Prophylactic transient hypoxia (preconditioning) increased neuron resistance to subsequent induction of severe hypoxia. Published data and results obtained by the authors on the molecular-cellular mechanisms of hypoxic preconditioning are presented. The roles of intracellular signal transduction, genome function, stress proteins, and neuromodulatory peptides in this process are discussed. The roles of glutamatergic as well as calcium and phosphoinositide regulatory systems and neuromodulatory factors as components of "volume" signal transmission are analyzed in hypoxic preconditioning-associated induction of functional tolerance mechanisms against the acute harmful effects of hypoxia on neurons in olfactory slices.

The aim of the present study was to explore 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 (IP3R1) 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 TPI and DPI hippocampal levels in juvenile and adult rats in group 1, however these changes were more pronounced in juvenile rats than in adults. In group 2, hypoxia upregulated TPI and DPI hippocampal levels in juvenile rats, but in adult animals of this group only a small TPI level upregulation was detected. Activation of IP3R1 expression was found to occur in the hippocampus both of juvenile and adult rats in groups 1 and 2. These data are consistent with our findings on impaired spatial learning ability 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.

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Studies reported here showed that the incubation medium used for frog muscle contains factors able to modulate the secretion of mediator from motor nerve terminals, with increases in release from low-efficiency synapses and decreases in release from high-efficiency synapses. Both the stimulatory and the inhibitory effects of the incubation medium are mediated by the corresponding changes in the number of available mediator quanta stored. Factors with stimulatory presynaptic actions were present mainly in the low-molecular-weight (<10 kDal) fraction of the incubation medium. The extent of the stimulatory action of this fraction on low-efficiency synapses correlated with the concentration of histidine-containing substances.