@article{
 title = {Calcium channel blockers ameliorate disease in a mouse model of multiple sclerosis},
 type = {article},
 year = {2004},
 identifiers = {[object Object]},
 keywords = {Multiple sclerosis,Spinal cord,White matter},
 pages = {5-9},
 volume = {189},
 id = {e2dbb6ce-f16a-3efc-bcc8-3826a6b7a87f},
 created = {2018-03-05T02:57:43.242Z},
 file_attached = {true},
 profile_id = {fc9ef84f-888b-33fd-b1d3-fbf022f2f0c8},
 group_id = {21bf6821-cbba-3be9-9d50-072f76d57584},
 last_modified = {2018-03-05T02:57:43.414Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {Brand-Schieber2004},
 private_publication = {false},
 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. ?? 2004 Elsevier Inc. All rights reserved.},
 bibtype = {article},
 author = {Brand-Schieber, Elimor and Werner, Peter},
 journal = {Experimental Neurology},
 number = {1}
}

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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. ?? 2004 Elsevier Inc. All rights reserved.","bibtype":"article","author":"Brand-Schieber, Elimor and Werner, Peter","journal":"Experimental Neurology","number":"1","bibtex":"@article{\n title = {Calcium channel blockers ameliorate disease in a mouse model of multiple sclerosis},\n type = {article},\n year = {2004},\n identifiers = {[object Object]},\n keywords = {Multiple sclerosis,Spinal cord,White matter},\n pages = {5-9},\n volume = {189},\n id = {e2dbb6ce-f16a-3efc-bcc8-3826a6b7a87f},\n created = {2018-03-05T02:57:43.242Z},\n file_attached = {true},\n profile_id = {fc9ef84f-888b-33fd-b1d3-fbf022f2f0c8},\n group_id = {21bf6821-cbba-3be9-9d50-072f76d57584},\n last_modified = {2018-03-05T02:57:43.414Z},\n read = {false},\n starred = {false},\n authored = {false},\n confirmed = {true},\n hidden = {false},\n citation_key = {Brand-Schieber2004},\n private_publication = {false},\n abstract = {Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS, are inflammatory demyelinating diseases of the central nervous system. 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