ArticleThe Journal of clinical investigation2005
TRPA1 induced in sensory neurons contributes to cold hyperalgesia after inflammation and nerve injury.
Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 283 papers.
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The trial behind it
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Who cites it
283 citing papers in PubMed.
- A Human TRPA1-Specific Pain Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Trial
- Saikosaponin D Attenuates Postherpetic Neuralgia and Reduces Inflammation by Regulating Gut Microbiota in a Rodent Model.Biochemical genetics · 2026Article
- Spared but Not Silent: Ion Channel Plasticity in Uninjured Sensory Neurons in Neuropathic Pain.International journal of molecular sciences · 2026Review
- Nanomedicine against oxaliplatin-induced peripheral neuropathy: hypotheses and research perspectives on ion channels and immune microenvironment.Journal of the Egyptian National Cancer Institute · 2026Review
- Place preference in a female adolescent rat model of neuropathic pain: The effects of cannabidiol and oxycodone on cerebellum cell density.Psychopharmacology · 2026Article
- An mTORC2-Lipid Signaling Axis Controls Stress-Induced Organismal Death.Research square · 2026Article
- CXCL9 and CXCL10 Induce Expression of Nociceptive Ion Channels in Primary Sensory Neurons in Models of HIV-Associated Distal Sensory Polyneuropathy.International journal of molecular sciences · 2026Article
- TRP Channels from Sensory Coding to Physiology.Metabolites · 2025Review
- High Prevalence of Cold Intolerance in Rheumatoid Arthritis: A Case-Control Study.Clinical case reports · 2025Article
- Targeting prostaglandin ENature communications · 2025Article
- Lysosomal ion channels and pain.Pain reports · 2025Review
- α2δ-1-Linked NMDA and AMPA Receptors in Neuropathic Pain and Gabapentinoid Action.Journal of neurochemistry · 2025Review
- Histone Methyltransferase G9a in Primary Sensory Neurons Promotes Inflammatory Pain and Transcription ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025Review
- Borneol's Pre-Clinical Analgesic Efficacy: Mediated by Receptor and Immune Mechanisms.Journal of pain research · 2025Review
- Santacruzamate A Alleviates Pain and Pain-Related Adverse Emotions through the Inhibition of Microglial Activation in the Anterior Cingulate Cortex.ACS pharmacology & translational science · 2024Article
- Neurochemical mechanism of muscular pain: Insight from the study on delayed onset muscle soreness.The journal of physiological sciences : JPS · 2024Review
- Human Transient Receptor Potential Ankyrin 1 Channel: Structure, Function, and Physiology.Sub-cellular biochemistry · 2024Review
- Parthenolide as a potential analgesic in the treatment of paclitaxel-induced neuropathic pain: the rat modeling.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Lipopolysaccharide-Induced TRPA1 Upregulation in Trigeminal Neurons is Dependent on TLR4 and Vesicular Exocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
223 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cold hyperalgesia is a well-documented symptom of inflammatory and neuropathic pain; however, the underlying mechanisms of this enhanced sensitivity to cold are poorly understood. A subset of transient receptor potential (TRP) channels mediates thermosensation and is expressed in sensory tissues, such as nociceptors and skin. Here we report that the pharmacological blockade of TRPA1 in primary sensory neurons reversed cold hyperalgesia caused by inflammation and nerve injury. Inflammation and nerve injury increased TRPA1, but not TRPM8, expression in tyrosine kinase A-expressing dorsal root ganglion (DRG) neurons. Intrathecal administration of anti-nerve growth factor (anti-NGF), p38 MAPK inhibitor, or TRPA1 antisense oligodeoxynucleotide decreased the induction of TRPA1 and suppressed inflammation- and nerve injury-induced cold hyperalgesia. Conversely, intrathecal injection of NGF, but not glial cell line-derived neurotrophic factor, increased TRPA1 in DRG neurons through the p38 MAPK pathway. Together, these results demonstrate that an NGF-induced TRPA1 increase in sensory neurons via p38 activation is necessary for cold hyperalgesia. Thus, blocking TRPA1 in sensory neurons might provide a fruitful strategy for treating cold hyperalgesia caused by inflammation and nerve damage.
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