期刊
BRITISH JOURNAL OF PHARMACOLOGY
卷 153, 期 2, 页码 319-334出版社
WILEY
DOI: 10.1038/sj.bjp.0707531
关键词
allodynia; hyperalgesia; endocannabinoid; central sensitization; nerve injury
资金
- NIDA NIH HHS [R01 DA021644, DA021644, DA022478, R21 DA022478, R21 DA022478-02, DA022702, R01 DA021644-03, R21 DA022702] Funding Source: Medline
- NATIONAL INSTITUTE ON DRUG ABUSE [R21DA022478, R21DA022702, R01DA021644] Funding Source: NIH RePORTER
Cannabinoids suppress behavioural responses to noxious stimulation and suppress nociceptive transmission through activation of CB1 and CB2 receptor subtypes. CB1 receptors are expressed at high levels in the central nervous system (CNS), whereas CB2 receptors are found predominantly, but not exclusively, outside the CNS. CB2 receptors are also upregulated in the CNS and dorsal root ganglia by pathological pain states. Here, we review behavioural, neurochemical and electrophysiological data, which identify cannabinoid CB2 receptors as a therapeutic target for treating pathological pain states with limited centrally, mediated side effects. The development of CB2-selective agonists (with minimal affinity for CB1) as well as mutant mice lacking CB2 receptors has provided pharmacological and genetic tools required to evaluate the effectiveness of CB2 agonists in suppressing persistent pain states. This review will examine the efficacy of cannabinoid CB2-selective agonists in suppressing acute, inflammatory and neuropathic nociception following systemic and local routes of administration. Data derived from behavioural, neurochemical and neurophysiological approaches are discussed to better understand the relationship between antinociceptive effects induced by CB2-selective agonists in behavioural studies and neural mechanisms of pain suppression. Finally, the therapeutic potential and possible limitations of CB2-based pharmacotherapies for pathological pain states induced by tissue and nerve injury are discussed.
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