Inhibition of pain responses by activation of CB(2) cannabinoid receptors.

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 Lipids

authors

Malan TP Jr,Ibrahim MM,Vanderah TW,Makriyannis A,Porreca F

doi

10.1016/s0009-3084(02)00155-x

subject

Has Abstract

pub_date

2002-12-31 00:00:00

pages

191-200

issue

1-2

eissn

0009-3084

issn

1873-2941

pii

S000930840200155X

journal_volume

121

pub_type

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