Journal de l'alcoolisme et de la toxicomanie
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ISSN: 2329-6488
ISSN: 2329-6488
Shushpanova TV
Graphical Abstract: Influence of maternal alcoholism on the brain benzodiazepine receptor development in human’s embryo and fetus showed decreases their affinity and increases density as compensatory adaptation of the fetal nervous system to the effects of alcohol.
Abstract: Signaling mechanisms that are required for proper neuronal development and how these processes are impaired by ethanol resulting in harmful consequences to brain development are very important for our understanding. The aim of the present work was to study the development of synaptic Benzodiazepine Receptors (BzDR) (functionally associated with the brain GABAergic system) in the brains of embryos and fetuses aged 8-15 weeks obtained from alcoholic female patients.
Material and method: Abortive material (samples of brain tissue) was obtained from 33 women with grade II alcoholism (ICD-10 F10.201 and F10.202) and 30 control women were studied. The properties of BzDR were studied by radioreceptor binding with the selective ligand [3H]-flunitrazepam using a crude embryo brain synaptosomal fraction.
Results: In contrast to controls, brain cells developing in conditions of prenatal alcoholization showed formation of synaptic benzodiazepine receptors and alterations in their properties: decreases in their affinity and increases in their density. A decrease in the ability of receptors to bind agonist ligands impairs the ligand: receptor protein ratio, leading to decreased binding of the major neurotransmitter GABA and impairment to synaptic transmission.
Conclusion: These are interpreted as compensatory reactions promoting adaptation of the fetal nervous system to the effects of alcohol and functional deficiency of the GABAergic system.