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Related Experiment Videos

Macrophage migration inhibitory factor increases neuronal delayed rectifier K+ current.

Tomokazu Matsuura1, Chengwen Sun, Lin Leng

  • 1Department of Physiology and Functional Genomics and McKnight Brain Institute, University of Florida, Gainesville, FL 32610-0274, USA.

Journal of Neurophysiology
|November 4, 2005
PubMed
Summary
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Macrophage migration inhibitory factor (MIF) stimulates neuronal firing by increasing delayed rectifier K+ current (I(Kv)). This effect, mediated by thiol-protein oxidoreductase activity and superoxide, highlights MIF's role in neuronal function.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Macrophage migration inhibitory factor (MIF) has diverse roles in the immune, endocrine, and nervous systems.
  • Previous research indicated that elevated intracellular MIF levels inhibit neuronal firing.
  • The specific mechanisms by which MIF influences neuronal activity remain incompletely understood.

Purpose of the Study:

  • To investigate the effect of MIF on the delayed rectifier K+ current (I(Kv)) in neurons.
  • To elucidate the molecular mechanisms underlying MIF's influence on I(Kv) and neuronal excitability.

Main Methods:

  • Patch-clamp electrophysiology was used to measure I(Kv) in cultured Sprague-Dawley rat neurons.
  • Intracellular perfusion of recombinant MIF (rMIF) and its variants (P1S-MIF, C60S-MIF) was performed.

Related Experiment Videos

  • MIF-neutralizing antibodies and superoxide scavengers (Tiron) were employed to assess mechanisms.

    • Main Results:

    • Intracellular MIF (80 nM) significantly increased I(Kv) density by approximately 32% within 3-30 minutes.
    • The stimulatory effect of MIF on I(Kv) was dependent on its thiol-protein oxidoreductase (TPOR) activity.
    • The effect was abolished by MIF-inactivating treatments, neutralizing antibodies, and the superoxide scavenger Tiron.

    Conclusions:

    • Neuronal MIF exerts a stimulatory effect on I(Kv), potentially enhancing neuronal firing.
    • This action appears to be mediated by MIF's TPOR activity and a superoxide-dependent pathway.
    • MIF represents a novel regulator of neuronal excitability through modulation of ion channel activity.