AI Article Synopsis
- After a spinal cord injury, normal sensory signals can cause harmful sympathetic nerve responses, leading to a condition called dysautonomia.
- Research shows that structural changes in the spinal autonomic circuitry contribute to these abnormal reflexes.
- Treating mice early with the drug gabapentin can prevent these reflex changes and reduce the symptoms of dysautonomia, even maintaining benefits after treatment ends, suggesting its potential use for preventing dysautonomia in high-level spinal cord injury patients.
Article Abstract
After spinal cord injury (SCI), normally innocuous visceral or somatic stimuli can trigger uncontrolled reflex activation of sympathetic circuitry, causing pathological dysautonomia. We show that remarkable structural remodeling and plasticity occur within spinal autonomic circuitry, creating abnormal sympathetic reflexes that promote dysautonomia. However, when mice are treated early after SCI with human-equivalent doses of the US Food and Drug Administration (FDA)-approved drug gabapentin (GBP), it is possible to block multi-segmental excitatory synaptogenesis and abolish sprouting of autonomic neurons that innervate immune organs and sensory afferents that trigger pain and autonomic dysreflexia (AD). This "prophylactic GBP" regimen decreases the frequency and severity of AD and protects against SCI-induced immune suppression. These benefits persist even 1 month after stopping treatment. GBP could be repurposed to prevent dysautonomia in at-risk individuals with high-level SCI.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8817229 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2020.108667 | DOI Listing |
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