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Protein kinase C co-expression and the effects of halothane on rat skeletal muscle sodium channels

J P Mounsey1, M K Patel, D Mistry

  • 1Department of Internal Medicine (Cardiovascular Division), Box 6012, MR4 Building, University of Virginia Health Sciences Center, Charlottesville, Virginia 22908, USA. pmounsey@virginia.edu

British Journal of Pharmacology
|November 11, 1999
PubMed

Insights

Protein kinase C (PKC) activity modulates how volatile anesthetics affect voltage-gated sodium channels. Halothane

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Voltage-gated sodium channels are targets for general anesthetics.
  • Protein kinase C (PKC) phosphorylates a key site on sodium channels.

Purpose of the Study:

  • To investigate if PKC modulates volatile anesthetic effects on sodium channels via phosphorylation.
  • To explore the interaction between halothane, PKC, and sodium channel inactivation.

Main Methods:

  • Expressed rat skeletal muscle sodium channel alpha-subunits in Xenopus oocytes.
  • Measured sodium currents using two-microelectrode voltage clamp.
  • Modulated PKC activity by co-expressing a constitutively active PKC alpha-isozyme.

Main Results:

  • Halothane alone had no effect on sodium currents.
  • Co-expression of PKC with halothane enhanced sodium current decay rate and reduced amplitude.
  • This enhancement of decay was abolished in a mutant lacking the inactivation gate phosphorylation site.

Conclusions:

  • PKC activity enables halothane to hasten sodium current decay and reduce amplitude, partly via the inactivation gate phosphorylation site.
  • The interaction between halothane and sodium channels may be direct, facilitated by PKC and phosphorylation.

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