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Rat Eyes (rat + eye)
Selected Abstracts2223: Carbon monoxide as a mediator in the retinaACTA OPHTHALMOLOGICA, Issue 2010C BUCOLO Purpose Carbonic monoxide (CO) is organic gas ubiquitously synthesized in mammalian tissues by enzyme that has constitutive and inducible forms. This gas is produced as metabolic end-product in specific cell life phases, and may acts as atypical neuronal messenger. Evidence has recently accumulated suggesting that CO may be cytoprotective because its bioactions, including inhibition of apoptosis, platelet aggregation, complement activation, and inflammatory cytokine production. CO appears to be important to counteract the cytotoxicity caused by excessive production of reactive oxygen (ROS) and nitrogen (RNS) species. Methods In vitro and in vivo models. Results Induction of heme oxygenase (HO)-1 by hemin has been found to prevent retinal cell death after ischemia provoked by ocular hypertension in rats. The LPS-induced expression of pro-inflammatory cytokines, in rat eye, is also inhibited by CO. Interestingly, drugs active as inhibitors of iNOS block CO-induced increases in cGMP in the retina.Drugs inhibiting NO formation by acting on iNOS activity have been found to potently reduce intraocular pressure. Studies from our lab showed that an increase of CO availability by hemin or carbon monoxide-releasing molecules lower the intraocular pressure, suggesting a suppress action of iNOS-derived NO production. Conclusion A better understanding of CO regulation may lead to new therapeutic options that are safer and more efficacious than currently available treatments for various sight-threatening eye diseases, such as retinal degenerations. [source] Toxicity testing of the VEGF inhibitors bevacizumab, ranibizumab and pegaptanib in rats both with and without prior retinal ganglion cell damageACTA OPHTHALMOLOGICA, Issue 5 2010Sebastian Thaler Abstract. Purpose:, To evaluate the effects of intravitreally introduced vascular endothelial growth factor (VEGF) inhibitors in rat eyes with healthy retinal ganglion cells (RGC) and into others with N-methyl-D-aspartate (NMDA)-induced RGC damage. Methods:, Bevacizumab, ranibizumab and pegaptanib were intravitreally injected each at two different concentrations. Respective vehicles of the three substances served as controls. In a different group, additionally a rat anti-VEGF antibody was injected after NMDA treatment. Retrogradely labelled RGC were counted on retinal wholemounts 1 week or 2 months after intravitreal introduction of the VEGF inhibitors. Electron microscopy (EM) was performed on normal rat eyes 2 months after introduction of the VEGF inhibitors. Results:, RGC counts in healthy rat eyes were essentially unchanged from those of the control animals after the administration of both low and high concentrations of bevacizumab, ranibizumab or pegaptanib. Compared to the other two substances, however, high doses of pegaptanib and its respective vehicle significantly decreased RGC after 1 week and led to a marked increase of mitochondrial swelling in EM. In eyes with NMDA-induced RGC damage, no changes of RGC numbers were detected after rat anti-VEGF antibody or bevacizumab, ranibizumab and pegaptanib at both tested concentrations. Conclusions:, Even at higher doses, bevacizumab and ranibizumab showed no toxic effects on RGC in vivo in either untreated rats or in the NMDA-induced RGC damage model. Also a rat anti-VEGF antibody showed no adverse effects after NMDA. Anti-VEGF therapy therefore appears safe even for eyes with additional excitotoxic RGC damage. Potential harm from the pegaptanib carrier solution at very high local concentrations cannot be excluded. [source] Excessive maternal caffeine exposure during pregnancy is cataractogenic for neonatal crystalline lenses in rats: a biomicroscopic and histopathologic studyACTA OPHTHALMOLOGICA, Issue 5 2004Cem Evereklioglu Abstract. Purpose:,To investigate histologically the influence of maternal caffeine exposure during pregnancy in vivo on crystalline lenses in neonatal rats. Methods:,Experimentally naive, female Wistar-albino rats (200,220 g) were mated