RESUMEN
Using immunohistochemical method, it was demonstrated that neurons of the cerebral cortex have the capacity to express hypoxia-inducible factor-1 alpha (HIF-1α) in normoxia. Intensity of this process is different for rats having unequal tolerance to hypoxia. Basal HIF-1α expression in neurons of rats with low-resistance (LR) to hypoxia is higher compared to rats with high-resistance (HR). Bilateral photochemically induced focal ischemic insult in the rat prefrontal cortex completely suppressed HIF-1α neuronal expression the in the ischemic zone and only partially--in the area of the penumbra. Neuronal injury was more pronounced in cortex of LR rats compared to HR rats. These findings suggest that functional significance of HIF-1α is greater in neurons of the cerebral cortex of LR rats compared to HR rats.
Asunto(s)
Isquemia Encefálica/metabolismo , Subunidad alfa del Factor 1 Inducible por Hipoxia/metabolismo , Hipoxia/metabolismo , Neocórtex/metabolismo , Corteza Prefrontal/metabolismo , Accidente Cerebrovascular/metabolismo , Animales , Hipoxia/fisiopatología , Subunidad alfa del Factor 1 Inducible por Hipoxia/genética , Neocórtex/patología , Neuronas/metabolismo , Especificidad de Órganos , Corteza Prefrontal/patología , RatasRESUMEN
Using quantitative immunohistochemistry, changes in the expression of the BDNF (Brain-Derived Neurotrophic Factor) were studied in the hippocampus and neocortex of 24 male Wistar rats during the development of post-stress-related anxiety state in the experimental model of posttraumatic stress disorder, and its correction by hypoxic postconditioning (PC). For the induction of anxiety state, combined severe psychoemotional stress was applied (immobilization, forced swimming, ether stress followed 7 days later by repeated immobilization - restress). Correction of the anxiety state was achieved by application of hypoxic PC, which included three sessions of mild hypobaric hypoxia (360 mm Hg, 2 h, daily). The formation of the anxiety pathology was accompanied by a significant reduction in the expression of immunoreactive BDNF in dorsal (CA1) and ventral (dentate gyrus) hippocampus and neocortex, while hypoxic PC resulted in partial (hippocampus) or complete (neocortex) restoration of BDNF expression. The results indicate that the neurotrophic factors, and BDNF in particular, seem to play an important role in the pathogenesis of the anxiety-depressive disorders as well as in mechanisms of proadaptive and neuroprotective effects of hypoxic PC.