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Regulation of calcium currents by chemokines and their receptors

Seog Bae Oh1, Takayuki Endoh, Arthur A Simen

  • 1Department of Molecular Pharmacology and Biological Chemistry, Northwestern University Medical School, 303 E. Chicago Avenue, Chicago, IL 60611, USA.

Journal of Neuroimmunology
|March 7, 2002
PubMed

Insights

Chemokines, like fractalkine and SDF-1alpha, inhibit voltage-dependent calcium currents (I(Ba)) by interacting with chemokine receptors. This modulation, mediated by Gi/Go proteins, affects neuronal signaling in specific neuron populations.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Chemokines are signaling proteins that regulate immune cell migration.
  • Chemokine receptors are G protein-coupled receptors involved in various cellular processes.
  • Voltage-dependent calcium currents play crucial roles in neuronal excitability and neurotransmitter release.

Purpose of the Study:

  • To investigate the role of chemokine receptors in modulating voltage-dependent calcium currents (I(Ba)).
  • To explore the potential of chemokines to influence neuronal signaling pathways.

Main Methods:

  • Heterologous expression systems (G1A1 cells) and primary neurons were used.
  • Electrophysiological techniques (e.g., whole-cell patch-clamp) were employed to measure I(Ba).
  • Specific chemokines (Fractalkine, SDF-1alpha, RANTES, MDC) and their corresponding receptors (CX3CR1, CXCR4, CCR5, CCR4) were studied.

Main Results:

  • Specific chemokines inhibited I(Ba) in cells expressing corresponding chemokine receptors.
  • The observed inhibition was voltage-dependent and showed prepulse facilitation.
  • Inhibition was blocked by N-ethylmaleimide and pertussis toxin, indicating Gi/Go protein mediation.
  • Some chemokines reduced I(Ba) in subpopulations of dorsal root ganglion and brainstem neurons.

Conclusions:

  • Chemokine receptors can modulate neuronal calcium currents.
  • Chemokines may influence neuronal signaling by inhibiting calcium influx via Gi/Go pathways.
  • These findings suggest a novel mechanism for chemokine-mediated neuroinflammation and neuromodulation.

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