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• W2087010345 endingPage "e73504" @default.
• W2087010345 startingPage "e73504" @default.
• W2087010345 abstract "Stress is an integral component of life that can sometimes cause a critical overload, depending on the qualitative and quantitative natures of the stressors. The involvement of actin, the predominant component of dendritic integrity, is a plausible candidate factor in stress-induced neuronal cytoskeletal changes. The major aim of this study was to compare the effects of three different stress conditions on the transcription and translation of actin-related cytoskeletal genes in the rat brain. Male Wistar rats were exposed to one or other of the frequently used models of physical stress, i.e. electric foot shock stress (EFSS), forced swimming stress (FSS), or psychosocial stress (PSS) for periods of 3, 7, 14, or 21 days. The relative mRNA and protein expressions of β-actin, cofilin and mitogen-activated protein kinase 1 (MAPK-1) were determined by qRT- PCR and western blotting from hippocampus and frontal cortex samples. Stressor-specific alterations in both β-actin and cofilin expression levels were seen after stress. These alterations were most pronounced in response to EFSS, and exhibited a U-shaped time course. FSS led to a significant β-actin mRNA expression elevation in the hippocampus and the frontal cortex after 3 and 7 days, respectively, without any subsequent change. PSS did not cause any change in β-actin or cofilin mRNA or protein expression in the examined brain regions. EFSS, FSS and PSS had no effect on the expression of MAPK-1 mRNA at any tested time point. These findings indicate a very delicate, stress type-dependent regulation of neuronal cytoskeletal components in the rat hippocampus and frontal cortex." @default.
• W2087010345 created "2016-06-24" @default.
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• W2087010345 date "2013-10-04" @default.
• W2087010345 modified "2023-09-23" @default.
• W2087010345 title "Cytoskeletal Protein Translation and Expression in the Rat Brain Are Stressor-Dependent and Region-Specific" @default.
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• W2087010345 doi "https://doi.org/10.1371/journal.pone.0073504" @default.
• W2087010345 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3790765" @default.
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