Progressive cortical atrophy after forebrain ischemia in diabetic rats

The morphological changes in the brain of diabetic rats were examined up to 8 weeks after transient forebrain ischemia produced by transient occlusion of both carotid arteries. Using histochemistry, we also examined the exten t and rate of development of atrophic changes in the brain, appearance of a strocytes, activated microglia, and glucose transporter 1 (GLUT1) in strept ozotocin-treated rat brains after forebrain ischemia. Atrophic changes appe ared in the hippocampus in both non-diabetic- and diabetic-ischemic groups 4 weeks after ischemia. In diabetic-ischemic rats, the atrophic changes wer e more severe and progressed more rapidly in the hippocampus, and were also observed in the frontal, temporal and parietal cortices, but not in any co rtical areas of the non-diabetic-ischemic rats and non-ischemic-diabetic ra ts. We observed reduced density of GLUT1 in all corticaI regions and hippoc ampus in ischemic-diabetic rats at 4-8 weeks, when the number of activated microglias and astroglias increased in all cortical regions. Although sever e atrophic changes were observed in the gray matter, no serious injury was noted in the white matter in the diabetic-ischemic group. Our results indic ate that brain ischemia in the presence of diabetes causes more severe late -onset damage culminating in brain atrophy, compared with non-diabetics. (C ) 2001 Elsevier Science Ireland Ltd and the Japan Neuroscience Society. All rights reserved.