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Interleukin-1 beta depresses calcium currents in CA1 hippocampal neurons at pathophysiological concentrations

C R Plata-Salamán1, J M Ffrench-Mullen

  • 1School of Life and Health Sciences, University of Delaware, Newark 19716.

Brain Research Bulletin
|August 1, 1992
PubMed

Insights

Interleukin-1 beta rapidly reduces calcium currents in brain cells at disease-relevant levels. This interaction in the central nervous system may influence neuronal excitability and neurodegeneration.

Area of Science:

  • Neuroscience
  • Neuroimmunology
  • Cellular Electrophysiology

Background:

  • Interleukin-1 (IL-1) is implicated in central nervous system (CNS) pathology.
  • The precise mechanisms of IL-1's neurobiological effects require further elucidation.

Purpose of the Study:

  • To investigate the effect of recombinant human interleukin-1 beta (rhIL-1 beta) on voltage-dependent calcium (Ca2+) currents.
  • To determine the physiological relevance of rhIL-1 beta's action on neuronal calcium influx.

Main Methods:

  • Whole-cell patch clamp electrophysiology on acutely dissociated guinea pig hippocampal CA1 neurons.
  • Application of rhIL-1 beta at pathophysiological concentrations.
  • Assessment of neuroactive specificity using rhIL-1 receptor antagonist.

Main Results:

  • rhIL-1 beta rapidly depressed voltage-gated Ca2+ currents in hippocampal neurons.
  • This effect was observed at concentrations greater than or equal to 1.97 pg/10 microliters.
  • The effect was specific, as demonstrated by the lack of response to rhIL-1 beta with receptor antagonist co-application.

Conclusions:

  • IL-1 beta significantly modulates neuronal calcium currents.
  • This modulation may contribute to altered neuronal excitability during disease states.
  • IL-1 beta's action on calcium influx could play a role in neurodegenerative processes.

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