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This study examined the effects of cannabinoid agonists on hyperalgesia in a model of neuropathic pain in the rat and investigated the possible sites of action. The antihyperalgesic activity of the cannabinoids was compared with their ability to elicit behavioral effects characteristic of central cannabinoid activity. WIN55, 212‐2 (0.3–10 mg/kg−1), CP‐55, 940 (0.03–1 mg/kg−1), and HU‐210 (0.001–0.03 mg/kg−1) were all active in a “tetrad” of tests consisting of tail‐flick, catalepsy, rotarod, and hypothermia following subcutaneous administration, with a rank order of potency in each of HU‐210> CP‐55, 940> WIN55, 212‐2. The effects of WIN55, 212‐2 in each assay were blocked by the Cannabinoid1 (CB1) antagonist SR141716A. In the partial sciatic ligation model if neuropathic pain WIN55, 212‐2, CP‐55, 940, and HU‐210 produced complete reversal of mechanical hyperalgesia within 3 hours of subcutaneous administration with D50 values of 0.52, 0.08, and 0.005 mg/kg−1, respectively. In this model WIN55, 212‐2 was also effective against thermal hyperalgesia and mechanical allodynia. WIN55, 212‐2 produced pronounced reversal of mechanical hyperalgesia following intrathecal administration that was blocked by the CB1 antagonist SR141716A. Following intraplantar administration into the ipsilateral hindpaw, WIN55, 212‐2 produced up to 70% reversal of mechanical hyperalgesia, although activity was also observed at high doses following injection into contralateral paw. The antihyperalgesic effect of WIN55, 212‐2 injected into the ipsilateral paw was blocked by subcutaneously administered SR141716A, but was not affected by intrathecally administered SR141716A. Conclude that cannabinoids are highly potent and efficacious antihyperalgesic agents in a model of neuropathic pain. This activity is likely to be mediated via action in both the CNS and in the periphery.
Pain Practice – Wiley
Published: Jan 1, 2001
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