Abstract
Hypobaric hypoxia (HH) is known to provoke neurological disorders and damage the cognitive function. Nitric oxide (NO), synthesized by NO synthases (NOS), plays some key functions in the striatum, a basal ganglion of the brain. Therefore, the appropriate activity and expression of NOS-expressing cells may be a key point in the control of the striatal function. This work examines NOS isoforms (neuronal, endothelial, and inducible) expression and activity, and NO production in the hypoxic striatum during the subsequent reoxygenation period. Wistar rats were submitted for 20 min to acute HH, which simulates an altitude of 8100 m. After the hypoxia period, animals were kept under normobaric normoxic conditions for different reoxygenation times (0 h, 24 h, and 5 days). In situ NOS activity (NADPH-diaphorase), NOS expression (RT-PCR and image quantification after inmunohistochemistry), and NO production (indirectly quantified as nitrate/nitrite and S-nitrose compounds, NOx) were evaluated in the striatum of adult rats. NOS isoforms mRNA did not modify the expression in any hypoxic group vs. control. However, quantification of immunoreaction revealed a decrease in eNOS and nNOS after hypoxia. NOx levels as well as NADPH-diaphorase activity, detected in some striatal neurons, significantly diminished throughout the reoxygenation period. These results reflect that NOS isoforms protein expression, in situ NOS activity, and NO concentration decreased after acute HH/reoxygenation in rat striatum, proposing that the NO pathway is altered during such situations in this basal ganglion of the brain.
Published Version
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