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Retinal Neurodegeneration (retinal + neurodegeneration)
Selected AbstractsRetinal neurodegeneration: early pathology in diabetesCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 1 2000Erich Lieth ABSTRACT Normal vision depends on the normal function of retinal neurons, so vision loss in diabetes must ultimately be explained in terms of altered neuronal function. However, to date relatively little attention has been paid to the impact of diabetes on the neural retina. Instead, the focus of most research has been primarily on retinal vascular changes, with the assumption that they cause altered neuronal function and consequently vision loss. An increasing body of evidence suggests that alterations in neuronal function and viability may contribute to the pathogenic mechanisms of diabetic retinopathy beginning shortly after the onset of diabetes. This view arises from neurophysiological, psychometric, histopathological and biochemical observations in humans and experimental animals. The collective evidence from past and recent studies supports the hypothesis that neurodegeneration, together with functional changes in the vasculature, is an important component of diabetic retinopathy. The authors invite other investigators to include the neural retina as a component of their studies so that the pathogenesis of diabetic retinopathy can be understood more clearly. [source] Non-viral gene therapy for diabetic retinopathyDRUG DEVELOPMENT RESEARCH, Issue 11 2006*Article first published online: 9 FEB 200, Toshiyuki Oshitari Abstract Diabetic retinopathy results from vascular abnormalities, such as an increase in the permeability of retinal vessels, and retinal neurodegeneration, which are irreversible changes that occur early in the course of diabetic retinopathy. To block the vascular and neuronal complications associated with the development and progression of diabetic retinopathy, a reasonable strategy would be to prevent the increased vascular permeability and to block the neuronal cell death. The purpose of this review is to present the non-viral strategies being used to block the neurovascular abnormalities and neuronal cell death that are observed in the early stages of diabetic retinopathy in order to prevent the onset or the progression of the diabetic retinopathy. Some of the non-viral gene therapeutic techniques being used are electroporation of selected genes, injections of antisense oligonucleotides, and injections of small interference RNAs. The results obtained by these methods are discussed as is the potential of these therapeutic strategies to prevent the onset or the progression of the neurovascular abnormalities in diabetic retinopathy. Drug Dev. Res. 67:835,841, 2006. © 2007 Wiley-Liss, Inc. [source] Neuropeptide Y inhibits [Ca2+]i changes in rat retinal neurons through NPY Y1, Y4, and Y5 receptorsJOURNAL OF NEUROCHEMISTRY, Issue 5 2009Ana Rita Álvaro Abstract Neuropeptide Y (NPY) and NPY receptors are widely distributed in the CNS, including the retina, but the role of NPY in the retina is largely unknown. The aim of this study was to investigate whether NPY modulates intracellular calcium concentration ([Ca2+]i) changes in retinal neurons and identify the NPY receptors involved. As NPY decreased the [Ca2+]i amplitudes evoked by 30 mM KCl in only 50% of neurons analyzed, we divided them in two populations: NPY-non-responsive neurons (,2/,1 , 0.80) and NPY-responsive neurons (,2/,1 < 0.80), being the ,2/,1 the ratio between the amplitude of [Ca2+]i increase evoked by the second (,2) and the first (,1) stimuli of KCl. The NPY Y1/Y5, Y4, and Y5 receptor agonists (100 nM), but not the Y2 receptor agonist (300 nM), inhibited the [Ca2+]i increase induced by KCl. In addition, the inhibitory effect of NPY on evoked-[Ca2+]i changes was reduced in the presence of the Y1 or the Y5 receptor antagonists. In conclusion, NPY inhibits KCl-evoked [Ca2+]i increase in retinal neurons through the activation of NPY Y1, Y4, and Y5 receptors. This effect may be viewed as a potential neuroprotective mechanism of NPY against retinal neurodegeneration. [source] Low sensitivity of retina to AMPA-induced calcificationJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2003Noemí Andrés Abstract Glutamate is involved in most CNS neurodegenerative diseases. In particular, retinal diseases such as retinal ischemia, retinitis pigmentosa, and diabetic retinopathy are associated with an excessive synaptic concentration of this neurotransmitter. To gain more insight into retinal excitotoxicity, we carried out a dose,response study in adult rats using ,-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), a glutamate analogue. AMPA intraocular injections (between 0.27 and 10.8 nmol) caused no morphologic modification, but a 10.8 + 21 nmol double injection in a 10-day interval produced a lesion characterized by discrete neuronal loss, astroglial and microglial reactions, and calcium precipitation. Abundant calcium deposits similar to those present in rat and human brain excitotoxicity or hypoxia-ischemia neurodegeneration were detected by alizarin red staining within the retinal surface and the optic nerve. Glial reactivity, associated normally with astrocytes in the nerve fiber, was assessed in Müller cells. GABA immunoreactivity was detected not only in neuronal elements but also in Müller cells. In contrast to the high vulnerability of the brain to excitotoxin microinjection, AMPA-induced retinal neurodegeneration may provide a useful model of low central nervous system sensitivity to excitotoxicity. © 2003 Wiley-Liss, Inc. [source] | |||||||||||||