Acclimatization to Middle Attitude Hypoxia Masks the Symptoms of Experimental Posttraumatic Stress Disorder, but Does Not Affect Its Pathogenetic Mechanisms.

The effects of acclimatization to middle attitude hypoxia on the resistance to acute emotional stress were studied on the model of posttraumatic stress disorder in rats. Anxyolitic, but not anxiogenic effect was observed in acclimatized rats. However, acclimatized rats with posttraumatic stress disorder were characterized by hypofunction of the pituitary-adrenocortical axis, which is typical of this pathology, and reduction in corticosterone/dehydroepiandrosterone ratio. At the neuroendocrine level, up-regulation of glucocorticoid receptors and a decrease in the level of corticotropin-releasing hormone in the hippocampus were revealed. The observed modifications of regulatory mechanisms can underlie hypofunction of the pituitary-adrenocortical axis. It was concluded that acclimatization to middle attitude hypoxia masks behavioral symptoms of posttraumatic stress disorder, but does not alter its pathogenetic neuroendocrine mechanisms.

Cerebral Mechanisms of Hypoxic/Ischemic Postconditioning.

This review analyzes recent data on mechanisms of cerebral hypoxia and the protective methods of hypoxic and ischemic postconditioning, as well as their interrelationship with the key mechanisms responsible for neuroprotection and neuroplasticity. Upregulation of expression of antiapoptotic factors and neurotrophins and modulation of activity of several protein kinases and transcription factors such as hypoxia-inducible factor-1 (HIF-1) are considered as the most important aspects in the neuroprotective potential of postconditioning. The presented information indicates substantial transformative promise of the noninvasive techniques of hypoxic postconditioning as well as significant similarity between the adaptive pathways activated by various postconditioning methods, which are far from being fully understood.

[Prenatal hypoxia modifies working memory and the activity of hippocampal polyphosphoinositide system in rats].

The present study was aimed at the analysis of spatial learning abilities in the Morris water maze (working memory) as well as hippocampal levels of phosphatidylinositol 4,5-diphosphates (TPI), phosphatidylinositol 4-phosphates (DPI), phosphotidylinositols (MPI), and expression of the type 1 inositol 1,4,5-trisphosphate receptor (IR3R1) in rats exposed to severe hypobaric hypoxia (ascent to 11 km, 3 h) on prenatal days 14-16 (group 1) or 17-19 (group 2). Exposure to severe hypoxia led to significant elevation of TP 1 and DPI hippocampal levels in juvenile and adult rats in the group 1, however these changes were more pronounced in juvenile rats than in adults. In the group 2, hypoxia up-regulated TPI and DPI hippocampal levels in juvenile rats, but in adult animals of this group just a small TPI level up-regulation was detected. Activation of IR3R1 expression was found to occur in the hippocampus both of juvenile and adult rats in the groups 1 and 2. These finding are consistent with the impaired spatial learning ability we revealed in the Morris water maze, indicative of a working memory deficit in the rat offspring exposed to hypobaric hypoxia during the first half of the last week of pregnancy.