Light and electron microscopy were used to study the characteristics of the formation of brain vascular structures at the early stages of development in conditions of maternal alcoholization during pregnancy. Computer morphometric methods using the Scion Image system for image analysis showed that fetuses at 11-12 weeks of development in conditions of prenatal alcohol exposure showed a decrease in the mean absolute cross-sectional area of vessels in the intermediate layer of the brain, with an increase in their relative area and an increase per unit area of sections, as compared with the control group. Vessels started to differentiate into arteries and veins from 10 weeks of development.

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Chronic alcohol intake induces neuroadaptive changes in benzodiazepine receptors modulating GABAA receptors that promote alcohol addiction. Analysis of benzodiazepine receptors in the brain of Wistar rats differing by alcohol preference has demonstrated that affinity of [(3)H]flunitrazepam and [(3)H]Ro5-4864 binding with membrane fraction was reduced, while the density of specific binding sites in the brain cortex of heavy drinking and low drinking rats was increased in comparison with rats nonpreferring alcohol. Administration of anticonvulsant meta-chlorobenzhydryl urea increased affinity of benzodiazepine receptors in the brain cortex of heavy drinking rats, which improved GABA neurotransmission in the brain of these animals and reduced alcohol consumption.

Prenatal exposure to ethanol has an impact on angiogenesis and synaptogenesis and formation of neurotransmitter receptors in the brain of the embryo and fetus. Compensatory mechanism of hypoxia in conditions of prenatal exposure to alcohol involves decrease in the perimeter of the vessel and the area of the vessel in the cross section and an increase in the number of vessels in the brain. A significant effect of prenatal exposure to ethanol on the development of synaptic structures in the developing brain of the fetus was expressed in the slowing down of the formation of synaptic contacts and in the reduction of their number in comparison with the norm. Shaping synaptic contact is one of the leading processes during which largely determine the future integrative brain capabilities. The properties of benzodiazepine receptors in the developing brain of the human's embryo and fetus under prenatal alcohol influence were characterized by a decrease in affinity and an increase in their density as compensatory adaptation of the fetal nervous system to the effects of alcohol. It is reflected on during synaptogenesis in the developing brain and can lay the basis of severe disorders in the unborn child. Alcohol abuse induces neuroadaptive alters of benzodiazepine receptor system in the brain in patients with alcoholism that can modulate GABA A R and mediation of GABA in the brain, which can cause alcohol addiction.