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A calcium-channel antagonist can prevent paramyxovirus-induced neurodegeneration
T Andersson1, P Wallén, S Grillner
1Clinical Research Center, Karolinska Institutet, Huddinge Hospital, Sweden.
Abstract:
Mumps virus caused a partially lytic infection in cultivated rat embryonic dorsal root ganglion neurons with a restricted formation of viral components. The neuronal degeneration was markedly enhanced by increasing the calcium concentration of the medium and could be almost totally inhibited by the dihydropyridine calcium channel antagonist nifedipine. The drug had no effect on a productive and completely lytic Sendai virus infection of the neurons. A previous neurophysiological study has shown that a reduced calcium influx occurs during the action potential early during the infection. The present study suggests a crucial role of calcium in neurodegeneration induced by certain viruses.
Insights
Mumps virus infection in neurons causes degeneration, which is worsened by increased calcium. Calcium channel blockers like nifedipine can prevent this neurodegeneration, highlighting calcium's role in viral-induced nerve cell damage.
Area of Science:
- Neuroscience
- Virology
- Cell Biology
Background:
- Mumps virus can cause neuronal damage.
- Calcium ions play a role in neuronal function and excitability.
- Understanding the mechanisms of viral neurodegeneration is crucial for developing treatments.
Purpose of the Study:
- To investigate the role of calcium in mumps virus-induced neurodegeneration in rat dorsal root ganglion neurons.
- To determine if calcium channel blockers can mitigate viral neurotoxicity.
Main Methods:
- Cultured rat embryonic dorsal root ganglion neurons were infected with mumps virus.
- Neuronal degeneration was assessed under varying calcium concentrations.
- The effect of the calcium channel antagonist nifedipine was evaluated.
- Comparison with Sendai virus infection was performed.
Main Results:
- Mumps virus induced a partially lytic infection with restricted viral component formation.
- Neuronal degeneration was enhanced by increased extracellular calcium.
- Nifedipine significantly inhibited mumps virus-induced neurodegeneration.
- Nifedipine did not affect Sendai virus-induced lytic infection.
Conclusions:
- Calcium influx plays a critical role in mumps virus-induced neurodegeneration.
- Targeting calcium channels may offer a therapeutic strategy against certain viral encephalopathies.
- The mechanism of neurodegeneration differs between mumps and Sendai viruses.