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PubMed1999

Retinal sparing by selective retinal pigment epithelial photocoagulation.

OBJECTIVE: To investigate whether photocoagulation of the retinal pigment epithelium is possible with sparing of the photoreceptors. METHODS: Mild laser effects of a neodymium:yttrium-lithium-fluoride (Nd:YLF) laser (527 nm) were applied to 17 patients. To establish the necessary energy, test exposures were performed to the lower macula (laser variables: 1.7 microseconds, 100 and 500 pulses applied in a train at 500 Hz, 20-130 microJ, 160 microm). Of 179 test lesions, 73 were followed up at various time intervals up to 1 year by performing microperimetry directly on top of the laser lesions. RESULTS: All of the test lesions were at the threshold of retinal pigment epithelial disruption, and none of the laser effects were visible by ophthalmoscopy during photocoagulation; they were detectable only by fluorescein angiography. After exposure with 500 pulses, retinal defects were detected in up to 73% of the patients (100 microJ) after the first day. Most of these defects were no longer detectable after 3 months. After exposure with 100 pulses, no defects could be detected with 70 and 100 microJ after 1 day. The absence of microscotomas in the follow-up period suggests that retinal damage was minimal or, if it occurred, was functionally repaired. CONCLUSION: By choosing proper energy and number of pulses, it is possible to produce retinal pigment epithelial effects with no subsequent retinal damage detectable by microperimetry.

Adult↗
PubMed2004

Vision change after sheet transplant of fetal retina with retinal pigment epithelium to a patient with retinitis pigmentosa.

OBJECTIVE: To report the subjective and objective improvement in vision in a patient with autosomal dominant retinitis pigmentosa after transplantation of a sheet of fetal neural retina together with its retinal pigment epithelium. DESIGN: A sheet of fetal neural retina with its retinal pigment epithelium was transplanted into the subretinal space under the fovea unilaterally in a patient with retinitis pigmentosa with visual acuity of 20/800 in the treated eye. Early Treatment Diabetic Retinopathy Study visual acuity testing, scanning laser ophthalmoscope, tissue typing of the donor and recipient, fluorescein angiography, multifocal electroretinogram, multifocal visually evoked potential, and clinical examination were used. RESULTS: No clinical evidence of rejection was observed. There was no retinal edema or scarring. The transplant sheet lost its pigmentation by 6 months. MAIN OUTCOME MEASURES: A change in visual acuity from 20/800 to 20/400 (7 months), 20/250 (9 months), and 20/160 (1 year) was observed by Early Treatment Diabetic Retinopathy Study visual acuity testing. Independently, scanning laser ophthalmoscope testing at a different institution at 9 months showed a visual acuity of 20/270 at a 40 degrees field of view. CONCLUSION: This study indicates that fetal retina transplanted with its retinal pigment epithelium can survive 1 year without apparent clinical evidence of rejection and show continued improvement in Early Treatment Diabetic Retinopathy Study visual acuity.

Electroretinography↗
PubMed1984

Assessment of possible transneuronal changes in the retina of rats with inherited retinal dystrophy: cell size, number, synapses, and axonal transport by retinal ganglion cells.

In pigmented RCS rats with inherited retinal dystrophy, most photoreceptor cells disappear between postnatal days 20 and 100. We have examined the time course of the degeneration of photoreceptor nuclei and synapses and determined whether transneuronal changes occur in the inner nuclear layer (INL), inner plexiform layer (IPL), and retinal ganglion cells following loss of photoreceptor cells in these animals. Electron microscopic photomontages of the entire thickness of the IPL of dystrophic (RCS-p+) and control (RCS-rdy+ p+) rats 334 to 515 days old were prepared, and synapses were counted and identified as either conventional (amacrine) or ribbon (bipolar) types. Neither the incidence of synapses in the IPL nor the ratio of conventional to ribbon synapses differed in the dystrophic and control retinas. Ganglion cell diameter, perimeter, area, and density were measured from drawings of wholemount preparations of dystrophic and control rats 105 days and older. Diameter, perimeter, area and number of ganglion cells were not significantly different in the two genotypes. Anterograde axonal transport was measured by studying the displacement of labeled material as it traveled along ganglion cell axons and accumulated in the superior colliculus. The normal and dystrophic rats showed no significant difference in (1) the rates of rapidly moving components (approximately 110-180 mm/day) and slowly moving components (1.7-2.5 mm/day) or (2) the amount of radioactive material transported to the superior colliculus. The absence of transneuronal changes in retinal ganglion cells of RCS rats contrasts with results obtained earlier in rd mice (Graftstein et al., '72). Unlike the RCS rat, retinal degeneration in rd mice occurs before the maturation of the retina. We hypothesize that the ganglion cells may be more affected by loss of input early in development, and, therefore, ganglion cells of retinal dystrophic rats are less affected despite little or no synaptic input for several months. Furthermore, any reduction in the electrical activity of retinal ganglion cells that might follow loss of photoreceptor cells does not result in a significantly decreased rate of axonal transport.

