Impaired visual evoked potential and primary axonopathy of the optic nerve in the diabetic BB/W-rat

Sima, Anders A. F.; Zhang, W. X.; Cherian, Paul; Chakrabarti, Subrata

doi:10.1007/bf00400249

Cited by 67 publications

(44 citation statements)

References 38 publications

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“…Optic nerves of spontaneously diabetic BB/W rats have significantly smaller nerve fiber with increased atrophy and dystrophic changes in the nerve fiber layer of the retina. The percentage of area occupied by glial cells was increased and the axonal component wasdecreased significantly (Sima et al, 1992). The irregularity was commonly found in the glucosamine-infused rats, and results were comparable to those of streptozotocin-induced diabetic model (Ino-ue et al, 1991(Ino-ue et al, , 1998a(Ino-ue et al, , 1998bWalker et al, 1999).…”

Section: Discussionsupporting

confidence: 66%

Dysfunction of Retinal Cell and Optic Nerve by Continuous Cerebroventricular Infusion of Glucosamine

Jang¹,

Han

Jun

et al. 2009

Biomolecules and Therapeutics

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-We have investigated the effect of glucosamine on the retinal cells after continuous infusion into cerebroventricle by using osmotic minipump to avoid peripheral effect. Continuous intracerebroventricular (i.c.v) infusion of glucosamine with the rate of 0.1 μmol/10 μl/hr for 7 days resulted in morphological changes of the optic nerve in electron microscopic level as well as morphological changes of the retina in light microscopic level. Retinal sections were immunostained for the detection of morphological changes of astrocytes. GFAP immunoreactivity appeared not only in the Muller cells but also many of the radial processes of Muller cells. The optic nerve showed deformed axon and slight lamellar separation of myelin sheath after continuous infusion of glucosamine in observing with electron microscope. Interestingly, vacuoles were observed in deformed axons and retinal layers were folded and detached. These results suggested that glucosamine plays a role in induction of morphological dysfunction in retina and optic nerves.

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Section: Discussionsupporting

confidence: 66%

Dysfunction of Retinal Cell and Optic Nerve by Continuous Cerebroventricular Infusion of Glucosamine

Jang¹,

Han

Jun

et al. 2009

Biomolecules and Therapeutics

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“…The latencies of auditory and visual potentials were found to be prolonged in streptozotocin-induced diabetic rats [118,119] and type 1 BB/Wor diabetic rats [120,121] in relation to controls. Likewise, in hippocampal slices from streptozotocininduced diabetic rats, LTP is impaired, whereas longterm depression (LTD) is enhanced when compared with control rats [90,91,122,123].…”

Section: Insulin-sensitive Diabetesmentioning

confidence: 99%

Metabolic Alterations Associated to Brain Dysfunction in Diabetes

Duarte¹

2014

aging dis

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From epidemiological studies it is known that diabetes patients display increased risk of developing dementia. Moreover, cognitive impairment and Alzheimer's disease (AD) are also accompanied by impaired glucose homeostasis and insulin signalling. Although there is plenty of evidence for a connection between insulin-resistant diabetes and AD, definitive linking mechanisms remain elusive. Cerebrovascular complications of diabetes, alterations in glucose homeostasis and insulin signalling, as well as recurrent hypoglycaemia are the factors that most likely affect brain function and structure. While difficult to study in patients, the mechanisms by which diabetes leads to brain dysfunction have been investigated in experimental models that display phenotypes of the disease. The present article reviews the impact of diabetes and AD on brain structure and function, and discusses recent findings from translational studies in animal models that link insulin resistance to metabolic alterations that underlie brain dysfunction. Such modifications of brain metabolism are likely to occur at early stages of neurodegeneration and impact regional neurochemical profiles and constitute non-invasive biomarkers detectable by magnetic resonance spectroscopy (MRS).Key words: Neurodegeneration, Diabetes, Alzheimer's disease, Insulin, Metabolism Diabetes mellitus can be defined as a chronic metabolic disorder characterized by hyperglycaemia, resulting from inappropriate insulin secretion and/or action [1]. The vast majority of the diabetes cases are included in two main categories, classified according to the underlying cause, which are type 1 diabetes (T1D) or insulindependent diabetes, generally caused by an autoimmune reaction to antigens of pancreatic β-cells, leading to impaired insulin production, and type 2 diabetes (T2D) or insulin-resistant diabetes, characterised by inefficiency of insulin action. While T1D is mainly observed in children and adolescents, T2D is more common among adults, accounting for more than 90% of the diabetes cases worldwide. The prevalence of diabetes and impaired glucose tolerance achieved now epidemic proportions, respectively at 6.9% and 8.3% of the world population, and predicted to raise to 8. 0% and 10.1% in 2035 [2]. Moreover, diabetes is nowadays a leading cause of death accounting for 8.4% of global mortality in people aged between 20 and 79 years [2]. The main contributor for the high prevalence of diabetes is the rise of obesity, related to the combination of ample food availability and a sedentary lifestyle, contrasting to less abundant food supplies and higher physical activity observed until a century ago.Diabetes is associated with the occurrence of well described microvascular complications that affect different organs, leading most commonly to retinopathy, nephropathy and peripheral neuropathy, which development is dependent on the duration of the disease and glycaemia control [3]. When the control of the disorder allowed patients to live longer and without these Volume 6, N...

