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Related Experiment Videos

Modulation of divalent cation-activated chloride ion currents.

R H Scott1, S M McGuirk, A C Dolphin

  • 1Department of Pharmacology, St George's Hospital Medical School, London.

British Journal of Pharmacology
|July 1, 1988
PubMed
Summary

This study reveals that chloride currents (ICl) in dorsal root ganglion neurons are modulated by G-protein activation and intracellular calcium stores. These findings suggest novel regulatory mechanisms for neuronal excitability and ion channel function.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Electrophysiology

Background:

  • Dorsal root ganglion (DRG) neurons exhibit voltage-sensitive calcium channel currents (ICa, IBa) followed by chloride tail currents (ICl).
  • The precise regulation of these chloride currents remains an area of active investigation.

Purpose of the Study:

  • To investigate the regulatory mechanisms of chloride currents (ICl) in cultured dorsal root ganglion neurons.
  • To determine the role of G-protein signaling and intracellular calcium stores in modulating these currents.

Main Methods:

  • Electrophysiological recordings of voltage-sensitive calcium channel currents (ICa, IBa) and chloride tail currents (ICl) in cultured DRG neurons.
  • Pharmacological manipulation using (-)-baclofen, Bay K 8644, and caffeine.

Related Experiment Videos

  • Intracellular application of GTP-gamma-S to activate G-proteins and assessment of pertussis toxin sensitivity.

    • Main Results:

    • (-)-Baclofen inhibited both IBa and ICl(Ba), while Bay K 8644 potentiated them.
    • Intracellular GTP-gamma-S increased the incidence and sustained amplitude of ICl(Ba), indicating G-protein involvement.
    • Caffeine selectively reduced ICl(Ba), suggesting a role for intracellular calcium release in its activation, particularly when barium served as the charge carrier.

    Conclusions:

    • Chloride currents in DRG neurons are regulated by both divalent cation entry through calcium channels and G-protein activation.
    • G-protein mediated regulation of ICl(Ba) may involve the release of calcium from intracellular stores.
    • These findings elucidate novel pathways controlling neuronal excitability and ion channel function.