ArticleThe journal of pain2014
Ablating spinal NK1-bearing neurons eliminates the development of pain and reduces spinal neuronal hyperexcitability and inflammation from mechanical joint injury in the rat.
Article in The journal of pain, 2014. 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.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Subfailure capsule strain as the cause of cervical zygapophysial joint pain after whiplash: a scoping review.Pain medicine (Malden, Mass.) · 2026Article
- PGC-1α Transcriptionally Regulated by ChREBP Mitigates Neuropathic Pain Through Promoting Microglial Fatty Acid Oxidation and Anti-Inflammatory Response.CNS neuroscience & therapeutics · 2026Article
- Article
- Blocking SP/NK1R signaling improves spinal cord hemisection by inhibiting the release of pro-inflammatory cytokines in rabbits.The journal of spinal cord medicine · 2023Article
- Spinal Cord Stimulation Increases Chemoefficacy and Prevents Paclitaxel-Induced Pain via CX3CL1.Neuromodulation : journal of the International Neuromodulation Society · 2023Article
- Characterization of the Dahl salt-sensitive rat as a rodent model of inherited, widespread, persistent pain.Scientific reports · 2022Article
- Astrocytes contribute to pain gating in the spinal cord.Science advances · 2021Article
- Common and discrete mechanisms underlying chronic pain and itch: peripheral and central sensitization.Pflugers Archiv : European journal of physiology · 2021Review
- Innervation of the Human Intervertebral Disc: A Scoping Review.Pain medicine (Malden, Mass.) · 2021Article
- Opioid-Induced Hyperalgesic Priming in Single Nociceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Article
- Ocular surface inflammation induces de novo expression of substance P in the trigeminal primary afferents with large cell bodies.Scientific reports · 2020Article
- Role of Nociceptor Toll-like Receptor 4 (TLR4) in Opioid-Induced Hyperalgesia and Hyperalgesic Priming.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Physiologic facet capsule stretch can induce pain & upregulate matrix metalloproteinase-3 in the dorsal root ganglia when preceded by a physiological mechanical or nonpainful chemical exposure.Clinical biomechanics (Bristol, Avon) · 2019Article
- Substance P and pain chronicity.Cell and tissue research · 2019Review
- Article
- Fentanyl Induces Rapid Onset Hyperalgesic Priming: Type I at Peripheral and Type II at Central Nociceptor Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- CD44 Signaling Mediates High Molecular Weight Hyaluronan-Induced Antihyperalgesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Ablation of IB4 non-peptidergic afferents in the rat facet joint prevents injury-induced pain and thalamic hyperexcitability via supraspinal glutamate transporters.Neuroscience letters · 2017Article
- Marked sexual dimorphism in 5-HTNeuroscience · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledThe facet joint is a common source of pain, especially from mechanical injury. Although chronic pain is associated with altered spinal glial and neuronal responses, the contribution of specific spinal cells to joint pain is not understood. This study used the neurotoxin [Sar(9),Met(O2)(11)]-substance P-saporin (SSP-SAP) to selectively eliminate spinal cells expressing neurokinin-1 receptor (NK1R) in a rat model of painful facet joint injury to determine the role of those spinal neurons in pain from facet injury. Following spinal administration of SSP-SAP or its control (blank-SAP), a cervical facet injury was imposed and behavioral sensitivity was assessed. Spinal extracellular recordings were made on day 7 to classify neurons and quantify evoked firing. Spinal glial activation and interleukin 1αα (IL1α) expression also were evaluated. SSP-SAP prevented the development of mechanical hyperalgesia that is induced by joint injury and reduced NK1R expression and mechanically evoked neuronal firing in the dorsal horn. SSP-SAP also prevented a shift toward wide dynamic range neurons that is seen after injury. Spinal astrocytic activation and interleukin 1α (IL1α) expression were reduced to sham levels with SSP-SAP treatment. These results suggest that spinal NK1R-bearing cells are critical in initiating spinal nociception and inflammation associated with a painful mechanical joint injury. PERSPECTIVE: Results demonstrate that cells expressing NK1R in the spinal cord are critical for the development of joint pain, spinal neuroplasticity, and inflammation after trauma to the joint. These findings have utility for understanding mechanisms of joint pain and developing potential targets to treat pain.
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Registered trials
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