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Na+,K(+)-ATPase and Mg(2+)-ATPase activities were studied in neurons and glial cells of the olfactory cortex of the rat by quantitative cytophotometry in conditions of long-term potentiation (LTP), and significant changes in direction and extent were found. Na+,K(+)-ATPase activity decreased in neurons in the first 15 min after LTP, with subsequent elevation by 30 min. Mg(2+)-ATPase activity remained unchanged in these conditions. Glial cells showed significant increases in Na+,K(+)-ATPase activity in the initial period after LTP, with return to control by 30 min. Again, there were no significant changes in Mg(2+)-ATPase activity. The formation and persistence of LTP in neurons and glial cells was accompanied by significant changes in Na+,K(+)-ATPase activity, which were reciprocal in nature.

The Nissl method and immunocytochemistry were used to study the effects of severe hypobaric hypoxia and its actions in combination with the preconditioning actions of moderate hypoxia on the expression of the early gene proteins c-Fos and NGFI-A as well as structural changes in hippocampal and neocortical neurons in the rat brain. Severe hypoxia was found to suppress c-Fos and NGFI-A synthesis (3-24 h after exposure) and to induce delayed (days 3-7) structural damage to neurons, of the "light" and predominantly the "dark" types, which appear to reflect the development of necrotic and apoptotic processes respectively. Preconditioning with the regime used here corrected these derangements, resulting in increases in the expression of early gene proteins and significant reductions in structural damage to neurons after severe hypoxia.

Previous studies have demonstrated that preconditioning (PC) with three sessions of moderate hypoxia significantly increases the expression of the antioxidant protein thioredoxin-1 (Trx-1) in the rat hippocampus by 3 h after subsequent acute severe hypoxia as compared with non-preconditioned animals. However, it remained unclear whether this increase in Trx-1 accumulation during PC is induced before severe hypoxia or is a modification of the response to severe hypoxia. This question was addressed in the present investigation using experiments on 12 adult male Wistar rats with studies of Trx-1 expression after PC without subsequent severe hypoxia. Immunocytochemical studies were performed 3 and 24 h after three episodes of moderate hypobaric hypoxia (three sessions of 2 h at 360 mmHg with 24-h intervals). Immunoreactivity to Trx-1 24 h after the last session was significantly decreased in neurons in all the areas of the hippocampus studied (CA1, CA2, CA3, and the dentate gyrus). Immunoreactivity in CA3 was also decreased 3 h after hypoxia. These results provide evidence that moderate preconditioning hypoxia itself not only does not increase, but even significantly decreases Trx-1 expression. Thus, increases in Trx-1 contents in the hippocampus of preconditioned animals after severe hypoxia are not associated with the accumulation of this protein during PC, but with a PC-induced modification of the reaction to severe hypoxia.

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