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Endocannabinoid metabolism and uptake: novel targets for neuropathic and inflammatory pain

Endocannabinoid metabolism and uptake: novel targets for neuropathic and inflammatory pain

  1. NeuroChi
    Cannabinoid CB1 and CB2 receptors are located at key sites involved in the relaying and processing of noxious inputs. Both CB1
    and CB2 receptor agonists have analgesic effects in a range of models of inflammatory and neuropathic pain. Importantly,
    clinical trials of cannabis-based medicines indicate that the pre-clinical effects of cannabinoid agonists may translate into
    therapeutic potential in humans. One of the areas of concern with this pharmacological approach is that CB1 receptors have a
    widespread distribution in the brain and that global activation of CB1 receptors is associated with adverse side effects. Studies
    of the endogenous cannabinoids (endocannabinoids) have demonstrated that they are present in most tissues and that in
    some pain states, such as neuropathic pain, levels of endocannabinoids are elevated at key sites involved in pain processing. An
    alternative approach that can be used to harness the potential therapeutic effects of cannabinoids is to maximise the effects
    of the endocannabinoids, the actions of which are terminated by re-uptake and metabolism by various enzymes, including
    fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL) and cyclooxygenase type 2 (COX2). Preventing the
    metabolism, or uptake, of endocannabinoids elevates levels of these lipid compounds in tissue and produces behavioural
    analgesia in models of acute pain. Herein we review recent studies of the effects of inhibition of metabolism of
    endocannabinoids versus uptake of endocannabinoids on nociceptive processing in models of inflammatory and neuropathic
    pain.

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