Neuroscience letters
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Neuroscience letters · Sep 2013
CB1 cannabinoid receptor agonist prevents NGF-induced sensitization of TRPV1 in sensory neurons.
The transient receptor potential vanilloid type 1 channel (TRPV1) and nerve growth factor (NGF) are important mediators of inflammatory pain. NGF released during inflammation sensitizes TRPV1 in afferent nerve endings of peripheral nociceptors, increasing pain sensation. Cannabinoids, by activating CB1 G protein-coupled receptors, produce analgesia in a variety of pain models, though the exact mechanisms are not known. ⋯ Neither this rate, nor the magnitude of the sensitization (198 ± 63% of baseline) were different from that seen in cells not treated with NGF (3 of 25 cells sensitized (12.0%), 253 ± 70% of baseline). Pretreatment with the CB1 antagonist AM-251 (100 nM) prevented the effect of ACEA on NGF-induced sensitization. These results support the hypothesis that cannabinoids, acting through CB1 receptors, may produce analgesia in part by preventing NGF-induced sensitization of TRPV1 in afferent nociceptor nerve endings.