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Multiple effects of protein kinase C activators on Na+ currents in mouse neuroblastoma cells

C M Godoy1, S Cukierman

  • 1Department of Physiology, Loyola University Medical Center, Maywood, Illinois 60153.

The Journal of Membrane Biology
|June 1, 1994
PubMed

Insights

Protein kinase C (PKC) activators differentially modulate sodium (Na+) currents in neuroblastoma cells. PKC activation affects Na+ channel gating, with varied effects depending on the activator, suggesting complex physiological regulation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Physiology

Background:

  • Protein kinase C (PKC) is a family of enzymes involved in cell signaling.
  • Sodium (Na+) channels are crucial for electrical excitability in neurons.
  • The precise mechanisms by which PKC modulates Na+ channel function remain incompletely understood.

Purpose of the Study:

  • To investigate the effects of various protein kinase C (PKC) activators on Na+ currents in mouse neuroblastoma cells.
  • To elucidate the specific mechanisms of Na+ channel modulation by different PKC activators.

Main Methods:

  • Utilized the perforated-patch (nystatin-based) whole-cell voltage clamp technique.
  • Applied diacylglycerol-like compounds (OAG, DOG), phorbol esters, and cis-unsaturated fatty acids as PKC activators.
  • Examined the impact on Na+ current amplitude, activation, inactivation kinetics, and steady-state properties.
  • Investigated the role of PKC inhibitors (calphostin C, H7, staurosporine, polymyxin B) in preventing observed effects.

Main Results:

  • Diacylglycerol-like compounds (OAG, DOG) and cis-unsaturated fatty acids attenuated Na+ currents, shifting steady-state inactivation to more hyperpolarized potentials.
  • Phorbol esters did not affect Na+ currents, while oleic acid enhanced them without altering kinetic or steady-state properties.
  • All observed modulatory effects were blocked by PKC inhibitors, confirming PKC involvement.
  • Trans-unsaturated or saturated fatty acids, which do not activate PKC, had no effect on Na+ currents.

Conclusions:

  • PKC activation modulates Na+ channel behavior through at least three distinct mechanisms, influencing gating properties.
  • Different PKC activators elicit qualitatively different responses, indicating complex regulation of Na+ currents.
  • The specific physiological consequences of PKC activation on Na+ currents remain unclear due to these varied effects.

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