with adult male rats over 2 days for copulation. After confirming pregnancy with a vaginal smear method, 50 gravid rats (dams) were randomly divided into five groups (n = 10 in each), consisting of one control and four experimental groups. Groups 1, 2 and 3 experimental dams were treated with intraperitoneal (i.p.) caffeine at doses of 25, 50 and 100 mg/kg/day, respectively, during pregnancy from gestational day 9 through to day 21. Group 4 dams were treated with caffeine in distilled water in a gavage at a dose of 50 mg/kg/day. Group 5 control dams were given i.p. saline solution daily for the same period. After normal delivery, the eyes were examined by slit-lamp biomicroscopy. The neonates were then killed by decapitation at postnatal days 1 or 30 and the eyes removed for histopathologic investigation of the lenses. Results:,Group 1 and control eyes had normal anterior lens capsules with a single layer of anterior cuboidal epithelial cells, regularly oriented cortical and nuclear lens fibres, and a clear posterior lens capsule with no lining epithelial cells behind the equator. In the remaining groups, histopathologic findings suggesting cataractogenesis included eosinophilic degeneration, lens fibre cell swelling and liquefaction, central lens fibres with retained nuclei, and prominent epithelial cells lining the posterior lens capsule behind the equator. Moreover, some lenses in group 3 had immature cataract on slit-lamp biomicroscopic examination at postnatal day 30. Conclusion:,Excessive maternal caffeine exposure during pregnancy had cataractogenic effects on developing crystalline lenses in newborn rat eyes, both macroscopically and histopathologically. If an appropriate dose of caffeine can be identified, caffeine-induced cataract formation may be used as a new experimental cataract model in animal studies. [source] Effects of binocular form deprivation on the excitatory post-synaptic currents mediated by N-methyl-D-aspartate receptors in rat visual cortexCLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 3 2004Wei Qin MD Abstract Purpose:,To investigate the effects of binocular form deprivation (BFD) on the excitatory post-synaptic currents (EPSCs) mediated by the N-methyl-D-aspartate (NMDA) receptor (NMDA-EPSCs), and the proportion of NMDA-EPSCs relative to glutamate receptor currents (glutamate-EPSCs) in rat visual cortex. Methods:,Binocular form deprivation was achieved by suturing the eyelids of Wistar rats at postnatal day (PD) 14, before eye-opening. Visual cortical slices (300 µm) were prepared from normal and BFD Wistar rats aged PD 14, 21 and 28. Recordings were obtained in slices from layer II to IV using the whole-cell patch-clamp technique. Glutamate-EPSCs were isolated in the presence of bicuculline methiodide (20 µmol/L) in the bathing medium, and NMDA-EPSCs were isolated with a combination of bicuculline methiodide (20 µmol/L) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 20 µmol/L). In addition, D,L-2-amino-5-phosphonovalerate (AP-5, 20 µmol/L) was applied to study the NMDA-only mediated currents. For each cell, the ratio of peak NMDA to glutamate EPSCs was calculated. Results:,During visual development, the decay time constant of NMDA-EPSCs became shorter after eye-opening in normal rats (F = 5.949, P <0.05; PD 28 vs PD 14, P = 0.027), but not in rats with BFD (P > 0.05). The weighted time constant of NMDA-EPSCs in the visual cortex became shorter after the rats' eyes were opened in the normal group (F2,37 = 4.727, P = 0.015; PD 28 vs PD 14, P = 0.035), but not in the BFD group (P > 0.05). However, the rise time constant and peak value of NMDA-EPSCs showed no significant changes in normal and BFD groups (P > 0.05). The ratio of NMDA-EPSCs to glutamate-EPSCs became gradually smaller with age in the normal rats (F = 4.661, P < 0.05; PD 28 vs PD 14, P = 0.025), but not in the BFD group (P > 0.05). Conclusions:,These studies reveal that the proportion of NMDA-EPSCs relative to glutamate-EPSCs and the decay time constant of NMDA-EPSCs are influenced by BFD. These changes may reflect important experience-dependent modifications of neuronal synapses in visual cortex. [source] | ||||||||||