Aging↗
PubMed1997

Lipids of plasma, retina, and retinal pigment epithelium in Swedish briard dogs with a slowly progressive retinal dystrophy.

Reduced blood levels of long chain polyunsaturated fatty acids have been reported in humans and animals with inherited retinal degenerations. The lipid and fatty acid compositions of plasma, retina, and retinal pigment epithelium of the Swedish Briard dog, which has a very slowly progressive retinal dystrophy that is inherited in an autosomal recessive manner were analysed. The lipid class composition of the pigment epithelium was not different between affected and normal dogs; however, significant differences were found between the retinas of the two groups. Affected dogs had relatively more phosphatidylethanolamine and phosphatidylinositol and less phosphatidylcholine than normal dogs. There was no difference in the fatty acid compositions of plasma and retinal pigment epithelium between affected and normal dogs. However, the retinas of affected dogs had significantly lower levels of 22:5n-3 and 22:6n-3 and higher levels of 18:2n-6, 20:4n-6, and 22:5n-6. The total n-3 fatty acid content was significantly lower in affected retinas (P < 0.001), whereas the content of n-6 fatty acids was significantly higher in affected retinas (P < 0.001). These studies provide evidence for yet another animal model of inherited retinal degeneration with a defect in retinal polyunsaturated fatty acid metabolism. The fatty acid pattern in affected dogs resembles that seen in the retina in n-3 fatty acid deficiency.

Animals↗
PubMed1993

Regulation of glucose transporter (GLUT 3) and aldose reductase mRNA inbovine retinal endothelial cells and retinal pericytes in high glucose and high galactose culture.

The regulation of GLUT-3 and aldose reductase mRNA in retinal endothelial cells and retinal pericytes was studied in response to variations in the extracellular concentration of hexoses. In physiological concentrations of glucose (5 mmol/l), an increase in the level of GLUT-3 mRNA was observed in cultured cells compared to the level of mRNA found in the absence of glucose. In contrast, there was little change in the level of GLUT-3 mRNA when the cells were cultured in the presence of 5 mmol/l galactose. In high concentrations of glucose, there was a decline in GLUT-3 mRNA indicating that the GLUT-3 mRNA is regulated by the extracellular concentration of glucose. In contrast, at both 5 mmol/l and 25 mmol/l glucose, the level of aldose reductase mRNA was increased. Furthermore, there were differences in the magnitude of the increase of aldose reductase mRNA between bovine retinal pericytes and bovine retinal endothelial cells with a greater increase being observed in the pericytes. We propose that this demonstration of a facilitative glucose transporter system within retinal cells, and in particular the specific response to different hexoses and the known distinct kinetic parameters of the transporter system in specific cell types, highlights the heterogeneity of hexose transport mechanisms in retinal cells. Thus, hypergalactosaemia as a model system for the study of diabetic retinopathy should be used with caution.

Aldehyde Reductase↗
PubMed1982

Phakic retinal detachment associated with cystic retinal tuft.

Of 200 consecutive cases with phakic nontraumatic rhegmatogenous retinal detachment, 15 cases (7.5%) were causally related to cystic retinal tuft. The cystic retinal tuft was characterized by a small, elevated and chalky-white lesion with cystic features and pigment proliferations. The lesions were present in the equatorial region of the retina, and two types of retinal breaks were found, i.e., horseshoe- or crescent-shaped flap tears and round opercular tears. Flap tears were found more frequently, which were located at the juxtabasal zone of the equator and induced acute, highly elevated detachments. Opercular tears were located at the extrabasal zone of the equator and caused relatively slowly developing, shallow detachments. It was concluded that the cystic retinal tuft is an important vitreoretinal abnormality predisposing to rhegmatogenous retinal detachment.

Adult↗
PubMed2004

Induction of IL-8, MCP-1, and bFGF by TNF-alpha in retinal glial cells: implications for retinal neovascularization during post-ischemic inflammation.

