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Updated: Aug 23, 2026
Measuring Progressive Neurological Disability in a Mouse Model of Multiple Sclerosis
Published on: November 14, 2016
Calcium channel blockers ameliorate disease in a mouse model of multiple sclerosis
Elimor Brand-Schieber1, Peter Werner
1Department of Neurology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Abstract:
Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS, are inflammatory demyelinating diseases of the central nervous system. The inflammatory attacks lead to glial dysfunction and death, axonal damage, and neurological deficits. Numerous studies in rat suggest that extracellular calcium influx, via voltage-gated calcium channels (VGCC), contributes to white matter damage in acute spinal cord injury and stroke. Our immunohistochemical finding that mouse spinal cord axons display subunits of L-type VGCC also supports this hypothesis. Furthermore, we hypothesized that VGCC also play a role in EAE, and possibly, MS. In our study, administration of the calcium channel blockers (CCB) bepridil and nitrendipine significantly ameliorated EAE in mice, compared with vehicle-treated controls. Spinal cord samples showed reduced inflammation and axonal pathology in bepridil-treated animals. Our data support the hypothesis that calcium influx via VGCC plays a significant role in the development of neurological disability and white matter damage in EAE and MS.
Insights
Calcium channel blockers significantly reduced inflammation and axonal damage in experimental autoimmune encephalomyelitis, a model for multiple sclerosis. This suggests targeting voltage-gated calcium channels could treat these central nervous system diseases.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), involve central nervous system inflammation and demyelination.
- Voltage-gated calcium channels (VGCC) are implicated in white matter damage in other neurological conditions.
Purpose of the Study:
- To investigate the role of VGCC in EAE pathogenesis.
- To determine if calcium channel blockers (CCB) can ameliorate EAE and associated pathology.
Main Methods:
- Mice with EAE were treated with CCBs bepridil or nitrendipine.
- Immunohistochemistry was used to assess spinal cord inflammation and axonal damage.
Main Results:
- CCB treatment significantly reduced EAE severity compared to controls.
- Bepridil administration led to decreased inflammation and axonal pathology in spinal cords.
Conclusions:
- VGCC activity contributes to neurological disability and white matter damage in EAE.
- Targeting VGCC with CCBs shows therapeutic potential for EAE and potentially MS.
