Cannabinoids in addiction therapy - Focus on cocaine
The endocannabinoid system, part of the body’s onboard cell-signaling network, has a role to play in cocaine addiction. Cocaine dysregulates neural cannabinoid receptor 1 (spoken of as ‘CB1’) and its downstream G protein-coupled receptor regulatory kinases 2, 3, and 5, and rapamicin and 70kDa ribosomal protein S6 kinase signaling. Moreover, chronic cocaine administration elicits increased CB1 receptor levels in numerous brain areas, and this is maintained over a long extinction period.
This may be what contributes to the neuroplasticity or neurotoxicity in brains in cocaine addiction. It is known experimentally that chronic stimulation of anandamide, an endogenous cannabinoid, reduces cue- and stress-induced relapse in animal models. Subchronic treatment with the synthetic agonist WIN 55,212-2 during cocaine abstinence also alters subsequent cocaine-seeking behavior animals.
CB1 receptors appear not to be directly involved in psychostimulant reward, or in dependence development, but they do play a role in reinstatement of extinguished drug-seeking behavior on re-exposure to the drug or associated cues. Enhancement CB1 neurotransmission counteracts these. Conversely, the CB1 antagonist AM251 inhibits cocaine relapse.
New evidence has also demonstrated that CB2 receptors in the brain, previously believed to express predominantly in peripheral immune cells, may also modulate some animal drug-seeking behaviors. CB2 receptors are expressed in mouse ventral tegmental area dopamine neurons, and activating these reduces neuronal excitability and subsequent cocaine-seeking behavior. For reinstatement, the same is true of TRPV1 receptors, though not for the rewarding effect of cocaine. Unlike CB1 receptors, neither of these plays a role in cue-induced reinstatement.
On the evidence of observational studies documenting users’ self-administration of crack-cocaine, distinct therapeutic benefits may be available specifically from cannabidiol (CBD). CBD is available in multiple formulations, is low in adverse risk potential, and could be offered easily in community-based settings for predominantly marginalized crack-cocaine user populations. Efficacy studies remain to be done first, however. Cocaine self-administration in animal models has not yet been attenuated by cannabidiol injections. Nor has cannabidiol treatment reduce cue-induced drug seeking in animals after withdrawal (though it has resulted in a statistically significant anxiolytic effect).
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The foregoing is a report on trends and developments in the cannabinoid industry. No product described herein is intended to diagnose, treat, cure or prevent any disease or syndrome.