BACKGROUND: We have demonstrated that macrophages/microglia were activated during post-ischemic inflammation in a mouse model of ischemic retinal neovascularization, and that the angiogenesis induced by tumor necrosis factor-alpha (TNF-alpha) appeared to be modulated through such angiogenic factors as interleukin-8 (IL-8), vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) in microvascular endothelial cells. We have extended these studies, and investigated whether TNF-alpha is localized in macrophages/microglia in the mouse model of retinal neovascularization, and whether TNF-alpha can induce angiogenic factors in retinal glial cells. METHODS: C57BL/6 J pups were placed in a 75% oxygen environment on postnatal day 7 (P7) for 5 days and then returned to room air. The co-localization of TNF-alpha with macrophages/microglia in the ischemic retina was examined by fluorescent immunohistochemistry. Bovine retinal glial cells were isolated for Northern blot analysis to quantify the expression levels of monocyte chemotactic protein-1 (MCP-1), IL-8, bFGF, and VEGF. RESULTS: Double staining of retinas revealed that the TNF-alpha expression level was enhanced in macrophages/microglia 4 days after the hypoxia. Cellular mRNA levels of MCP-1, IL-8, and bFGF, but not VEGF, were increased after treating retinal glial cells with TNF-alpha (100 U/ml). CONCLUSIONS: The results indicate that TNF-alpha is produced by activated macrophages/microglia and may participate in retinal neovascularization during post-ischemic inflammation through the induction of potent angiogenic factors in an autocrine or paracrine manner.

Animals↗
PubMed2005

Increased nitric oxide (NO) pathway metabolites in the vitreous fluid of patients with rhegmatogenous retinal detachment or diabetic traction retinal detachment.

BACKGROUND: Nitric oxide (NO) plays a significant role in physiological and pathological processes in the retina. In the L-arginine-NO pathway, NO synthase (NOS) converts L-arginine to NO and L-citrulline. Increased NO production, mediated by inducible NOS has been implicated in the pathogenesis of various vitreoretinal diseases. In the present study it is hypothesized that in rhegmatogenous retinal detachment (RRD), the production of NO pathway metabolites might be upregulated. METHODS: Using high-pressure liquid chromatography citrulline, arginine and nitrite were measured in vitreous fluid of 93 eyes with RRD, nine eyes with a traction retinal detachment due to proliferative diabetic retinopathy (PDR), and in 49 control samples of vitreous fluid from eyes without retinal detachment. RESULTS: The mean vitreous concentrations of citrulline and arginine were significantly increased in eyes with RRD (9.6+/-4.3 and 97.3+/-29.2; respectively) or in eyes with a traction retinal detachment (25.8+/-10.3 and 130.7+/-23.7; respectively) as compared to control eyes (7.1+/-3.2 and 75.9+/-18.1; respectively). The mean level of nitrite was also higher in vitreous fluid of patients with RRD (2.24+/-1.4) or patients with a traction retinal detachment (2.21+/-0.72) than in the controls (2.01+/-0.72), although not significantly so. CONCLUSIONS: We found increased levels of NO pathway metabolites in the vitreous fluid of eyes with retinal detachment, which may reflect a possible role of NO in the pathogenesis of this disease.

Aged↗
PubMed1992

Morphologic and clinical study of the retinal circulation in the miniature pig. A: Morphology of the retinal microvasculature.

The microvasculature of the retina was studied in 20 miniature pigs by means of vascular corrosion casts and semithin histological sections. These techniques provided information useful for a better understanding of retinal fluoangiography. Various characteristics of the porcine retinal vessels, which are similar in the human retinal vasculature, were demonstrated in this study: the holangiotic retina, the trilaminar organization of the retinal capillaries and the presence of particular avascular zones, radial peridiscal capillaries and initial annular constrictions of certain arteriolar side-branches. The intrinsic retinal vasculature also shows some dissimilarities between both species. The major retinal blood vessels of the pig lie very superficially in the nerve fibre layer, in contrast to their deeper location in man. The streak-shaped macular area of the pig contains no major vessels but, unlike the central fovea in the human eye, it is not completely avascular. Another interesting finding is the presence of a large anterior border venule in the porcine retina.

Animals↗
PubMed1985

Class II antigen expression and gamma interferon modulation of monocytes and retinal pigment epithelial cells from patients with retinitis pigmentosa.

