ArticleCell reports2021
Acute post-injury blockade of α2δ-1 calcium channel subunits prevents pathological autonomic plasticity after spinal cord injury.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.Neural regeneration research · 2026Article
- Gabapentin and cognitive impairment after traumatic brain injury: A multinational cohort of 49,925 patients.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Isolation, characterization and testing of RNA aptamers targeting glutamate receptors in a rat spinal cord injury pain model.Communications biology · 2025Article
- Article
- NF-κB inhibition attenuates sympathetic hyperreflexia and concomitant development of autonomic dysreflexia and immune dysfunction after spinal cord injury.Communications biology · 2025Article
- α2δ-1-Linked NMDA and AMPA Receptors in Neuropathic Pain and Gabapentinoid Action.Journal of neurochemistry · 2025Review
- Data reporting quality and semantic interoperability increase with community-based data elements (CoDEs). Analysis of the open data commons for spinal cord injury (ODC-SCI).Experimental neurology · 2025Article
- Neuroinflammation: targeting microglia for neuroprotection and repair after spinal cord injury.Frontiers in immunology · 2025Review
- Evolving insights on the role of microglia in neuroinflammation, plasticity, and regeneration of the injured spinal cord.Frontiers in immunology · 2025Review
- Reactive Astrocytes and Emerging Roles in Central Nervous System (CNS) Disorders.Cold Spring Harbor perspectives in biology · 2024Review
- α2δ1-mediated maladaptive sensory plasticity disrupts adipose tissue homeostasis following spinal cord injury.Cell reports. Medicine · 2024Article
- Drug Repurposing for Spinal Cord Injury: Progress Towards Therapeutic Intervention for Primary Factors and Secondary Complications.Pharmaceutical medicine · 2023Review
- Consequences of spinal cord injury on the sympathetic nervous system.Frontiers in cellular neuroscience · 2023Review
- Proinflammatory and Immunomodulatory Gene and Protein Expression Patterns in Spinal Cord and Spleen Following Acute and Chronic High Thoracic Injury.Journal of inflammation research · 2023Article
- Natural and targeted circuit reorganization after spinal cord injury.Nature neuroscience · 2022Review
- Review
- Maladaptation of renal hemodynamics contributes to kidney dysfunction resulting from thoracic spinal cord injury in mice.American journal of physiology. Renal physiology · 2022Article
- Harnessing cortical plasticity via gabapentinoid administration promotes recovery after stroke.Brain : a journal of neurology · 2022Article
- Immune dysfunction after spinal cord injury - A review of autonomic and neuroendocrine mechanisms.Current opinion in pharmacology · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.