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“…There is increasing evidence that retinal ganglion cell (RGC) death occurs early in diabetes, and that neurodegeneration is an important component of diabetic retinopathy (Barber et al, 1998;Abu-El-Asrar et al, 2004). Several studies have established that there are significantly more neuronal cells undergoing apoptosis, particularly in the ganglion cell layer, in retinas of diabetic rats than in those of control rats (Sima et al, 1992;Barber et al, 1998;Asnaghi et al, 2003). When diabetes exerts its primary damage on vascular cells and increases permeability or vascular occlusion, neuronal and glial cell integrity is compromised by the entry of circulating macrophages, antibodies, inflammatory cytokines, and excitotoxic amino acids into the retina (Antonetti et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Cilostazol on Retinal Ganglion Cell Damage in Diabetic Rats

Jung

Kim

2013

J Pharmacol Exp Ther

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Neurodegeneration is an important component of diabetic retinopathy, with increasing evidence that retinal ganglion cell (RGC) death occurs early in diabetes. We investigated the effects of cilostazol, which has been widely used to manage diabetic complications, on retinal ganglion cell death in the diabetic retina. Four-week-old Otsuka Long-Evans Tokushima fatty (OLETF) rats and Long-Evans Tokushima Otsuka (LETO) rats as matched nondiabetic controls were treated with daily oral cilostazol at 30 mg/kg or 0.9% saline solution. In OLETF rats at the age of 40 weeks, glial fibrillary acidic protein (GFAP) immunofluorescence staining was upregulated in vertical sections, and showed a more ramified pattern in whole-mount retinas compared with that in LETO rats. Vascular endothelial growth factor (VEGF) expression was limited to the ganglion cell layer in LETO rats, but extended into the outer plexiform layer in OLETF rats. Immunofluorescence staining and Western blotting demonstrated that cilostazol treatment reduced GFAP and VEGF expression in the retinas of OLETF rats. Terminal deoxynucleotidyl transferase-mediated terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine nick-end labeling (TUNEL) staining revealed an increase in the RGC layer in OLETF compared with LETO rats (P , 0.05), and cilostazol treatment reduced the number of TUNEL-positive cells in OLETF rats (P , 0.05). Relieving retinal ischemia by systemic cilostazol treatment had a noticeable protective effect on RGCs in diabetic rats. Cilostazol treatment may be useful for the management of diabetic retinal vascular dysfunction and neuronal degeneration.

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Impaired visual evoked potential and primary axonopathy of the optic nerve in the diabetic BB/W-rat

Cited by 67 publications

References 38 publications

Dysfunction of Retinal Cell and Optic Nerve by Continuous Cerebroventricular Infusion of Glucosamine

Dysfunction of Retinal Cell and Optic Nerve by Continuous Cerebroventricular Infusion of Glucosamine

Metabolic Alterations Associated to Brain Dysfunction in Diabetes

Neuroprotective Effects of Cilostazol on Retinal Ganglion Cell Damage in Diabetic Rats

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