Depressive disorders and alcohol dependence are among the most common psychopathologies. It is known that disorders in the serotonergic and dopaminergic brain systems functioning lie in the pathogenesis of alcoholism and affective disorders. In this work, we studied the effects of prolonged administration of ethanol (1.5 g/kg, 20%, 10 days, i.p.) on behavior, functional activity of 5-HT1A and 5-HT2A receptors and expression of genes encoding serotonin (Htr1a, Htr2a) and dopamine (Drd1, Drd2) receptors in brain structures in mice of ASC strain (with the genetic predisposition to depressive-like behavior) and mice of the parental (“non-depressive”) CBA strain. It has been shown that alcoholization leads to an increase in motor activity in animals of both lines and an increase in the level of exploratory behavior in ASC mice. No significant effect of ethanol on social and depression-like behavior was found. The functional activities of 5-HT1A and 5-HT2A receptors (determined by the response to the administration of corresponding receptor agonists) were reduced by ethanol only in ASC animals. A decrease in 5-HT2A receptor gene expression was found in the frontal cortex of CBA mice treated with alcohol. At the same time, ethanol led to an increase in the mRNA levels of the 5-HT1A receptor gene in the striatum and the DRD1 receptor gene in the hypothalamus, as well as a decrease in the expression of the DRD2 receptor gene in the hippocampus of ASC mice. Thus, changes in the serotonergic and dopaminergic brain systems induced by chronic ethanol were more significant in ASC mice with a genetic predisposition to depression-like behavior.
Read full abstract