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The effect of preconditioning (PC) on the changes of nerve growth factor-induced gene A (NGFI-A) expression induced by severe hypobaric hypoxia was studied by in situ hybridization. A PC consisted of three trials of mild hypobaric hypoxia (360 Torr, 2 h) spaced at 24 h. The last trial was followed by severe hypoxia (SH; 180 Torr, 3 h) 24 h later. The PC hypoxia prevented the NGFI-A messenger RNA (mRNA) increase in the cortex, neostriatum, piriform cortex, amygdala and hippocampus detected 3 h after SH. The preconditioned SH caused a peak in NGFI-A mRNA expression at the 24 h time-point and thus abolished the dramatic decrease of the mRNA in vulnerable areas seen by 24 and 72 h after SH. The findings suggest a role of brain NGFI-A in the protective effect of hypoxic/ischemic PC. [Copyright &y& Elsevier]

Abstract: The aim of this work was to study effects of mild preconditioning hypobaric hypoxia (380Torr for 2h, repeated 3 or 6 times spaced at 24h) on brain NGFI-A immunoreactivity and passive avoidance (PA) behavior in rats exposed to severe hypoxia (160Torr for 3h). Severe hypobaric hypoxia produced extensive neuronal loss in hippocampal CA1, while the preceding hypoxic preconditioning had clear protective effect on neuronal viability of vulnerable hippocampal cells. Besides, the hypoxic preconditioning prevented impairment of acquisition and retention of PA caused by severe hypoxia. The six-trial hypobaric preconditioning was more effective in protection against PA learning deficits in severe hypoxia exposed rats than the three-trial preconditioning. The preconditioning up-regulated severe hypoxia-suppressed neocortical and hippocampal expression of NGFI-A, suggesting a possible role for NGFI-A in the neuroprotective mechanisms activated by hypoxic preconditioning. [Copyright &y& Elsevier]

Induction of endogenous antioxidants is one of the key molecular mechanisms of cell resistance to hypoxia/ischemia. The effect of severe hypoxia on the expression of cytosolic antioxidant thioredoxin-1 (Trx) in hippocampus and neocortex was studied in preconditioned and non-preconditioned rats. The preconditioning consisted of three trials of mild hypobaric hypoxia (360Torr, 2h) spaced at 24h. Twenty-four hours after the last trial rats were subjected to severe hypobaric hypoxia (180Torr, 3h). Trx expression was studied by immunocytochemistry. In hippocampus severe hypobaric hypoxia rapidly induced Trx expression, which remained elevated still at 24h. In neocortex the enhanced expression appeared only at 24h. The preconditioning significantly augmented severe hypoxia-induced Trx-immunoreactivity at 3h but not at 24h. These findings point out that Trx contributes to mechanisms of brain tolerance to hypobaric hypoxia, especially in early periods after the exposure. [Copyright &y& Elsevier]