Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P21554 (cannabinoid receptor)
3,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antinociceptive action of cannabinoids in acute and inflammatory pain states have been well-documented. There is also accumulating evidence suggesting that cannabinoids are effective analgesics in chronic pain conditions. WIN 55,212-2, a mixed CB1 and CB2 cannabinoid receptor agonist, has been shown to be effective against hyperalgesia and allodynia in painful peripheral mononeuropathy. Recently, in addition to their spinal and supraspinal antinociceptive action, cannabinoids have also reported to exert local analgesic effects. The aim of this study is to observe the effect of a high affinity cannabinoid, WIN 55,212-2, on tactile allodynia and thermal hyperalgesia in diabetic rats. Diabetes was produced with the injection of a single dose of streptozocin (50 mg/kg, i.p.) and this procedure resulted in neuropathic pain behaviors in the hindlimbs. Mechanical allodynia was detected by application of von Frey filaments to the plantar surface of the foot, and thermal hyperalgesia was studied using the Hargreaves' method; however, thermal hyperalgesia did not develop in diabetic rats. With its higher doses, both systemic (3 and 10 mg/kg, i.p.) and peripheral (30 microg, i.p.l.) injections of WIN 55,212-2 reduced mechanical allodynia. These results suggest that WIN 55,212-2 has an antiallodynic effect in streptozocin-induced diabetic rats and may be a promising approach in the treatment of diabetic neuropathy.
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PMID:The effect of WIN 55,212-2, a cannabinoid agonist, on tactile allodynia in diabetic rats. 1551 50

Rodent models of neuropathic pain are used to investigate the underlying mechanisms of pain associated with damage to peripheral nerves and to evaluate the efficacy of novel compounds. However, few models have been adequately characterized and the validity of many models remains unclear. The present experiment examined the activity of known anti-allodynic compounds in the L5 spinal nerve ligation (SNL) model of peripheral mononeuropathy in the rat, a modified version of the L5/L6 SNL model [S.H. Kim, J.M. Chung, An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat, Pain 50 (1992) 355-363]. Tactile sensitivity was measured 7-21 days post-surgery using von Frey monofilaments before and following treatment with gabapentin (30, 60 and 120 mg/kg), morphine (1, 3 and 6 mg/kg), amitriptyline (1.5, 3 and 10 mg/kg), fluoxetine (3, 10 and 30 mg/kg), WIN55,212-2 (0.5, 1 and 2.5 mg/kg), indomethacin (1 and 5 mg/kg) or U-50,488H (3 and 6 mg/kg). Compared to sham-operated control animals, L5 SNL animals displayed significant tactile allodynia in the ipsilateral hindpaw that was completely reversed by treatment with gabapentin, morphine, and WIN55,212-2, partially reversed by amitriptyline and fluoxetine, and unaffected by U-50,488H or indomethacin. The robust effects of the non-selective cannabinoid receptor agonist WIN55,212-2 and morphine support reports in the literature that systemic cannabinoid receptor agonists and opioids are active in neuropathic pain. These results suggest that the L5 SNL model can be utilized to determine the anti-allodynic activity of novel compounds.
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PMID:Pharmacological evaluation of the selective spinal nerve ligation model of neuropathic pain in the rat. 1591 Sep 75