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Levels of endocannabinoids are different in certain areas of the brains of people who have undergone chronic alcohol exposure. This raises the possibility that by targeting the endocannabinoid system (ECS) in the brain, alcohol addiction could be treated and/or the symptoms of alcohol exposure lessened.
This study looked at the patterns of changes in the endocannabinoid system, including endocannabinoid levels in the blood and serum, and the expression of ECS receptors in the areas of the brain that mediate and regulate reward. Using rats who had been subjected to equivalent levels of addiction, such as alcoholization, the effects of alcohol deprivation were observed in these parts of the brain; and the changes that occur alongside voluntary consumption of alcohol.
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By investigating whether activating or blocking endocannabinoid receptors in these areas changed the consumption of rats, both the mechanisms of addiction are explored and a potential method of treating alcohol addiction is revealed. THC and CP55940 are both cannabinoid agonists, reduced alcohol intake without significantly changing dopamine or GABA signaling (which is seen in other models of addiction).
Levels of endocannabinoids 2-AG and AEA were measured in the brains of rats in three phases of alcoholism: alcoholization, deprivation, and relapse.
Results were interesting, showing that in the limbic forebrain, the two most common CB1 receptor agonists, anandamide (AEA) and arachidonoylglycerol (2-AG) increased during and after 7 days of alcoholization, decreased after 2 days of deprivation, and 2-AG decreased further when the rats were allowed to relapse into alcoholism. In other parts of the brain, the patterns were different during different phases of the test.
In the midbrain, AEA was reduced but not 2-AG, after alcoholization. Both AEA and 2-AG were reduced when alcohol was reintroduced. Interestingly, the levels of CB1R expression were largely unchanged, even though the endocannabinoid levels were changed.
Two agonists, THC and CP55, 940, both reduced the amount of fluid and ethanol the rats chose to drink. Another (selective) agonist, SR141716, reduced fluid and ethanol intake as well. Other addiction-related signaling pathways, dopamine and GABA, were unaffected. This strongly suggests that the ECS is an important pathway in the development, maintenance, and recovery from addiction
The authors conclude that a large part of the rewards system for alcoholism (and presumably other addictive substances) is mediated by the ECS, independently of other classic addiction pathways, and therefore presents a target for therapy.
A large part of alcoholism is the reward the brain gets from alcohol. Physical dependency aside, it is one of the biggest reasons it is hard to quit alcohol. This study suggests that the rewards system of the brain is controlled in part by the endocannabinoid system, and could therefore be targeted by cannabinoid receptor agonists like the ones used here to alter the behavior of addicted individuals in a positive way.
The discovery of an important addiction mechanism that is mediated by the ECS promises another avenue for treating alcoholism and potentially other addictions. Blocking or activating endocannabinoid receptors already looks like it could be a way of reducing the reward from alcohol.