A cannabinoid is one of a great collection of complex chemical compounds that operates on cannabinoid receptors in cells that fluxuates neurotransmitter release in the brain. Cannabinoids for these receptors include the endocannabinoids, that are made naturally in the body by animals, the phytocannabinoids in cannabis and some other plants, and synthetic cannabinoids. The main cannabinoid is the phytocannabinoid tetrahydrocannabinol (THC), the primary psychoactive chemical in cannabis. Cannabidiol (CBD) is another main constituent of the plant and produces a non psychotic effect. This paper will look at how the cannabinoid receptors could be possible sites to target when trying to reduce alcohol consumption.
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Cannabinoids receptor 1 has regulatory role in alcohol consumption
The actions underlying predisposition to alcohol addiction and alcoholism are not very well known. This research, reviews the role of cannabinoid (CB1) receptors in voluntary alcohol use, and acute alcohol‐induced dopamine release, using mice that lack the CB1 receptor gene. These mice showed massively cut down on alcohol consumption, and didn’t show one bit of alcohol‐induced dopamine release, when paralleled to wild‐type mice. The gender difference, with female mice using vast amounts of more alcohol than wild‐type male mice, was seen in wild‐type mice, whereas this gender difference was not coherent in CB1 mutant male and female mice. There was also a massive gender difference, with the wild‐type, heterozygous, and mutant females using more liquid and food than wild‐type, heterozygous and mutant males. However, the net amount of fluid utility and food intake did not change between wild‐type, heterozygous, and mutant mice. These conclusions firmly indicate that the CB1 receptor system has a massive job in controlling the good wielding abilities of alcohol.
Male and Female’s cannabinoid receptor 1 works differently
This research evaluated the impact of targeted mutation of the CB1 receptor gene on oral self‐administration of alcohol, and on acute alcohol‐induced DA release. The conclusions show, for the very first time, that the mice that do not bare the CB1 receptor use less alcohol than their wild‐type comrades. These results are near the same to those reported in D2‐receptor‐deficient mice, where it was shown that mice that do not have the D2 DA receptor used less alcohol and were less sensitive to the locomotor depressant and ataxic impacts of alcohol.