Cited by 195Pain Mechanisms and TreatmentsCannabis and Cannabinoid ResearchPain Management and Treatment

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Upregulation of spinal cannabinoid-1-receptors following nerve injury enhances the effects of Win 55,212-2 on neuropathic pain behaviors in rats

Lim, Grewo, Sung, Backil, Ji, Ru-Rong, Mao, Jianren·2003·Pain

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Abstract

Exogenous cannabinoids are effective in attenuating neuropathic pain behaviors induced by peripheral nerve injury, but the mechanisms of their effectiveness remain unclear. Here we examined the expression of spinal cannabinoid-1-receptors (CB1Rs) following chronic constriction sciatic nerve injury (CCI) and its relation to the effects of a CBR agonist (Win 55,212-2) on neuropathic pain in rats. CCI induced a time-dependent upregulation of spinal CB1Rs primarily within the ipsilateral superficial spinal cord dorsal horn as revealed by both Western blot and immunohistochemistry. This CCI-induced CB1R upregulation was at least in part mediated through tyrosine kinase receptors (Trk), because intrathecal treatment with the Trk inhibitor K252a (1 microg) for postoperative days 1-6 significantly reduced the CB1R upregulation in CCI rats. At the intracellular level, the mitogen-activated protein kinase (ERK-MAPK) inhibitor PD98059 (1 microg) prevented, while the protein kinase C inhibitor chelerythrine (10 microg) partially reduced, the CCI-induced CB1R upregulation when each agent was administered intrathecally for postoperative days 1-6. Importantly, the CCI-induced upregulation of spinal CB1Rs enhanced the effects of Win 55,212-2 on both thermal hyperalgesia and mechanical allodynia, since inhibition of the CB1R upregulation by PD98059 resulted in a significant reduction of the effects of Win 55,212-2 in CCI rats. These results indicate that upregulation of spinal CB1Rs following peripheral nerve injury may contribute to the therapeutic effects of exogenous cannabinoids on neuropathic pain.

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Authors: Lim, G., Sung, B., Ji, R.-R., & Mao, J.
Affiliations: Harvard University (US)
Brigham and Women's Hospital (US)
Corresponding author: Mao, Jianren
ORCID: Ji, Ru-Rong
Mao, Jianren
Venue: Pain
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2003-09
Volume: 105
Issue: 1
Pages: 275-283
ISSN: 0304-3959 (ISSN-L)
DOI: 10.1016/s0304-3959(03)00242-2
OpenAlex: W2007715028
Cited by: 195
References: 91
Citations by year: 2026: 6 · 2025: 8 · 2024: 5 · 2023: 6 · 2022: 7 · 2021: 8 · 2020: 9 · 2019: 4 · 2018: 7 · 2017: 11 · 2016: 7 · 2015: 10 · 2014: 5 · 2013: 8 · 2012: 8
FWCI: 7.30
Type: journal article
Language: en
Open access: closed
Locations: Pain (publishedVersion)
PubMed (publishedVersion)
Funders: Massachusetts General Hospital
National Institutes of Health
National Institute on Drug Abuse (DA 08835, R01DA008835)
National Institute of Neurological Disorders and Stroke (R01NS040698, R01NS042661, R01 NS42661)
Topics: Health Sciences › Medicine › Physiology (medical) › Pain Mechanisms and Treatments
Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
Health Sciences › Medicine › Anesthesiology and Pain Medicine › Pain Management and Treatment
Keywords: cannabinoid 1 receptor, dorsal horn, neuropathic pain, chronic constriction injury, sciatic nerve injury, WIN 55,212-2, exogenous cannabinoids, receptor up-regulation, Trk receptors, K252a, ERK signaling, protein kinase C, thermal hyperalgesia, mechanical allodynia, intrathecal administration
MeSH terms: Analgesics, Animals, Behavior, Animal, Enzyme Inhibitors, Flavonoids, Ligation, Male, Morpholines, Naphthalenes, Neuralgia, Pain, Protein Kinase C, Receptors, Drug, Sciatic Nerve, Spinal Cord, Time Factors, Wounds and Injuries, Up-Regulation, Rats, Sprague-Dawley, Receptor Protein-Tyrosine Kinases, Mitogen-Activated Protein Kinases, Receptors, Cannabinoid, Benzoxazines, Rats

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Upregulation of spinal cannabinoid-1-receptors following nerve injury enhances the effects of Win 55,212-2 on neuropathic pain behaviors in rats

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