TY - JOUR

T1 - The Effects of Chronic Alcoholization on the Expression of Brain-Derived Neurotrophic Factor and Its Receptors in the Brains of Mice Genetically Predisposed to Depressive-Like Behavior

AU - Bazovkina, D. V.

AU - Kondaurova, E. M.

AU - Tsybko, A. S.

AU - Kovetskaya, A. I.

AU - Ilchibaeva, T. V.

AU - Naumenko, V. S.

PY - 2017/9/14

Y1 - 2017/9/14

N2 - Brain-derived neurotropic factor (BDNF) plays an important role in mechanisms of depression. Precursor protein of this factor (proBDNF) can initiate apoptosis in the brain, while the mature form of BDNF is involved in neurogenesis. It is known that chronic alcoholization leads to the activation of apoptotic processes, neurodegeneration, brain injury, and cognitive dysfunction. In this work, we have studied the influence of long-term ethanol exposure on the proBDNF and BDNF protein levels, as well as on the expression of genes that encode these proteins in the brain structures of ASC mice with genetic predisposition to depressive-like behavior and in mice from parental nondepressive CBA strain. It was shown that chronic alcoholization results in a reduction of the BDNF level in the hippocampus and an increase in the amount of TrkB and p75 receptors in the frontal cortex of nondepressive CBA mice. At the same time, the long-term alcoholization of depressive ASC mice results in an increase of the proBDNF level in the frontal cortex and a reduction in the p75 protein level in the hippocampus. It has also been shown that, in depressive ASC mice, proBDNF and BDNF levels are significantly lower in the hippocampus and the frontal cortex compared with nondepressive CBA strain. However, no significant differences in the expression of genes encoding the studied proteins were observed. Thus, changes in the expression patterns of proBDNF, BDNF, and their receptors under the influence of alcoholization in the depressive ASC strain and nondepressive CBA strain mice are different.

AB - Brain-derived neurotropic factor (BDNF) plays an important role in mechanisms of depression. Precursor protein of this factor (proBDNF) can initiate apoptosis in the brain, while the mature form of BDNF is involved in neurogenesis. It is known that chronic alcoholization leads to the activation of apoptotic processes, neurodegeneration, brain injury, and cognitive dysfunction. In this work, we have studied the influence of long-term ethanol exposure on the proBDNF and BDNF protein levels, as well as on the expression of genes that encode these proteins in the brain structures of ASC mice with genetic predisposition to depressive-like behavior and in mice from parental nondepressive CBA strain. It was shown that chronic alcoholization results in a reduction of the BDNF level in the hippocampus and an increase in the amount of TrkB and p75 receptors in the frontal cortex of nondepressive CBA mice. At the same time, the long-term alcoholization of depressive ASC mice results in an increase of the proBDNF level in the frontal cortex and a reduction in the p75 protein level in the hippocampus. It has also been shown that, in depressive ASC mice, proBDNF and BDNF levels are significantly lower in the hippocampus and the frontal cortex compared with nondepressive CBA strain. However, no significant differences in the expression of genes encoding the studied proteins were observed. Thus, changes in the expression patterns of proBDNF, BDNF, and their receptors under the influence of alcoholization in the depressive ASC strain and nondepressive CBA strain mice are different.

KW - BDNF precursor proBDNF

KW - brain-derived neurotrophic factor BDNF

KW - chronic alcoholization

KW - hereditary predisposition to depressive-like behavior

KW - mice

KW - mRNA and protein levels

KW - TrkB and p75 receptors

KW - Alcoholism/complications

KW - Animals

KW - Brain-Derived Neurotrophic Factor/genetics

KW - Depressive Disorder/complications

KW - Disease Models, Animal

KW - Ethanol/toxicity

KW - Frontal Lobe/drug effects

KW - Gene Expression Regulation

KW - Genetic Predisposition to Disease

KW - Hippocampus/drug effects

KW - Male

KW - Mice

KW - Mice, Inbred CBA

KW - Mice, Transgenic

KW - Protein Precursors/genetics

KW - Receptor, trkB/genetics

KW - Receptors, Nerve Growth Factor/genetics

KW - Signal Transduction

UR - http://www.scopus.com/inward/record.url?scp=85044236844&partnerID=8YFLogxK

U2 - 10.7868/S002689841704005X

DO - 10.7868/S002689841704005X

M3 - Article

C2 - 28900083

AN - SCOPUS:85044236844

VL - 51

SP - 647

EP - 655

JO - Molekulyarnaya Biologiya

JF - Molekulyarnaya Biologiya

SN - 0026-8984

IS - 4

ER -