Journal
SCIENCE TRANSLATIONAL MEDICINE
Volume 12, Issue 539, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scitranslmed.aay0167
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Funding
- European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program [693038]
- Novo Nordisk Foundation Laureate Program
- Faculty of Health and Medical Sciences, University of Copenhagen
- Laege Sofus Carl Emil Friis og hustru Olga Doris Friis' Legat
- European Research Council (ERC) [693038] Funding Source: European Research Council (ERC)
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Spasticity, one of the most frequent comorbidities of spinal cord injury (SCI), disrupts motor recovery and quality of life. Despite major progress in neurorehabilitative and pharmacological approaches, therapeutic strategies for treating spasticity are lacking. Here, we show in a mouse model of chronic SCI that treatment with nimodipine-an L-type calcium channel blocker already approved from the European Medicine Agency and from the U.S. Food and Drug Administration-starting in the acute phase of SCI completely prevents the development of spasticity measured as increased muscle tone and spontaneous spasms. The aberrant muscle activities associated with spasticity remain inhibited even after termination of the treatment. Constitutive and conditional silencing of the L-type calcium channel Ca(V)1.3 in neuronal subtypes demonstrated that this channel mediated the preventive effect of nimodipine on spasticity after SCI. This study identifies a treatment protocol and suggests that targeting Ca(V)1.3 could prevent spasticity after SCI.
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