeability

H Pasantes-Morales1, R A Murray, L Lilja

  • 1Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City.

The American Journal of Physiology
|January 1, 1994
PubMed
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Regulatory volume decrease (RVD) in astrocytes involves specific cation and anion pathways. Swelling-activated K+ and Cl- fluxes likely occur via channels, not cotransporters, with K+ permeability being rate-limiting.

Area of Science:

  • Cell Physiology
  • Neuroscience
  • Astrocyte Biology

Background:

  • Detached cerebellar astrocytes in culture exhibit regulatory volume decrease (RVD) upon acute exposure to hyposmolarity.
  • Understanding the ionic mechanisms of RVD is crucial for comprehending astrocyte volume regulation.
  • Previous studies have initiated the characterization of RVD in these cells.

Purpose of the Study:

  • To characterize the ionic pathways involved in hyposmolarity-induced regulatory volume decrease (RVD) in detached cerebellar astrocytes.
  • To elucidate the role of cation and anion fluxes in astrocyte volume regulation.
  • To differentiate between channel-mediated and cotransporter-mediated ion transport during RVD.

Main Methods:

  • Investigated RVD under varying extracellular calcium concentrations, pH, and temperatures.

Related Experiment Videos

  • Substituted Na+ with various cations (K+, Rb+, Li+, choline, etc.) and Cl- with different anions to assess pathway specificity.
  • Utilized pharmacological blockers (bumetanide, furosemide, quinidine, DIDS, dipyridamole) and ionophores (gramicidin) to probe transport mechanisms.

    • Main Results:

    • RVD was independent of extracellular calcium, accelerated at alkaline pH, and reduced at lower temperatures.
    • The cationic pathway was specific for K+ and Rb+, while the anion pathway was unselective, with a permeability rank of SCN- = I- > NO3- > Cl- > benzoate > acetate >> SO3- > gluconate.
    • Quinidine inhibited RVD, suggesting involvement of K+ channels, and gramicidin accelerated RVD, indicating K+ permeability is rate-limiting.

    Conclusions:

    • Swelling-activated K+ and Cl- fluxes in astrocytes likely occur via diffusion through channels, rather than cotransporters.
    • K+ permeability appears to be the rate-limiting step for RVD, especially under conditions of low Cl- permeability.
    • These findings provide insights into the molecular mechanisms of astrocyte volume regulation and response to osmotic stress.