Abstract:
:Cannabinoid receptor agonists diminish responses to painful stimuli. Extensive evidence demonstrates that CB(1) cannabinoid receptor activation inhibits pain responses. Recently, the synthesis of CB(2) cannabinoid receptor-selective agonists has allowed testing whether CB(2) receptor activation inhibits pain. CB(2) 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 CB(2) receptor agonists inhibit pain responses by acting at peripheral sites. CB(2) receptor activation also inhibits edema and plasma extravasation produced by inflammation. CB(2) receptor-selective agonists do not produce central nervous system (CNS) effects typical of cannabinoids retaining agonist activity at the CB(1) receptor. Peripheral antinociception without CNS effects is consistent with the peripheral distribution of CB(2) receptors. CB(2) receptor agonists may have promise for the treatment of pain and inflammation without CNS side effects.
journal_name
Chem Phys Lipidsjournal_title
Chemistry and physics of lipidsauthors
Malan TP Jr,Ibrahim MM,Vanderah TW,Makriyannis A,Porreca Fdoi
10.1016/s0009-3084(02)00155-xsubject
Has Abstractpub_date
2002-12-31 00:00:00pages
191-200issue
1-2eissn
0009-3084issn
1873-2941pii
S000930840200155Xjournal_volume
121pub_type
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