Date: 22.11.2010
Many studies have previously suggested a possibility that behind the susceptibility to abuse of alcohol and other substances there is a genetic predisposition to this addiction. Now a new study published in the journal Alcoholism Clinical Experimental Research (Thanos, 2010) provides with a direct evidence based on tests performed on mice.
The study of the Brookhaven National Laboratory of the Department of the Energy in the United States took two different strains of animals into acount. One of them was missing a gene coding for the dopamine receptor called D2, the other one was normal. Scientists were analyzing a different response to consumption of alcohol.
As it´s known, dopamine is a neurotransmitter responsible for feelings of pleasure, wellbeing and reward. Scientists in this case were particularly interested in the dopaminergic system, because a large amount of studies has shown that the deficit of specific receptors make animals and people less able to experience the most common delights and they are more prone to abuse of alcohol, drugs and also obesity.
The ability to obtain strains with a complete lack of the D2 gene and to control their intake of alcohol has made possible, for the first time, verification of the importance of the genetic component of the brain response to alcohol.
Half of each group of mice was given only water while the other one received a solution of 20 per cent ethanol to simulate the high consumption of this substance. After six months, researchers compared the levels of different types of cannabinoid receptor 1 (CB1) in various parts of the brain in all groups. These receptors are located close to the dopamine receptors and play a role in alcohol consumption and abuse. It is known, that the two types of receptors influence each other.
Recently researchers have found out that animals wich lack of D2 receptors had increased levels of CB1 receptors in brain regions associated with addiction compared to animals in the control group which received only water. "This may mean that active D2 receptors in normal mice in some way inhibit the expression of the CB1 gene and that the absence of D2 leads to an increase in the expression of CB1," said Panayotis Thanos, who led the research.
Chronic consumption of alcohol, however, seems to counteract this effect: mice without D2 who drank alcohol showed about the half of the the level of CB1 compared to animals with the same deficit that drank only water. "We have observed an up-regulation of CB1 in mice deficient in D2, which was reversed by the consumption of ethanol," said Thanos. "This down-regulation of CB1 after alcohol intake in animals deficient in D2 could be based on the small effects of reinforcing of ethanol in these mice."
Translation: Pavla Čermáková
Story source: http://lescienze.espresso.repubblica.it/
Original work: Thanos, P. K., Gopez, V., Delis, F., Michaelides, M., Grandy, D. K., Wang, G.-J., Kunos, G. and Volkow, N. D. , Upregulation of Cannabinoid Type 1 Receptors in Dopamine D2 Receptor Knockout Mice Is Reversed by Chronic Forced Ethanol Consumption. Alcoholism: Clinical and Experimental Research, no. doi: 10.1111/j.1530-0277.2010.01318.x
Photografs: www.sxc.hu
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