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Control Retinas (control + retina)
Selected AbstractsDark-rearing-induced reduction of GABA and GAD and prevention of the effect by BDNF in the mouse retinaEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2006Eun-Jin Lee Abstract Gamma-aminobutyric acid (GABA) is an important retinal neurotransmitter. We studied the expression of GABA, glutamate decarboxylase 65 (GAD65) and GAD67 by immunocytochemistry and Western blot, in the retinas of control and dark-reared C57BL/6J black mice. This study asked three questions. First, is visual input necessary for the normal expression of GABA, GAD65 and GAD67? Second, can the retina recover from the effects of dark-rearing if returned to a normal light,dark cycle? Third, does BDNF prevent the influence of dark-rearing on the expression of GABA and GAD? At postnatal day 10 (P10), before eye opening, GABA immunoreactivity was present in the ganglion cell layer (GCL), in the innermost rows of the inner nuclear layer (INL) and throughout the inner plexiform layer (IPL) of control and dark-reared retinas. In P30 control retinas, GABA immunoreactivity showed similar patterns to those at P10. However, in P30 dark-reared retinas, the density of GABA-immunoreactive cells was lower in both the INL and GCL than in control retinas. In addition, visual deprivation retarded GABA immunoreactivity in the IPL. Western blot analysis showed corresponding differences in the levels of GAD65 but not of GAD67 expression between control and dark-rearing conditions. In our study, dark-rearing effects were reversed when the mice were put in normal cyclic light,dark conditions for 2 weeks. Moreover, dark-reared retinas treated with BDNF showed normal expression of both GABA and GAD65. Our data indicate that normal expression of GABA and GAD65 is dependent on visual input. Furthermore, the data suggest that BDNF controls this dependence. [source] Pigment epithelium-derived factor supports normal Müller cell development and glutamine synthetase expression after removal of the retinal pigment epitheliumGLIA, Issue 1 2001Monica M. Jablonski Abstract In conditions in which the retinal pigment epithelium (RPE) is dystrophic, carries a genetic mutation, or is removed physically, Müller cells undergo degenerative changes that contribute to the retinal pathology. We previously demonstrated that pigment epithelium-derived factor (PEDF), a glycoprotein secreted by the RPE cells with neuroprotective and differentiation properties, protects against photoreceptor degeneration induced by RPE removal. The purpose of the present study was to analyze the putative gliosupportive activity of PEDF on Müller cells of RPE-deprived retinas and assess whether protection of Müller cells was correlated with improved photoreceptor outer segment assembly. Eyes were dissected from Xenopus laevis tadpoles, and the RPE was removed before culturing in medium containing purified PEDF, PEDF plus anti-PEDF, or medium alone. Control eyes matured with an adherent RPE or in medium containing PEDF plus nonimmune serum. Müller cell ultrastructure was examined. Glial fibrillary acidic protein (GFAP) and glutamine synthetase were localized immunocytochemically, and the corresponding protein levels were quantified. In control retinas, Müller cells were structurally intact and formed adherens junctions with neighboring photoreceptors. In addition, they did not express GFAP, whereas glutamine synthetase expression was high. RPE removal dramatically altered the ultrastructure and biosynthetic activity of Müller cells; Müller cells failed to form adherens junctions with photoreceptors and glutamine synthetase expression was suppressed. PEDF prevented the degenerative glial response; Müller cells were ultrastructurally normal and formed junctional complexes with photoreceptors. PEDF also preserved the expression of glutamine synthetase at near-normal levels. The morphogenetic effects of PEDF were blocked by the anti-PEDF antibody. Our study documents the glioprotective effects of PEDF and suggests that maintenance of the proper Müller cell ultrastructure and expression of glutamine synthetase may be necessary to support the proper assembly of photoreceptor outer segments. GLIA 35:14,25, 2001. © 2001 Wiley-Liss, Inc. [source] Activation of immature microglia in response to stab wound in embryonic quail retinaTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 1 2005Ana M. Sánchez-López Abstract Activation of mature (ramified) microglia in response to injury in the adult central nervous system (CNS) is well documented. However, the response of immature (ameboid) microglia to injury in the developing CNS has received little attention. In this study, a stab wound was made in embryonic quail retinas at incubation days 7 and 9, and the response of retinal microglial cells was analyzed at different times between days 1 and 37 postinjury. The appearance of microglial cells within the wound occurred at the same time as the arrival of the first migrating ameboid microglial cells at an equivalent area in control retinas. Therefore, no specific attraction of microglia toward the wound was observed. Microglial cells in the wound had phenotypic features similar to those of activated microglia in the adult CNS. Thus, their shape was more compact compared with microglial cells outside the wound, expression of the molecule recognized by the QH1 antibody was up-regulated, and their lysosomal compartment was markedly increased. Transitional forms between normal ameboid and activated-like microglial cells were seen at the wound edge, supporting the view that ameboid microglia become activated when they contact the wound during the normal course of their migration in the retina. The microglial reaction was maintained within the wound at 37 days postinjury. In addition to the stab wound, secondary damage areas were found in experimental retinas. Activated cells could still be observed in these areas at 37 days postinjury. J. Comp. Neurol. 492:20,33, 2005. © 2005 Wiley-Liss, Inc. [source] The role of CTGF in the diabetic rat retina and its relationship with VEGF and TGF-,2, elucidated by treatment with CTGFsiRNAACTA OPHTHALMOLOGICA, Issue 6 2010Hongwei Yang Acta Ophthalmol. 2010: 88: 652,659 Abstract. Purpose:, The critical association of connective tissue growth factor (CTGF) with diabetic retinopathy (DR) remains to be clarified. We detected alterations in the gene and protein expression of CTGF and related cytokines, including vascular endothelial growth factor (VEGF) and transforming growth factor-,2 (TGF-,2), and their response to small interfering RNA (siRNA) targeting the CTGF (CTGFsiRNA) in the retina of diabetic rats. The relationships between CTGF, VEGF and TGF-,2 levels, as well as the degree of apoptosis in the diabetic retina, were also investigated. Methods:, Diabetes was induced in rats by the ,-cell toxin streptozotocin (STZ). Retinas were obtained from control and diabetic rats and similar animals treated with CTGFsiRNA by intravitreal injection. mRNA level and protein expression of CTGF, VEGF and TGF-,2 were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, and located by immunohistochemistry. Retinal apoptosis was detected by TUNEL staining. Results:, The levels of CTGF, VEGF and TGF-,2 and the number of TUNEL-positive nuclei were significantly higher in diabetic retinas than in control retinas (p < 0.01). The level of CTGF rose at 8 weeks, earlier than levels of VEGF and TGF-,2, which rose at 12 weeks after the onset of diabetes. The difference was significant (p < 0.05). siRNA-mediated inhibition of CTGF mRNA inhibited retinal VEGF and TGF-,2 and also resulted in a significant decrease in apoptosis. Significant correlations were found between CTGF and VEGF (p = 0.009), CTGF and TGF-,2 (p = 0.01), and apoptosis and these three cytokines (p < 0.01) in the rat retina early in diabetes. Conclusions:, These results suggest that the diabetes-mediated increase in CTGF upregulates VEGF and TGF-,2 expression and induces apoptosis in the retina. This elevation may be inhibited by treatment with CTGFsiRNA. Connective tissue growth factor may serve as a potential target for the prevention and treatment of DR. [source] | ||||||||||