Analysis of diabetes-related cerebellar changes in streptozotocin-induced diabetic rats

Abstract

IntroductionDiabetes mellitus (DM) comprises a group of common metabolic disorders that share the phenotype of hyperglycemia, leading to damage in a number of tissues. Retinas, neurons, and kidneys are especially affected (1). Acute and chronic complications may occur. Chronic complications are divided into vascular and nonvascular complications. Vascular complications are subdivided into microvascular (retinopathy, neuropathy, nephropathy) and macrovascular complications (coronary artery disease, peripheral vascular disease, cerebrovascular disease). Oxidative stress, glycosylation, and protein kinase-C activation are shown in all tissues affected by microvascular complications (1-3). Glucose homeostasis in humans is important for the functioning of the nervous system. The brain is an insulin-sensitive organ with widespread and selective expression of the insulin receptor in the olfactory bulb, hypothalamus, hippocampus, amygdala, cerebral cortex, and cerebellum; hypoglycemia and hyperglycemia affect the central and peripheral nervous system, leading to severe dysfunction (1-3).Chronic hyperglycemia is associated with functional and structural blood-brain barrier (BBB) changes in cerebral microvessels (3). Diabetes is also associated with gradually developing end-organ damage in the central nervous system, known as diabetic encephalopathy, characterized by impairment of cognitive functions and electrophysiological changes. Chronically increased intracellular glucose concentration leads to functional, structural, and neurodegenerative changes (1).Studies performing biochemical and structural analysis of the brain relevant to the ultrastructural features of diabetes are limited, and the number of cerebellar studies are even more so. This study aimed to analyze the structural and ultrastructural cerebellar changes in streptozotocin (STZ)-induced diabetic rats (2,4-6). Materials and methodsTwenty male adult Sprague Dawley rats weighing 200-220 g were obtained from the Experimental Medicine Research Institute (DETAE). Fourteen of these animals were selected as the diabetic group, and after 12 h of Background/aim: Diabetic peripheral neuropathy has been extensively studied and reported, but the number of studies that have investigated diabetes-related changes in the central nervous system are limited, with even fewer studies on the cerebellum. The aim of this experimental study was to perform a histologic analysis of the diabetes-related changes in the cerebellums of diabetic rats.Materials and methods: Twenty Sprague Dawley rats weighing between 200 and 220 g were included in the study. Diabetes was induced in 14 of these rats by a single intraperitoneal injection of 65 mg/kg streptozotocin dissolved in saline, while 6 animals constituted the control group. The induction of diabetes was confirmed by measuring the blood glucose levels in the tail blood with a glucometer. Levels equal to or above 200 mg/dL were considered diabetic. Induction of diabetes failed in 3 animals, who were then excluded from the study.Results...

The Effect of Induced Diabetes Mellitus on the Cerebellar Cortex of Adult Male Rat and the Possible Protective Role of Oxymatrine: A Histological, Immunohistochemical and Biochemical Study

“…Our electron microscopic results revealed further ultrastructural changes as irregularity and splitting of myelin sheaths in the molecular layer. This result came in agreement with (Ozdemir et al, 2016) who demonstrated separations and breaks of myelin sheaths in cerebellar cortex of diabetic rats. These alterations of the myelin sheaths were demonstrated to occur as a part of brain neuropathy that develops in different brain regions secondary to DM.…”

Influence of green tea on alcohol aggravated neurodegeneration of cortex, cerebellum and hippocampus of STZ-induced diabetic rats

“…Anomalies in brain structure have been linked to diabetes on multiple occasions. Neuronal degeneration and injuries in STZ-induced diabetes have been consistently shown in various regions of the brain [ 52 ]. Our present data support these earlier studies, and in addition, we noted that severe congestion, necrotic and degenerative changes in cortex, cerebellum and hippocampus, following alcohol administration to diabetic rats.…”

Gastrodin Ameliorates Motor Learning Deficits Through Preserving Cerebellar Long-Term Depression Pathways in Diabetic Rats

“…More importantly, we have shown that gastrodin could protect Purkinje cells and preserve LTD pathways, which may account for the improvement of motor learning. Although many studies have reported diabetes-induced cerebellar damage and motor function deficiency (Hernandez-Fonseca et al, 2009; Nagayach et al, 2014; OzdemIr et al, 2016), the role of cerebellar LTD pathways in diabetes-induced cognitive dysfunction remains elusive. We have provided morphological and biochemical evidence to suggest that NMDAR-dependent and AMPAR-dependent LTD in the cerebellum was compromised due to Purkinje cell injury.…”