title: [Dynamics of initial manifestations of experimental diabetic encephalopathy].
abstract: We established that alloxan diabetes leads to early development of diabetic encephalopathy on the background of marked hyperglycemia. Initial manifestations of experimental diabetic encephalopathy are based on fast progressing loss of neurons and glial cells in the structures of primary somatosensory cortex (field Par 1) and hippocampus (field CAl) between 4th and 17th day after alloxan administration. This is accompanied by accumulation oflipofuscin in neocortex neurons. Manifestations of diabetic encephalopathy on diencephalic level is registered only 10 days after alloxan administration, specifically in paraventricular nucleus where decrease in the number of neurocytes is observed between 10th and 17th day after diabetes induction. Initial manifestations of experimental diabetic encephalopathy correspond to progressing inhibition of orientation and exploratory behavior in animals and decrease of their capacity for conditioning.
authors.forename: I A
authors.initials: IA
authors.lastname: Volchegorskiĭ
authors.forename: L M
authors.initials: LM
authors.lastname: Rassokhina
authors.forename: I Iu
authors.initials: IIu
authors.lastname: Miroshnichenko
mesh_terms: D000496:Alloxan / Q000633:toxicity; D000818:Animals; D001522:Behavior, Animal; D001928:Brain Diseases, Metabolic / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology*; D001931:Brain Mapping; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000150:complications / Q000503:physiopathology; D005260:Female; D006624:Hippocampus / Q000503:physiopathology*; D006801:Humans; D006943:Hyperglycemia / Q000150:complications / Q000503:physiopathology*; D008062:Lipofuscin / Q000378:metabolism; D008297:Male; D019579:Neocortex / Q000503:physiopathology*; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D051381:Rats
chemical_list: D008062:Lipofuscin; D000496:Alloxan