Monocytes from retinitis pigmentosa patients express diminished amounts of class II (HLA-DR) antigens in comparison to normal individuals, normal siblings of retinitis pigmentosa patients, glaucoma patients, and macular degeneration patients. This observation is correlated with a subnormal production of IFN-gamma, a potent regulator of class II antigen expression. When monocytes from retinitis pigmentosa patients are treated with IFN-gamma, the decreased expression of HLA-DR on the cell surface is restored to levels found on monocytes from normal individuals. HLA-DR antigens were detected on the surfaces of human retinal pigment epithelial cells grown in vitro and the expression of these antigens can be enhanced following IFN-gamma treatment. These data demonstrate an altered expression and regulation of class II, HLA-DR, antigens in a human eye disease. Since class II antigens and IFN-gamma are currently known to be necessary regulating proteins for efficient immune reactivity, these findings may indicate an immune disturbance in retinitis pigmentosa patients. Alternatively, this alteration may have nonimmune implications. For example, these studies may demonstrate an imbalance in systemic regulatory control systems and hence raise the possibility that these or related regulatory proteins and cell surface receptors may be instrumental in maintaining retinal integrity.

Cells, Cultured↗
PubMed2006

Aberrant retinal tight junction and adherens junction protein expression in an animal model of autosomal dominant Retinitis pigmentosa: the Rho(-/-) mouse.

Retinitis pigmentosa (RP) comprises a heterogeneous group of inherited diseases that are characterised by primary degeneration of rod photoreceptors and secondary degeneration of cone photoreceptors in the retina. Additional pathological changes include vascular changes and invasion of the inner retina by retinal pigment epithelial (RPE) cells. RP represents a major cause of progressive retinal disease worldwide. Using a mouse model of autosomal dominant Retinitis pigmentosa (adRP) with retinopathy induced by targeted disruption of the rhodopsin gene Rho(-/-), we have analysed the levels of expression of a range of tight and adherens junction associated proteins, in order to further elucidate the pathogenic mechanisms occurring at an early stage of this condition. Using western blot analysis and indirect immunostaining of retinal cryosections from 6-week-old mice from a C-129 background we have determined changes, if any, in the levels of expression and localisation of a series of tight and adherens junction associated proteins, including Zonula Occludens-1 (ZO-1), occludin, N-Cadherin, p120-Catenin, alpha-Catenin, gamma-Catenin, beta-Catenin, and E-Cadherin. We have found an up-regulation of the tight junction and adherens junction associated protein Zonula Occludens-1 (ZO-1) in the neural retina of 6-week-old Rho(-/-) knockout mice compared with 6-week-old Wild-Type (WT) mice. Following immunohistochemistry, however, it appears, that ZO-1, beta-Catenin and p120-Catenin expression at the Outer Limiting Membrane (OLM) of the Rho(-/-) retina is compromised, in part, compared to WT animals of the same age. We hypothesise that these retinal changes following photoreceptor cell death may contribute to the pathogenesis of adRP. Our findings of changes in the levels of expression of ZO-1 and associated adherens junction proteins beta-Catenin and p120-Catenin at the OLM in 6-week-old Rho(-/-) mice provide evidence for tight junction and adherens junction associated protein modifications in an animal model of autosomal dominant RP (adRP).

Adherens Junctions↗
PubMed2005

Retinal G-substrate, potential downstream component of NO/cGMP/PKG pathway, is located in subtype of retinal ganglion cells and amacrine cells with protein phosphatases.

The aim of this study was to determine the distribution and function of G-substrate, a specific substrate of the nitric oxide (NO)-cyclic guanosine monophosphate (cGMP)-cGMP-dependent protein kinase (PKG) signaling pathway, in normal rat retina and in G-substrate knockout mice. The retinas of adult wild-type rats and mice and G-substrate knockout mice were studied immunohistologically to characterize the upstream and downstream components of the NO-cGMP-PKG pathway. Immunoblot analysis showed that the molecular weight of retinal G-substrate was similar to that of cerebellar G-substrate. In adult rats and mice, retinal G-substrate was located in a subpopulation of amacrine cells and in C38-positive retinal ganglion cells (RGCs) but not in alpha RGCs. In addition, retinal G-substrate was co-expressed with other upstream and downstream signaling components of the NO-cGMP-PKG-G-substrate-phosphatase pathway in the adult retina. Electroretinographic (ERG) analysis demonstrated that there was no significant difference between the ERGs of wild-type and G-substrate knockout mice. These results suggest that retinal G-substrate plays a role as a downstream component of the NO-cGMP-PKG pathway. The co-localization of retinal G-substrate with protein Ser/Thr phosphatases suggests that it acts as an endogenous protein phosphatase inhibitor as in the cerebellum.

