Peripheral Cannabinoid Analgesia: Neuronal and Immune Mechanisms
There is a wealth of animal data demonstrating cannabinoids to be analgesic. However, the well-known psychoactive central side effects resulting from cannabinoid action on neuronal cannabinoid CB1 receptors in the brain have limited the human use of cannabinoids in pain management. Exploitation of peripheral mechanisms potentially allows dissociation between analgesia and the unwanted cannabinoid “high.” This could involve singling out actions of peripheral neuronal cannabinoid receptors or utilization of receptors outwith the central nervous system, such as the cannabinoid CB2 receptor, expressed predominantly on immune cells. Multiple lines of evidence report peripheral analgesia via both CB1 and CB2 receptors. Neuronal actions and alteration of immune processes involved in the development of pain states are implicated. Therefore, development of cannabinoid analgesics directed at these peripheral targets offer a feasible therapeutic strategy devoid of central side effects.
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Document Type: Review Article
Affiliations: Royal Marsden Hospital, Fulham Road, London, UK
Publication date: 2005-02-01
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- Reviews in Analgesia (formerly Analgesia) is an international journal that publishes in English original reviews by experts on topics related to the basic mechanisms and therapeutics of pain relief. Reviews are invited that focus on pain mechanisms, endogenous mediators of pain, mechanisms of analgesia, and the synthesis, testing, or mechanism of action study of known or experimental analgesic compounds-including nonanalgesic and side effect endpoints and abuse liability. In addition, reviews of clinical studies or practice are invited that help elucidate the mechanism of action of known analgesic drugs, or that report on the use of experimental compounds or combinations. Reviews on new or standard methodological approaches, statistical analyses, and theoretical or mathematical treatments are also invited.