K. A. Baranova1, E. A. Rybnikova, and M. O. Samoilov
Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia
Received April 9, 2011
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 anx-
iety 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 associ-
ated 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 hypothala-
mus. 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 overex-
pression of the c-Fos transcription factor in the neocortex, hippocampus, and hypothalamus apparently partic-
ipates 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.
Keywords: c-Fos, hypoxic preconditioning, post-traumatic stress disorder, neuroprotection
DOI: 10.1134/S1819712411040039
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