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Effects of short-term exposure to lithium on antiapoptotic Bcl-xL protein expression in cortex and hippocampus of rats after acute stress. / Dygalo, N. N.; Bannova, A. V.; Sukhareva, E. V. и др.

в: Biochemistry (Moscow), Том 82, № 3, 01.03.2017, стр. 345-350.

Результаты исследований: Научные публикации в периодических изданияхстатьяРецензирование

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Dygalo NN, Bannova AV, Sukhareva EV, Shishkina GT, Ayriyants KA, Kalinina TS. Effects of short-term exposure to lithium on antiapoptotic Bcl-xL protein expression in cortex and hippocampus of rats after acute stress. Biochemistry (Moscow). 2017 март 1;82(3):345-350. doi: 10.1134/S0006297917030130

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BibTeX

@article{db2eb09b497e48fe8fc79a5de8f12687,
title = "Effects of short-term exposure to lithium on antiapoptotic Bcl-xL protein expression in cortex and hippocampus of rats after acute stress",
abstract = "The antiapoptotic protein Bcl-xL is involved in development of neurobiological resilience to stress; hence, the possibility of use of psychotropic drugs to increase its expression in brain in response to stress is of considerable interest. Lithium is a neurotropic drug widely used in psychiatry. In work, we studied effects of lithium administration (for 2 or 7 days) on the expression of Bcl-xL mRNA and protein in the hippocampi and cortices of rats subjected to stress that induced depression-like behavior in the animals. In contrast to the brain-derived neurotrophic factor (BDNF), whose expression decreased in the hippocampus in response to acute stress, stress increased the level of Bcl-xL mRNA in the hippocampus, but decreased it in the frontal cortex. Treatment of stressed animals with lithium for 2 or 7 days increased Bcl-xL protein levels 1.5-fold in the hippocampus, but it decreased them in the cortex. Therefore, Bcl-xL expression in the brain can be modulated by both stress and psychotropic drugs, and the effects of these factors are brain region-specific: both stress exposure and lithium administration activated Bcl-xL expression in the hippocampus and suppressed it in the frontal cortex. The activation of Bcl-xL expression in the hippocampus by lithium, demonstrated for the first time in this study, suggests an important role of this protein in the therapeutic effects of lithium in the treatment of stress-induced psychoemotional disorders.",
keywords = "Bcl-xL, BDNF, frontal cortex, gene expression, hippocampus, lithium chloride, stress",
author = "Dygalo, {N. N.} and Bannova, {A. V.} and Sukhareva, {E. V.} and Shishkina, {G. T.} and Ayriyants, {K. A.} and Kalinina, {T. S.}",
year = "2017",
month = mar,
day = "1",
doi = "10.1134/S0006297917030130",
language = "English",
volume = "82",
pages = "345--350",
journal = "Biochemistry (Moscow)",
issn = "0006-2979",
publisher = "Maik Nauka-Interperiodica Publishing",
number = "3",

}

RIS

TY - JOUR

T1 - Effects of short-term exposure to lithium on antiapoptotic Bcl-xL protein expression in cortex and hippocampus of rats after acute stress

AU - Dygalo, N. N.

AU - Bannova, A. V.

AU - Sukhareva, E. V.

AU - Shishkina, G. T.

AU - Ayriyants, K. A.

AU - Kalinina, T. S.

PY - 2017/3/1

Y1 - 2017/3/1

N2 - The antiapoptotic protein Bcl-xL is involved in development of neurobiological resilience to stress; hence, the possibility of use of psychotropic drugs to increase its expression in brain in response to stress is of considerable interest. Lithium is a neurotropic drug widely used in psychiatry. In work, we studied effects of lithium administration (for 2 or 7 days) on the expression of Bcl-xL mRNA and protein in the hippocampi and cortices of rats subjected to stress that induced depression-like behavior in the animals. In contrast to the brain-derived neurotrophic factor (BDNF), whose expression decreased in the hippocampus in response to acute stress, stress increased the level of Bcl-xL mRNA in the hippocampus, but decreased it in the frontal cortex. Treatment of stressed animals with lithium for 2 or 7 days increased Bcl-xL protein levels 1.5-fold in the hippocampus, but it decreased them in the cortex. Therefore, Bcl-xL expression in the brain can be modulated by both stress and psychotropic drugs, and the effects of these factors are brain region-specific: both stress exposure and lithium administration activated Bcl-xL expression in the hippocampus and suppressed it in the frontal cortex. The activation of Bcl-xL expression in the hippocampus by lithium, demonstrated for the first time in this study, suggests an important role of this protein in the therapeutic effects of lithium in the treatment of stress-induced psychoemotional disorders.

AB - The antiapoptotic protein Bcl-xL is involved in development of neurobiological resilience to stress; hence, the possibility of use of psychotropic drugs to increase its expression in brain in response to stress is of considerable interest. Lithium is a neurotropic drug widely used in psychiatry. In work, we studied effects of lithium administration (for 2 or 7 days) on the expression of Bcl-xL mRNA and protein in the hippocampi and cortices of rats subjected to stress that induced depression-like behavior in the animals. In contrast to the brain-derived neurotrophic factor (BDNF), whose expression decreased in the hippocampus in response to acute stress, stress increased the level of Bcl-xL mRNA in the hippocampus, but decreased it in the frontal cortex. Treatment of stressed animals with lithium for 2 or 7 days increased Bcl-xL protein levels 1.5-fold in the hippocampus, but it decreased them in the cortex. Therefore, Bcl-xL expression in the brain can be modulated by both stress and psychotropic drugs, and the effects of these factors are brain region-specific: both stress exposure and lithium administration activated Bcl-xL expression in the hippocampus and suppressed it in the frontal cortex. The activation of Bcl-xL expression in the hippocampus by lithium, demonstrated for the first time in this study, suggests an important role of this protein in the therapeutic effects of lithium in the treatment of stress-induced psychoemotional disorders.

KW - Bcl-xL

KW - BDNF

KW - frontal cortex

KW - gene expression

KW - hippocampus

KW - lithium chloride

KW - stress

UR - http://www.scopus.com/inward/record.url?scp=85014903825&partnerID=8YFLogxK

U2 - 10.1134/S0006297917030130

DO - 10.1134/S0006297917030130

M3 - Article

C2 - 28320276

AN - SCOPUS:85014903825

VL - 82

SP - 345

EP - 350

JO - Biochemistry (Moscow)

JF - Biochemistry (Moscow)

SN - 0006-2979

IS - 3

ER -

ID: 10063947