Abstract
A quantitative immunocytochemical method was used to study the dynamics of the expression of the transcription factor c-Fos in the hypothalamus, hippocampus, and neocortex during the development of anxiety in the post-traumatic stress disorder (PTSD) model in control rats and rats preconditioned by hypoxia, which is known to have an anxiolytic effect. It was found that the induction of experimental PTSD was associated with a significant and stable increase in the level of c-Fos in all investigated brain areas. The maximum increase according to amplitude (up to 30 times) and duration (about 10 days) was observed in the hypothalamus. This overexpression may be associated with corticotropin-releasing hormone hyperproduction, which is typical of PTSD. In animals that were subjected to triple hypoxic preconditioning with mild repetitive hypobaric hypoxia (360 mm Hg for 2 hours daily, for 3 days), which prevented the traumatic stress-induced pathology, c-Fos overexpression was completely or partially blocked. These data indicate that stable overexpression of the c-Fos transcription factor in the neocortex, hippocampus, and hypothalamus apparently participates in the mechanisms of PTSD development, whereas its blockade plays an important role in increasing the brain’s tolerance to stresses and in protection against stress-induced pathologies.
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Original Russian Text © K.A. Baranova, E.A. Rybnikova, M.O. Samoilov, 2011, published in Neirokhimiya, 2011, Vol. 28, No. 4, pp. 294–299.
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Baranova, K.A., Rybnikova, E.A. & Samoilov, M.O. Involvement of the transcription factor c-Fos in the protective effect of hypoxic preconditioning in a model of post-traumatic stress disorder in rats. Neurochem. J. 5, 257–262 (2011). https://doi.org/10.1134/S1819712411040039
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DOI: https://doi.org/10.1134/S1819712411040039