ArticleMolecular pain
Exercise training modulates glutamic acid decarboxylase-65/67 expression through TrkB signaling to ameliorate neuropathic pain in rats with spinal cord injury.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Research progress in neuropathic pain after spinal cord injury: a bibliometric study from 2013 to 2024.Frontiers in neurology · 2024Pooled it
- Restoration of gamma-aminobutyric acid homeostasis: A novel approach to alleviating central nervous system injury-associated immunodepression syndrome.Neural regeneration research · 2026Article
- Body weight-supported treadmill training enhances motor recovery and ameliorates neuron injury through the MDK/LRP-1 signaling pathway in T10 incomplete spinal cord-injured rats.Neurochemical research · 2026Article
- Exercise training promotes nerve cell repair and regeneration after spinal cord injury.Neural regeneration research · 2026Article
- Mechanisms and Clinical Application Progress of Exercise in the Treatment of Neuropathic Pain.Cellular and molecular neurobiology · 2026Review
- Article
- SKF-38393 regulates the expression of glutamic acid decarboxylase 67 via heparanase-1 in 6-hydroxydopamine-induced neurodegeneration.Scientific reports · 2025Article
- Curcumin reduces pain after spinal cord injury in rats by decreasing oxidative stress and increasing GABAA receptor and GAD65 levels.Scientific reports · 2025Article
- BDNF-TrkB Signaling Pathway in Spinal Cord Injury: Insights and Implications.Molecular neurobiology · 2025Review
- Exercise therapy facilitates neural remodeling and functional recovery post-spinal cord injury via PKA/CREB signaling pathway modulation in rats.Burns & trauma · 2025Article
- Effect of high-intensity exercise training on functional recovery after spinal cord injury.Frontiers in neurology · 2025Review
- Role of Exercise on Inflammation Cytokines of Neuropathic Pain in Animal Models.Molecular neurobiology · 2024Review
- Neuropathic Pain Induced by Spinal Cord Injury from the Glia Perspective and Its Treatment.Cellular and molecular neurobiology · 2024Review
- Exercise, Spinal Microglia and Neuropathic Pain: Potential Molecular Mechanisms.Neurochemical research · 2024Review
- Treadmill running on neuropathic pain: via modulation of neuroinflammation.Frontiers in molecular neuroscience · 2024Review
- The Role of Exercise in the Alleviation of Neuropathic Pain Following Traumatic Spinal Cord Injuries: A Systematic Review and Meta-analysis.Neurospine · 2023Article
- Exercise combined with administration of adipose-derived stem cells ameliorates neuropathic pain after spinal cord injury.Neural regeneration research · 2023Article
- High intensity interval training attenuates osteoarthritis-associated hyperalgesia in rats.The journal of physiological sciences : JPS · 2023Article
- The Rehabilitation-Related Effects on the Fear, Pain, and Disability of Patients With Lumbar Fusion Surgery: A Systematic Review and Meta-Analysis.Neurospine · 2023Article
- Effects of exercise training on neurological recovery, TGF-β1, HIF-1α, and Nogo-NgR signaling pathways after spinal cord injury in rats.Clinics (Sao Paulo, Brazil) · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain is one of the most frequently stated complications after spinal cord injury. In post-spinal cord injury, the decrease of gamma aminobutyric acid synthesis within the distal spinal cord is one of the main causes of neuropathic pain. The predominant research question of this study was whether exercise training may promote the expression of glutamic acid decarboxylase-65 and glutamic acid decarboxylase-67, which are key enzymes of gamma aminobutyric acid synthesis, within the distal spinal cord through tropomyosin-related kinase B signaling, as its synthesis assists to relieve neuropathic pain after spinal cord injury. Animal experiment was conducted, and all rats were allocated into five groups: Sham group, SCI/PBS group, SCI-TT/PBS group, SCI/tropomyosin-related kinase B-IgG group, and SCI-TT/tropomyosin-related kinase B-IgG group, and then T10 contusion SCI model was performed as well as the tropomyosin-related kinase B-IgG was used to block the tropomyosin-related kinase B activation. Mechanical withdrawal thresholds and thermal withdrawal latencies were used for assessing pain-related behaviors. Western blot analysis was used to detect the expression of brain-derived neurotrophic factor, tropomyosin-related kinase B, CREB, p-REB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord. Immunohistochemistry was used to analyze the distribution of CREB, p-CREB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord dorsal horn. The results showed that exercise training could significantly mitigate the mechanical allodynia and thermal hyperalgesia in post-spinal cord injury and increase the synthesis of brain-derived neurotrophic factor, tropomyosin-related kinase B, CREB, p-CREB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord. After the tropomyosin-related kinase B signaling was blocked, the analgesic effect of exercise training was inhibited, and in the SCI-TT/tropomyosin-related kinase B-IgG group, the synthesis of CREB, p-CREB, glutamic acid decarboxylase-65, and glutamic acid decarboxylase-67 within the distal spinal cord were also significantly reduced compared with the SCI-TT/PBS group. This study shows that exercise training may increase the glutamic acid decarboxylase-65 and glutamic acid decarboxylase-67 expression within the spinal cord dorsal horn through the tropomyosin-related kinase B signaling, and this mechanism may play a vital role in relieving the neuropathic pain of rats caused by incomplete SCI.
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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 Socratic graph.