Amacrine Cells↗
PubMed1998

Cytomegalovirus retinitis and viral resistance: 3. Culture results. CMV Retinitis and Viral Resistance Study Group.

PURPOSE: To evaluate the relationship between blood and urine cultures for cytomegalovirus and clinical outcomes in patients with cytomegalovirus retinitis. METHODS: Prospective epidemiologic study of 108 patients with newly diagnosed cytomegalovirus retinitis. Blood and urine were cultured for cytomegalovirus at diagnosis of retinitis, at 1 month and 3 months after diagnosis, and every 3 months thereafter. RESULTS: Of the patients, 80.6% were found to have either a positive blood culture or urine culture for cytomegalovirus at the time of diagnosis of retinitis, and a positive blood culture at diagnosis was associated with an increased mortality (odds ratio = 1.91, P = .012). Follow-up cultures were positive in approximately 20% of patients, and the rate was constant over time. The development of a positive blood or urine culture during follow-up correlated with the occurrence of cytomegalovirus retinitis in the contralateral eye in those patients with unilateral disease at diagnosis (odds ratio = 5.74, P = .001). CONCLUSIONS: Patients with cytomegalovirus retinitis and positive blood cultures for cytomegalovirus have a poorer prognosis.

AIDS-Related Opportunistic Infections↗
PubMed2002

Detection using the multifocal electroretinogram of mosaic retinal dysfunction in carriers of X-linked retinitis pigmentosa.

PURPOSE: To examine whether a mosaic pattern of retinal dysfunction in obligate carriers of X-linked retinitis pigmentosa (XLRP) could be observed in local electroretinographic responses obtained with the multifocal electroretinogram (mfERG). DESIGN: Prospective observational case series. PARTICIPANTS: Five obligate carriers of XLRP (mean age, 53.2 years) were recruited into the study. METHODS: Examination of each subject included a complete ocular examination, Humphrey visual field, standard full-field electroretinogram (ERG), and mfERG testing. For the mfERG, we used a 103-scaled hexagonal stimulus array that subtended a retinal area of approximately 40 in diameter. The amplitudes and implicit times in each location for the mfERG was compared with the corresponding value determined for a group of normally sighted, age-corrected control subjects. MAIN OUTCOME MEASURES: Mapping of 103 local electroretinographic response amplitudes and implicit times within the central 40 with the multifocal electroretinogram. RESULTS: Localized regions of reduced mfERG amplitudes and/or delayed implicit times were found in four of five carriers. In one of these four carriers, a mosaic pattern of mfERG dysfunction was present even in the absence of any clinically apparent retinal changes, retinal sensitivity losses on Humphrey field testing, or abnormal full-field cone ERG responses. However, one carrier with a typical tapetal-like reflex demonstrated no deficit on any functional tests. CONCLUSIONS: The mfERG demonstrated patchy areas of retinal dysfunction in some carriers of XLRP. This mosaic pattern of dysfunction may be observed in some patients with a normal-appearing fundus, normal psychophysical thresholds, and normal amplitude and implicit time full-field ERG cone responses.

Adult↗
PubMed2002

Single cell RT-PCR analysis of tyrosine kinase receptor expression in adult rat retinal ganglion cells isolated by retinal sandwiching.

We describe a protocol for analysis of gene expression in single, acutely dissociated adult rat retinal ganglion cells using RT-PCR. Retrograde tracing of retinal ganglion cells from the superior colliculi was conducted using Fluorogold. Retinas were dissected and ganglion cells isolated using retinal layer separation (sandwiching). Single, fluorescently labelled retinal ganglion cells were aspirated using a micropipette and used for PCR. Two PCR protocols are described where single cell cDNA was analysed for TrkB and GAPDH or TrkB, TrkC, Ret, Met, ErbB2 and Beta-actin by multiplex-PCR. All five tyrosine kinase receptors were amplified from single retinal ganglion cells. The method will prove useful for the molecular characterization of adult retinal ganglion cells.

Animals↗
PubMed1989

Nonuniform retinal expansion during the formation of the rabbit's visual streak: implications for the ontogeny of mammalian retinal topography.

