The role of C-Fos protein, somatostatin and neuropeptide Y in the pathogenesis of ischemic brain injuries based on animal model of cerebral ischemia.

The aim of this study was to define all the areas of changes in expression of nuclear c-Fos protein (c-Fos), cytoplasmic somatostatin (SS) and neuropeptide Y (NPY) in rat brain during experimental ischemia. Using the immunohistochemical method, brain mapping (based on the atlas by Paxinos & Watson) of immunoreactivity for c-Fos, SS and NPY in 39 rats, was studied in telencephalon, diencephalon and midbrain after resistant and transitory ischemia. The first experimental group (R group) was exposed to resistant ischemia by occlusion (10 minutes) of four vessels according to the Pulsinelli method. The second group was first exposed to transitory (4 minutes) ischemia (preconditioning) and, after 72 hours, to total ischemia as in the R group. There was a statistical difference between the R and T group in the c-Fos reaction, especially in the parietofrontal cortex, anterior amygdaloid area, claustrum, reuniens nucleus and suprachiasmatic nucleus. The dominant immunohistochemical reactivity was found for c-Fos protein, and the most reactive in terms of co-localization of c-Fos with SS and NPY was periventricular area of hypothalamus. The mapping showed that both, phylogenetically new as well as phylogenetically older brain structures reacted immunohistochemically. The results of our study, regarding the impact of preconditioning with a short period of ischemia on c-Fos activity and co-localization of c-Fos with SS and NPY immunoreactivity, showed the need for future studies of brain neuropeptides related to regional and time effects, and indicated brain structures which may require pharmacological targeting to achieve neuroprotective level of proto-oncogene activity in populations at risk.