ArticleScientific reports2022
Monoamine control of descending pain modulation after mild traumatic brain injury.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Therapeutic potential of CMPP, a novel maleimide derivative, in a reserpine-induced mouse model of pain-depression dyad.Biochemistry and biophysics reports · 2026Article
- Neuropathic pain in traumatic brain injury: consequences, mechanisms, and therapeutic avenues.Inflammopharmacology · 2026Review
- Dissection of Microglial Heterogeneity and Identification of Pain-Related Subpopulations After Traumatic Brain Injury.Pain research & management · 2026Article
- Exercise plasma improves traumatic brain injury outcomes in mice.Scientific reports · 2025Article
- Diffuse Noxious Inhibitory Controls in Chronic Pain States: Insights from Pre-Clinical Studies.International journal of molecular sciences · 2025Review
- Mechanisms and treatments of chronic pain after traumatic brain injury.Neurochemistry international · 2023Review
- Repeated closed-head mild traumatic brain injury-induced inflammation is associated with nociceptive sensitization.Journal of neuroinflammation · 2023Article
- Diffuse noxious inhibitory controls in chronic joint inflammatory Pain: Study of the descending serotonergic modulation mediated through 5HT3 receptors.Neurobiology of pain (Cambridge, Mass.)Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a significant public health concern, with the majority of injuries being mild. Many TBI victims experience chronic pain. Unfortunately, the mechanisms underlying pain after TBI are poorly understood. Here we examined the contribution of spinal monoamine signaling to dysfunctional descending pain modulation after TBI. For these studies we used a well-characterized concussive model of mild TBI. Measurements included mechanical allodynia, the efficacy of diffuse noxious inhibitory control (DNIC) endogenous pain control pathways and lumber norepinephrine and serotonin levels. We observed that DNIC is strongly reduced in both male and female mice after mild TBI for at least 12 weeks. In naïve mice, DNIC was mediated through α2 adrenoceptors, but sensitivity to α2 adrenoceptor agonists was reduced after TBI, and reboxetine failed to restore DNIC in these mice. The intrathecal injection of ondansetron showed that loss of DNIC was not due to excess serotonergic signaling through 5-HT
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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 OpenQuestion graph.