ArticlePain2014
Peripheral noxious stimulation reduces withdrawal threshold to mechanical stimuli after spinal cord injury: role of tumor necrosis factor alpha and apoptosis.
Article in Pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
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Who cites it
49 citing papers in PubMed, 67 citations in OpenAlex.
- Role of A-delta low threshold mechanoreceptors and tropomyosin receptor kinase B plasticity in at-level aversive pain after spinal cord injury.Experimental neurology · 2026Article
- Early Changes in Respiration and Motor Activity after Spinal Cord Injury Predict Pain-Related Outcomes in Mice.bioRxiv : the preprint server for biology · 2025Article
- Disuse plasticity limits spinal cord injury recovery.iScience · 2025Article
- BDNF: New Views of an Old Player in Traumatic Brain Injury.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Chemogenetic Attenuation of Acute Nociceptive Signaling Enhances Functional Outcomes Following Spinal Cord Injury.Journal of neurotrauma · 2024Article
- Updating perspectives on spinal cord function: motor coordination, timing, relational processing, and memory below the brain.Frontiers in systems neuroscience · 2024Review
- Progress in treatment of pathological neuropathic pain after spinal cord injury.Frontiers in neurology · 2024Review
- General Anesthesia Blocks Pain-Induced Hemorrhage and Locomotor Deficits After Spinal Cord Injury in Rats.Journal of neurotrauma · 2023Article
- Inflammatory-associated apoptotic markers: are they the culprit to rheumatoid arthritis pain?Molecular biology reports · 2022Review
- Neuroimmune Mechanisms Underlying Neuropathic Pain: The Potential Role of TNF-α-Necroptosis Pathway.International journal of molecular sciences · 2022Review
- Review
- Noxious Stimulation Induces Acute Hemorrhage and Impairs Long-Term Recovery after Spinal Cord Injury (SCI) in Female Rats: Evidence Estrous Cycle May Have a Modulatory Effect.Neurotrauma reports · 2022Article
- C-low threshold mechanoreceptor activation becomes sufficient to trigger affective pain in spinal cord-injured mice in association with increased respiratory rates.Frontiers in integrative neuroscience · 2022Article
- Pharmacogenetic inhibition of TrkB signaling in adult mice attenuates mechanical hypersensitivity and improves locomotor function after spinal cord injury.Frontiers in cellular neuroscience · 2022Article
- Inhibition of LncRNA Vof-16 expression promotes nerve regeneration and functional recovery after spinal cord injury.Neural regeneration research · 2022Article
- Spinal Cord Injury Increases Pro-inflammatory Cytokine Expression in Kidney at Acute and Sub-chronic Stages.Inflammation · 2021Article
- Exercise-Induced Plasticity in Signaling Pathways Involved in Motor Recovery after Spinal Cord Injury.International journal of molecular sciences · 2021Review
- The DNA Repair Enzyme XPD Is Partially Regulated by PI3K/AKT Signaling in the Context of Bupivacaine-Mediated Neuronal DNA Damage.Oxidative medicine and cellular longevity · 2021Article
- Learning to promote recovery after spinal cord injury.Experimental neurology · 2020Review
- Pharmacological Transection of Brain-Spinal Cord Communication Blocks Pain-Induced Hemorrhage and Locomotor Deficits after Spinal Cord Injury in Rats.Journal of neurotrauma · 2020Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
We previously showed that peripheral noxious input after spinal cord injury (SCI) inhibits beneficial spinal plasticity and impairs recovery of locomotor and bladder functions. These observations suggest that noxious input may similarly affect the development and maintenance of chronic neuropathic pain, an important consequence of SCI. In adult rats with a moderate contusion SCI, we investigated the effect of noxious tail stimulation, administered 1 day after SCI on mechanical withdrawal responses to von Frey stimuli from 1 to 28 days after treatment. In addition, because the proinflammatory cytokine tumor necrosis factor alpha (TNFα) is implicated in numerous injury-induced processes including pain hypersensitivity, we assessed the temporal and spatial expression of TNFα, TNF receptors, and several downstream signaling targets after stimulation. Our results showed that unlike sham surgery or SCI only, nociceptive stimulation after SCI induced mechanical sensitivity by 24h. These behavioral changes were accompanied by increased expression of TNFα. Cellular assessments of downstream targets of TNFα revealed that nociceptive stimulation increased the expression of caspase 8 and the active subunit (12 kDa) of caspase 3, indicative of active apoptosis at a time point consistent with the onset of mechanical allodynia. In addition, immunohistochemical analysis revealed distinct morphological signs of apoptosis in neurons and microglia at 24h after stimulation. Interestingly, expression of the inflammatory mediator NFκB was unaltered by nociceptive stimulation. These results suggest that noxious input caudal to the level of SCI can increase the onset and expression of behavioral responses indicative of pain, potentially involving TNFα signaling.
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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.