Phases of intermediate filament composition in Bergmann glia following cerebellar injury in adult rat.

In contrast to other astroglial populations, Bergmann glia (BG) form a strictly arranged system where each cell contacts the pia, with an architecture and function resembling that of immature radial glia. As a consequence, a post-lesion glial reaction is expected to differ from that observed in other parts of the brain. The present study describes the characteristic phases of intermediate filament protein formation during the different stages of BG response following injury and compares them with reactive glial patterns of other brain areas and patterns of glial development. The progress of Bergmann glial repair shares similar features with glial development. Following injury, BG developed nestin immunopositivity; then, colocalization of nestin and GFAP was observed. Finally, exclusively GFAP-immunopositive BG were restituted, denser, and thicker than before. The changes of intermediate filament composition appeared at first at the proximal and distal ends of BG fibers, i.e., at the perikaryal "root" and in the pial endfeet. No astrocytic invasion was present in the molecular layer, nor any distinct rearrangement of BG. These results demonstrate the role of the resident glia in glial reactions and refer to the priority of gliomeningeal connections.

Dynamics of dystroglycan complex proteins and laminin changes due to angiogenesis in rat cerebral hypoperfusion.

Permanent bilateral carotid occlusion is a well known cerebral hypoperfusion model in rats. The aim of our study was to investigate the different stages of vascular reaction by detecting changes in the extracellular martix proteins and to examine their relationship to angiogenesis after occlusion. Experiments were performed on adult male rats. Brain samples were investigated from day 1 to day 30 post-surgery. Immunohistochemical analysis was performed on the whole hippocampus and on the adjacent cortex in order to investigate extracellular martix proteins, such as the markers of dystroglycan complex (ß-dystroglycan, α-dystrobrevin and utrophin) and a marker of basal lamina (laminin). The levels of the proteins were estimated by western blot analysis. Vascular density as well as blood-brain barrier permeability were studied on brain slices from the same regions. Our results showed altered laminin and ß-dystroglycan immunoreactivity beginning 2 days after the onset of occlusion followed by an increased utrophin immunoreactivity without blood-brain barrier disruption 5 days later. By day 30 of hypoperfusion, when increased vascular density was detected, all changes returned to baseline levels. Western blot analysis showed significant differences in ß-dystroglycan and utrophin expression. Our results indicate that the different stages of neovascularisation resulting from cerebral hypoperfusion can be well defined by the markers laminin, ß-dystroglycan, and utrophin and that these markers are more likely to correlate with glio-vascular decoupling than does altered blood-brain barrier function.