HYPOTHALAMIC AND CORTICAL-NEURONS OF NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS ARE DIFFERENTLY AFFECTED BY STREPTOZOTOCIN DIABETES

Diabetic encephalopathy is a relatively frequent late complication in human and experimental diabetes mellitus. Although it is generally assumed that microangiopathy plays a major role in its pathogenesis, many aspects of the latter are still poorly understood. The detect possible correlations between vascular and cellular changes, we examined in normotensive and spontaneously hypertensive streptozotocin diabetic rats the neurons of hypothalamic and cortical regions in which the capillary basement membrane thickness had been known from a previous study. Arcuate and ventromedial nucleus neurons of normotensive diabetic rats compared to those of corresponding controls showed a reduced cytoplasmic area after 4 but not after 8 months of experiment. No difference was found between hypertensive control and diabetic rats after eight 4 or 8 months of experiment. After the 8th month cortical neurons of normotensive controls were smaller in an occipital than in a frontal region and within the same region in the following layer order: deep < superficial < intermediate. Neurons of hypertensive controls behaved comparably yet were generally smaller than those of normotensive controls in each corresponding region. Compared to those of control, cortical neurons of normotensive diabetic rats were smaller in superficial and deep layers of both regions and in the intermediate layer of the frontal region. Hypertension appeared to antagonize diabetes. Despite an arcuate nucleus microangiopathy found in rats from both strains after 4 and 8 months of diabetes, neuronal changes were seen only in normotensive animals after 4 months. In the intermediate cortical layer, where microangiopathy was most marked after 8 months of experiment, neurons were not or only slightly reduced in size. Further, hypertension, which aggravated microangiopraphy in both cortical regions, antagonized diabetes-induced neuronal changes. In conclusion, it appears rather unlikely that microangiopathy plays a major pathogenic role in diabetic encephalopathy.