Objective(s): The alteration of glucose transporters is closely related with the pathogenesis of brain edema.We compared neuronal damage/death in the hippocampus between adult and young gerbils following transient cerebral ischemia/reperfusion and changes of glucose transporter-1(GLUT-1)-immunoreactive microvessels in their ischemic hippocampal CA1 region.Materials and Methods: Transient cerebral ischemia was developed by 5-min occlusion of both common carotid arteries.Neuronal damage was examined by cresyl violet staining, NeuN immunohistochemistry and Fluoro-Jade B histofluorescence staining and changes in GLUT-1 expression was carried out by immunohistochemistry.
Results: About 90% of pyramidal neurons only in the adult CA1 region were home damaged after ischemia/reperfusion; in the young, about 53 % of pyramidal neurons were damaged from 7 days after ischemia/reperfusion.The density of GLUT-1-immunoreactive microvessels was significantly higher in the young sham-group than that in the adult sham-group.In the ischemia-operated-groups, the density of GLUT-1-immunoreactive microvessels was significantly decreased in the adult and young at 1 and 4 days post-ischemia, respectively, thereafter, the density of GLUT-1-immunoreactive microvessels was gradually increased in both groups after ischemia/reperfusion.Conclusion: CA1 pyramidal neurons of the young gerbil were damaged much later Dice than that in the adult and that GLUT-1-immunoreactive microvessels were significantly decreased later in the young.
These data indicate that GLUT-1 might differently contribute to neuronal damage according to age after ischemic insults.