We have studied the distribution of retinal ganglion cells (RGCs) which have been retrogradely labeled from massive bilateral injections of the enzyme horseradish peroxidase into the retino-recipient nuclei of foetal and postnatal albino rabbits aged from the 24th postconceptional day (24PCD) to adulthood. The number of labeled RGCs increases from about 447,000 on the 24PCD to a peak of about 525,000 on the 27PCD. From the 29PCD to birth (31/32PCD), the number of RGCs rapidly declines to about 375,000. During the next 20 d, the number of RGCs stabilizes at about 335,000. After the 51PCD, the number of RGCs gradually declines to the adult value of about 280,000. Retinal area steadily increases from about 40 mm2 on the 24PCD to about 500 mm2 in the adult, while RGC density decreases. However, the reduction in RGC density is nonuniform: RGC density in the visual streak drops from 18,600 RGCs mm2 on the 24PCD to 4700 RGCs/mm2 in the adult, whereas RGC densities at the superior and inferior edges of the retina decreases proportionally much more (from 9300 to 105 RGCs/mm2 and from 12,000 to 170 RGCs/mm2, respectively). As a result of this differential reduction in RGC density, the streak/inferior edge ratio changes from 1.6:1 to about 28:1. In the periods from the 24PCD to the 29PCD and from the 32PCD to adulthood, the proportional increases in the streak/superior edge and streak/inferior edge RGC density ratios are linearly related to the proportional increases in retinal area. However, between the 29PCD and 32PCD, the RGC density ratios increase at a greater rate than retinal area. We conclude that (1) the centro-peripheral difference in RGC density that is already present on the 24PCD might be attributable to differential RGC generation; (2) the redistribution of RGCs between the 24PCD and adulthood is mainly due to nonuniform expansion of the retina, with minimal expansion of the visual streak and maximal expansion at the superior and inferior retinal edges; and (3) a small component of the increase in the centro-peripheral RGC density ratio, which becomes apparent between the 29PCD and 32PCD, is probably due to differential RGC loss. We discuss the pattern of retinal expansion in the rabbit and the factors which might contribute to it.

Animals↗
PubMedDate not supplied

Alpha-2 adrenoceptor agonist protects retinal function after acute retinal ischemic injury in the rat.

Alpha-2 adrenoceptor agonists have previously been shown to enhance neuronal survival in an optic nerve mechanical injury model and to protect photoreceptors in a light-induced degeneration model. The purpose of this study was to examine the effect of the alpha-2 adrenoceptor agonist in a pressure-induced retinal ischemia model. Brown-Norway rats were treated systemically or topically with alpha-2 adrenoceptor specific agonist brimonidine. Retinal ischemia was induced by increasing the intraocular pressure to 110 mm Hg for 50 min. The effect of brimonidine on retinal ischemic injury was functionally assessed in the rats 7 d later using electroretinography (ERG). Ischemia-induced retinal cell death was studied using the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. We found that brimonidine treatment significantly protected the retina from retinal ischemic injury in a dose- and time-dependent manner. This protection can be achieved either by systemic or topical application and can be blocked by pretreatment with the alpha-2 adrenoceptor antagonist, yohimbine. Using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis, we found that brimonidine can up-regulate the expression of basic fibroblast growth factor, bcl-2 and bcl-xl in the retina. The drug also can activate two major cell survival signaling pathways in the retina: the extracellular-signal-regulated kinases (ERKs) and phosphatidylinositol-3' kinase/protein kinase Akt pathways. All these aforementioned factors may potentially contribute in mediating brimonidine's protective effect in this acute retinal ischemia model.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1999

Susceptibility of retinal ganglion cells to excitotoxicity depends on soma size and retinal eccentricity.

PURPOSE: This study was undertaken to determine if retinal ganglion cell sensitivity to intraocular N-methyl-D-aspartate or kainate injections varied as a function of retinal location (eccentricity) or cell soma size. METHODS: Rat retinal ganglion cells surviving intraocular N-methyl-D-aspartate or intraocular kainate induced lesions were retrogradely labeled with horseradish peroxidase and analyzed using an image analysis system. Control animals were retrogradely labeled after vehicle injection only. Cell counting was performed at 48 sampling points over the entire retina and represented a total area of 1.92 mm2 per retina. RESULTS: Larger cells were more sensitive to kainate than to N-methyl-D-aspartate excitotoxicity; smaller cells more vulnerable to N-methyl-D-aspartate excitotoxicity. Further from the optic nerve, more smaller cells survived kainate administration. After N-methyl-D-aspartate administration, larger cells survived most, noticeably in the central retina. CONCLUSIONS: Our results suggest that loss of retinal ganglion cells after N-methyl-D-aspartate or kainate administration affects distinct populations of retinal ganglion cells, dependent upon soma size and retinal location. The mechanism by which certain classes of cells survive or succumb to such insults has yet to be determined.

Animals↗