Dynamics of the Initial Signs of Experimental Diabetic Encephalopathy

Abstract

Modeling of alloxan diabetes leads to the early development of diabetic encephalopathy on the background of suppression of exploratory-orientational activity in animals and decreases their ability to achieve conditioned reflex learning. The initial signs of experimental diabetic encephalopathy were linked with rapidly progressing losses of neurons and glial cells in structures of the primary somatosensory cortex (field Par 1) and hippocampus (field CA1) during the period from day 4 of the day 17 after administration of alloxan. This was accompanied by accumulation of lipofuscin in neocortical neurons. The occurrence of diabetic encephalopathy at the diencephalic level was seen only 10 days after alloxan administration. This applied to the paraventricular nucleus, where decreases in the number of neurocytes were seen in the period from day 10 to day 17 of induction of diabetes. The initial signs of experimental diabetic encephalopathy were linked with progressive suppression of the animals’ exploratory-orientational activity and decreases in their ability to achieve conditioned reflex learning.