Alterations in the dopamine system have been hypothesized as a predisposing factor in alcoholism. The presence of the TaqI A1 and B1 alleles adjacent to the dopamine D 2-receptor gene (DRD2) was studied in Scandinavian alcoholic inpatients (n = 74), alcoholics autopsied at a forensic clinic (n = 19) and controls (n = 81). There were no significant differences between controls and the alcoholics, but a tendency of increased DRD2 TaqI A1 or B1 allele frequencies in alcoholic groups selected for severity (i.e. severity according to DSM-III-R criteria, early onset or severe medical complications due to alcohol abuse) and decreased frequencies in the corresponding less severe alcoholic group. The present study does not yield evidence for the hypothesis of an association between the DRD2 TaqI A1 or B1 alleles and alcoholism.
Almost every third injury event in females and in almost every other event in males is alcohol-related, showing that alcohol plays an important part in fatal injuries in females even though it is mostly a male problem.
Chronic ethanol ingestion by mice resulted in the loss of high-affinity beta-adrenergic agonist binding sites and a significant decrease in activation of adenylate cyclase by guanine nucleotides and beta-adrenergic agonists in the hippocampus, although no significant change was noted in the total number of beta-adrenergic receptors, as defined by the binding of the antagonist [125]iodocyanopindolol. In cerebellum, chronic ethanol ingestion resulted in a 16% decrease in the total concentration of beta-adrenergic receptors and in a decrease in the affinity for agonist of the high-affinity beta-adrenergic agonist binding sites. However, neither the amount of the high-affinity agonist binding sites nor the activation of adenylate cyclase by agonist was affected. The different responses to ethanol in hippocampus and cerebellum may result from quantitative differences in distribution of beta 1- and beta 2-adrenergic receptors in the tested brain areas and/or differential effects of ethanol on stimulatory guanine nucleotide binding protein in these brain areas.
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