The involvement of the calcium and phosphoinositide intracellular regulatory systems in the molecular-cellular mechanisms of adaptation of the brain to hypoxia induced by transient anoxia were studied in slices of rat olfactory cortex. Anoxia lasting 2 min initiated the development of moderate but stable activation of intracellular regulatory systems during the reoxygenation period, with increases in binding of Ca2+ to intracellular hydrophobic domains and increases in the level of polyphosphoinositide metabolism. During this period, cells in the slices released neuromediator factors into the perfusion fluid; transfer of these to recipient slices induced similar changes in the activities of intracellular regulatory system components in the recipient slices. After anoxia lasting 10 min, NMDA-mediated pathogenic hyperactivity of the calcium and phosphoinositide systems developed. Preliminary moderate activation of these systems by transient anoxia or neuromodulator factors released by cells in response to transient anoxia prevented disruption of intracellular regulatory system activity induced by subsequent longer-lasting anoxia.
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 effects of DTNB on changes in intracellular Ca(2+) content in slices of rat cortex induced by 2- or 10-min anoxia were studied fluorometrically. DTNB (200 microM) prevented excessive intracellular Ca(2+) accumulation during and after 10-min anoxia and moderate increase in Ca(2+) content induced by 2-min anoxia. Our results suggest that redox sites of NMDA receptors participates in both pathogenic and adaptive Ca(2+)-mediated processes activated by anoxia.
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