You are currently viewing the abstract.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Preventing spinal cord injury comorbidity
Subjects with spinal cord injury (SCI) often develop spasticity, a condition in which an increase in muscle tone causes continuous muscle contraction. Strategies for treating spasticity are lacking. Now, Marcantoni et al. investigated the mechanisms mediating spasticity in a mouse model of chronic SCI and showed that the L-type calcium channel CaV1.3 is involved in the development of this condition. Treating animals early after SCI with nimodipine, an L-type calcium channel blocker approved for the treatment of brain hemorrhage, prevented the development of spasticity in mice. Early prolonged blockade of L-type calcium channels might be effective for preventing spasticity in subjects with SCI.
Abstract
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 CaV1.3 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 CaV1.3 could prevent spasticity after SCI.
- Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works
This is an article distributed under the terms of the Science Journals Default License.
