Inhibition of pain responses by activation of CB2 cannabinoid receptors

被引:74
作者
Malan, TP
Ibrahim, MM
Vanderah, TW
Makriyannis, A
Porreca, F
机构
[1] Univ Arizona, Dept Anesthesiol, Tucson, AZ 85724 USA
[2] Univ Connecticut, Dept Med Chem, Storrs, CT 06269 USA
[3] Univ Connecticut, Dept Mol & Cell Biol, Storrs, CT 06269 USA
[4] Univ Arizona, Dept Pharmacol, Tucson, AZ 85724 USA
关键词
CB2; cannabinoid; pain; inflammation; hyperalgesia; allodynia; neuropathic;
D O I
10.1016/S0009-3084(02)00155-X
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cannabinoid receptor agonists diminish responses to painful stimuli. Extensive evidence demonstrates that CB1 cannabinoid receptor activation inhibits pain responses. Recently, the synthesis of CB2 cannabinoid receptor-selective agonists has allowed testing whether CB2 receptor activation inhibits pain. CB2 receptor activation is sufficient to inhibit acute nociception, inflammatory hyperalgesia, and the allodynia and hyperalgesia produced in a neuropathic pain model. Studies using site-specific administration of agonist and antagonist have suggested that CB2 receptor agonists inhibit pain responses by acting at peripheral sites. CB2 receptor activation also inhibits edema and plasma extravasation produced by inflammation. CB2 receptor-selective agonists do not produce central nervous system (CNS) effects typical of cannabinoids retaining agonist activity at the CB1 receptor. Peripheral antinociception without CNS effects is consistent with the peripheral distribution of CB2 receptors. CB2 receptor agonists may have promise for the treatment of pain and inflammation without CNS side effects. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:191 / 200
页数:10
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