Impairment of hippocampal neurogenesis in streptozotocin-treated diabetic rats

Abstract

Objectives – Adult neurogenesis in dentate gyrus (DG) is an evolutionarily preserved trait in most mammals examined thus far. Neuronal proliferation and subsequent integration of new neurons into the hippocampal circuit are regulated processes that can have profound effects on an animal’s behaviour. A streptozotocin model of type I diabetes, characterized by low insulin and high plasma glucose levels, affects not only body’s overall metabolism but also brain activity. Materials and methods – Neurogenesis was measured within the DG of the hippocampus using immunohistochemical markers Ki67, Doublecortin, Calbindin (CaBP) and bromodeoxyuridine (BrdU). Results – Cell proliferation, measured with the endogenous marker Ki67, was reduced by 45%, and cell survival, measured with BrdU, was reduced by 64% of the control. Combined effects on proliferation and survival produced dramatically lower neuronal production. Among the surviving cells only 33% matured normally as judged by the co‐labelling of BrdU and CaBP. Conclusion – Such a reduction lowered the number of surviving cells with neuronal phenotype by over 80% of the control values and this is expected to cause a significant functional impairment of learning and memory in diabetic animals. These results may shed light on causes of diabetic neuropathology and provide an explanation for the memory deficiencies seen in some diabetic patients.

Effect of environmental enrichment exposure on neuronal morphology of streptozotocin-induced diabetic and stressed rat hippocampus

“…Increasing evidence points toward an association between diabetes mellitus and deficit in learning and memory. [5,7] Findings of the research and evidences in the literature revealed reduced neurogenesis in the dentate gyrus of diabetic hippocampus [8] and decreased dendritic arborization. [9] Stress exposure triggered fear memory and anxiety, and decreased the hippocampal-dependent memory performance in mice.…”

Article Withdrawal Statement

“…administration of STZ (0.1 ml volume) for five consecutive days at a dose of 50 mg STZ/kg body weight. Body weight and blood glucose levels (determined from tail blood by glucometer) were monitored once every two days during the STZ treatment week and thereafter once weekly for the rest of the study [13][14][15]. OA treatment was performed by subcutaneously implanted ALZET Micro-osmotic pumps (Model 1004, Alzet, Cupertino, CA) at a rate of 3.5 pM/kg/min.…”

Environmental enrichment exposure restrains the neuronal damage induced by diabetes and stress in the motor cortex of rat brain

“…The drug STZ induction into the body causes decreased insulin discharge by destructing the b-cells of the pancreas in the islets of Langerhans. With the help of minute quantity of left over insulin in the pancreas animal can survive for several months but, the disease is fatal without any treatment (Zhang et al, 2008). Highly signifi cant nissl body damage was seen in the motor cortex neurons of rats in DI+S group when compared to the NC rats.…”