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The Journal of Neuroscience, June 1, 2002, 22(11):4720-4727

⁹-Tetrahydrocannabinol and Cannabinol Activate Capsaicin-Sensitive Sensory Nerves via a CB₁ and CB₂ Cannabinoid Receptor-Independent Mechanism

Peter M. Zygmunt, David A. Andersson, and Edward D. Högestätt

Department of Clinical Pharmacology, Institute of Laboratory Medicine, Lund University Hospital, SE-221 85 Lund, Sweden

Although ⁹-tetrahydrocannabinol (THC) produces analgesia, its effects on nociceptive primary afferents are unknown. These neurons participate not only in pain signaling but also in the local response to tissue injury. Here, we show that THC and cannabinol induce a CB₁/CB₂ cannabinoid receptor-independent release of calcitonin gene-related peptide from capsaicin-sensitive perivascular sensory nerves. Other psychotropic cannabinoids cannot mimic this action. The vanilloid receptor antagonist ruthenium red abolishes the responses to THC and cannabinol. However, the effect of THC on sensory nerves is intact in vanilloid receptor subtype 1 gene knock-out mice. The THC response depends on extracellular calcium but does not involve known voltage-operated calcium channels, glutamate receptors, or protein kinases A and C. These results may indicate the presence of a novel cannabinoid receptor/ion channel in the pain pathway.

Key words: calcitonin gene-related peptide; cannabinoids; cannabinol; cannabis; capsaicin; nociceptors; pain; receptors, sensory; tetrahydrocannabinol

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Copyright © 2002 Society for Neuroscience  0270-6474/02/22114720-08$05.00/0

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