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 GABAAR and mediation of GABA in the brain, which can cause alcohol addiction.
Part of the book: Drug Addiction