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Loss of functional voltage-gated sodium channels in persistent mumps virus-infected PC12 cells

E K Stauffer1, R J Ziegler

  • 1Department of Physiology, School of Medicine, University of Minnesota-Duluth 55812-2487.

Insights

Mumps virus (MV) infection in rat PC12 cells impairs sodium channels, preventing normal action potentials. However, calcium and potassium channels remain functional, suggesting MV specifically targets voltage-gated sodium channels.

Area of Science:

  • Neuroscience
  • Virology
  • Cell Biology

Background:

  • Mumps virus (MV) can establish persistent infections in host cells.
  • Neuronal function relies on voltage-gated ion channels, including sodium (Na+), calcium (Ca2+), and potassium (K+) channels.

Purpose of the Study:

  • To investigate the impact of persistent mumps virus infection on ion channel function in rat pheochromocytoma (PC12) cells.
  • To determine which specific voltage-gated ion channels are affected by MV infection.

Main Methods:

  • Intracellular electrophysiological recordings were used to examine stimulus-evoked action potentials (SEAPs) in MV-infected PC12 cells.
  • Pharmacological agents including tetrodotoxin (TTX), tetraethylammonium ions, and cobalt ions (Co2+) were applied to assess ion channel function.

Main Results:

  • MV-infected PC12 cells exhibited reduced SEAPs, with TTX showing minimal effect, suggesting impaired voltage-gated Na+ channel function.
  • MV-infected cells generated normal Ca2+ spikes in the presence of TTX and high extracellular Ca2+.
  • Superfusion with Co2+ in TTX-treated cells restored a SEAP profile characteristic of functional voltage-gated K+ channels only.

Conclusions:

  • Persistent mumps virus infection in PC12 cells significantly affects voltage-gated Na+ channels.
  • Voltage-gated Ca2+ and K+ channels appear to be spared from the detrimental effects of MV infection in these cells.

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