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PubMed1977

Complicated colobomatous microphthalmos in the BW rat: a new form of inherited retinal degeneration.

A new model of inherited retinal degeneration has been found in the rat. It is inherited in association with a number of other ocular defects, including microphthalmos, coloboma, retinal dysplasia, optic nerve hypoplasia and/or aplasia, as well as medullation of the nerve fiber layer of the retina. Together, these abnormalities constitute a condition referred to as complicated colobomatous microphthalmos. This condition was originally discovered in the Bmn strain of rats but subsequently transferred to a new genetic background in the Bmn-wys strain of rats (BW). This facilitated the histological evaluation of both the developmental and degenerative ocular defects in the adult animals. A well defined pattern emerged relating eye size, optic nerve size and retinal histology. Normal-sized eyes had normal-sized optic nerves and normal retinal histology while intermediate-sized eyes with no optic nerves had uniformly thin retinas. In contrast, intermediate-sized eyes with small optic nerves had areas of both normal thickness and thin retina. All of these eyes developed retinal degeneration characterized by a late onset and slow progression associated with normal phagocytic activity in the pigment epithelium and a tendency for the rod outer segments to fragment into very thin structures rather than accumulate as lamellar debris. This indicates that the retinal degeneration in the BW model differs in many respects from the well studied RCS model.

Animals↗
PubMed1988

Biochemical characterization of retinal protein and phospholipid synthesis in mice exposed transplacentally to N-methyl-N-nitrosourea.

Transplacental exposure to the DNA alkylating agent N-methyl-N-nitrosourea on day 16 of gestation in CD-1 albino mice induces a degeneration of the retina, the severity of which depends upon the dosage level of the drug. A 1 mg kg-1 dose provokes a progressive retinal degeneration in the offspring which begins at about 4-6 weeks of age and is characterized by gradual thinning of the retinal layers. A 15 mg kg-1 dosage of MNU provokes severe retinal dysplasia characterized morphologically by rosettes in the outer nuclear layer and loss of rod outer segments (ROS). In the present biochemical experiments, retinal protein synthesis was examined in mice 2-, 4-, and 6 weeks of age exposed to 1 mg kg-1 MNU and 2- and 5 weeks of age exposed to 15 mg kg-1 MNU. Phospholipid synthesis was examined in mice 2-, 4-, 6- and 12 weeks of age exposed to 1 mg kg-1 MNU and at 2 weeks in mice exposed to 15 mg kg-1 MNU. Retinas were incubated for 2 hr at 37 degrees C in media supplemented with either [3H]leucine for protein synthesis studies or [3H]glycerol for phospholipid synthesis experiments. Aliquots of crude ROS and the retinal debris were taken for protein determination, scintillation counting, SDS-PAGE separation of labeled opsin, phosphorus determination and TLC separation of phospholipids. Results indicated that mice exposed to 1 mg kg-1 MNU did not differ significantly from age-matched controls in these measurements, whereas mice exposed to 15 mg kg-1 MNU were significantly different from controls. These results suggest that even as early as 2 weeks of age protein and lipid metabolism are adversely affected in mice exposed to the higher dose of the alkylating agent at a critical time in retinal development, but general protein and lipid synthesis is not affected in animals exposed to 1 mg kg-1 MNU at least up to 12 weeks of age. These studies suggest further investigation of more subtle derangement in the retinal function in animals exposed to low levels of MNU.

Animals↗
PubMed2004

Developmental plasticity of NMDA receptor function in the retina and the influence of light.

Despite the early expression of NMDA receptors (NMDARs) in the retina, not much is known about their regulation and involvement in plasticity processes during retinal development and synapse formation. Here we report that NMDAR function in the inner retina is developmentally regulated and controlled by ambient light condition. A prominent down-regulation after eye opening of NMDAR function was observed in rat retinal ganglion cells (RGCs), which was prevented by dark rearing the animals for 1 month but was again induced by subsequent light exposure. As shown by molecular analysis of single RGCs, alterations in the subunit composition of NMDAR did not account for the light-dependent regulation of NMDAR function. Immunocytochemistry showed no differences in the NMDAR protein expression pattern between normal and dark-reared animals. In conclusion, our data clearly demonstrate that NMDAR function is modulated during periods of retinal plasticity independent of structural alterations in its subunit composition and thus different from mechanisms observed in higher visual centers.

Electric Conductivity↗
PubMed1981

The emergence, localization, and maturation of neurotransmitter systems during development of the retina in Xenopus laevis. III. Dopamine.

The uptake, synthesis, and release of dopamine was studied in retinas of Xenopus laevis. In the tadpole and adult retina, 3H-dopamine is accumulated by cells located in the inner nuclear layer. Retinas preloaded with 3H-dopamine release this compound in response to high K+ concentrations in the medium. This release is probably Ca++-dependent as it is inhibited by Co++ in the medium. Adult retinas are also capable of synthesizing 3H-dopamine from 3H-tyrosine. The appearance and maturation of these dopaminergic properties were followed during retinal development. Our data indicate that synthesis of dopamine can first be detected as early as stage 35/36 whereas uptake of dopamine first occurs at stage 43. K+-stimulated release of preloaded 3H-dopamine from putative dopaminergic neurons is, however, not evident until stage 46. These results show that similar to the development of GABA-ergic and glycinergic properties, the uptake, synthesis, and release mechanisms for dopamine emerge at different stages during retinal differentiation in Xenopus Laevis.

Acetylcholine↗
PubMed2000

The effects of natural cell loss on the regularity of the retinal cholinergic arrays.

