Use of sodium hydroxybutyrate and nooglutyl to correct dopamine release in the striatum of prenatally alcoholized rat pups

Abstract

Alcohol consumption by pregnant females is known to result in the development of mental abnormalities and mental retardation in their offspring [8]. It has been found experimentally that substances with nootropic activity such as sodium hydroxybutyrate and nooglutyl are capable of correcting these abnormalities resulting from prenatal alcoholization [3,4]. As shown by Trofnnov et al. [4], the neurocheinical mechanisms responsible for the pathology as weU as those by which the pharmacotherapeutic effect of nooglutyl is achieved, involve alterations in the levels of serotonin and dopamine and of their main metabolites 5-HIAA and DOPAC in the cortex and hippocampus of young rats [4]. It has also been shown that slowed dopamine turnover in the striatum is a characteristic neurochemical sign of the ethanol withdrawal syndrome [7]. In the study described here the prenatal alcoholization model was used to explore how the functional activity of the presynaptic dopaminergic system of the striatum in rat pups is influenced by (a) maternal alcoholization and (b) sodium hydroxybutyrate and nooglutyl.