The retina provides a paradigmatic example of the modularity of neuronal circuitry. Different cells are stacked in layers, and neurons of the same type are commonly regularly spaced within their layer. Although the orderly arrays formed by homotypic neurons provide the basis for parallel processing, the mechanisms responsible for regular cell spacing are just beginning to be elucidated. All the developing retinal arrays for which early markers have been identified are regular before being complete. This indicates that the positional constraints controlling mosaic formation are active at times when cell genesis, migration, and death also occur in the retina. To begin investigating how these different processes are coordinated, we have focused here on the effects of cell death on the spatial organization of the two rat cholinergic mosaics, the only arrays for which the development of spatial ordering has been described quantitatively to date. We have chosen an age interval when new cell genesis is over and death predominantly or nearly exclusively controls cell number in one of these array. We found that the regularity of this array is not improved by the loss of cells occurring in this age period. Rather, death appears to be largely independent of cell position.

Animals↗
PubMed1992

Vanishing retinal arterial aneurysms: a case report.

An 18-year-old woman with retinal vasculitis developed multiple retinal arterial aneurysms over a period of 3 years. Subsequently she developed macular oedema, peripheral neovascularisation, and vitreous haemorrhage and was treated with systemic steroids, laser photocoagulation, and vitreoretinal surgery. No systemic cause for vasculitis was found. Serial fluorescein angiography demonstrated gradual resolution of the arterial aneurysms over the subsequent 7 years.

Adolescent↗
PubMed1980

Postnatal development of GABA-ergic neurons in the rabbit retina.

Uptake, synthesis, storage, and release of gamma-aminobutyric acid (GABA) are some of the characteristic properties of GABA-ergic neurons. In the present study, we have used these properties as physiological probes to follow the emergence and maturation of GABA-ergic neurons during postnatal development of the rabbit retina. There is autoradiographic, immunocytochemical, and pharmacological evidence that some amacrine cells and certain neurons in the ganglion cell layer probably use GABA as the neurotransmitter. These neurons take up GABA, contain the GABA-synthesizing enzyme L-glutamic acid decarboxylase (GAD, EC 4.1.1.15), and release the accumulated GABA by a CA++-dependent mechanism when depolorized with high extracellular K+ concentration. In this study, we show that certain neurons in the newborn retina already possess a specific mechanism for GABA uptake. The positions and numbers of these cells in the developing retina suggest that they will become GABA-ergic neurons in the adult retina. These putative GABA-ergic neurons are, however, probably immature at birth because newborn retinas contain only low levels of GABA and GAD. Additionally, there is relatively little K+-stimulated, Ca++-dependent release of (3H)-GABA from the newborn retinas. GABA concentrations and GAD activities in developing retinas increase steadily postnatally, reaching about 80% of the adult levels by day 9. The activities of the GABA-degrading enzyme, GABA-glutamate transaminase (GABA-T, EC 2.6.1.19), follow a similar pattern of maturation during retinal development. K+ stimulated GABA release, however, remains low until about day 6, and then increases dramatically from 20% to 85% of the adult level over the next 3 days. Taken together, our results indicate that in the rabbit retina, the commitment by certain neurons to use GABA as the transmitter is made prenatally. These neurons are immature at birth but are biochemically, physiologically, and probably functionally mature by about 9 days after birth.

4-Aminobutyrate Transaminase↗
PubMed2006

SSEA-1 marks regionally restricted immature subpopulations of embryonic retinal progenitor cells that are regulated by the Wnt signaling pathway.

Identification and expansion of retinal progenitor cells are critical issues from both scientific and clinical aspects. Here, we identified SSEA-1 (CD15) as a novel surface antigen that can be used to define immature retinal progenitor cells. SSEA-1-expressing retinal cells were found in the peripheral region of the early embryonic mouse retina, and then their number dramatically disappeared along with retinal development. FACS analysis showed that the cells strongly positive for SSEA-1 co-expressed Ki67 proliferation antigen in all the developmental stages examined. The SSEA-1-expressing cells formed larger colonies than the non-expressing ones in retinal re-aggregation cultures. Moreover, late onset of rhodopsin expression was observed in SSEA-1-positive progenitor cells, supporting the idea that these cells have an intrinsically immature character. Differential expression of Wnt signal-related genes between SSEA-1-positive and -negative subpopulations of retina cells was revealed, and the expression of constitutively active forms of Wnt signaling molecules resulted in a greater number of SSEA-1-positive cells. In light of all of the data taken together, we propose SSEA-1 to be a surface marker to define a regionally restricted immature subset of progenitor cells of mouse neural retina, with SSEA-1 expression by them positively regulated by Wnt signals.

Animals↗
PubMed1985

Retinal detachment following endophthalmitis.

Fifty-five consecutive patients with a clinical diagnosis of bacterial endophthalmitis were reviewed. All patients were treated with systemic, periocular, topical, and intravitreal antibiotics. In addition, 33 of the patients underwent a pars plana vitrectomy. Nine retinal detachments occurred within six months of initial diagnosis. The higher frequency of retinal detachment in the vitrectomy group (21%) as compared to those patients managed without vitrectomy (9%) may be explained by a combination of surgical complications and the increased severity of endophthalmitis in the vitrectomy group. The two patients who developed retinal detachment during vitrectomy surgery rapidly progressed to no light perception. Conversely, the repair of retinal detachments diagnosed postoperatively had a good prognosis.

Adolescent↗
PubMed1994

Digenic retinitis pigmentosa due to mutations at the unlinked peripherin/RDS and ROM1 loci.

In spite of recent advances in identifying genes causing monogenic human disease, very little is known about the genes involved in polygenic disease. Three families were identified with mutations in the unlinked photoreceptor-specific genes ROM1 and peripherin/RDS, in which only double heterozygotes develop retinitis pigmentosa (RP). These findings indicate that the allelic and nonallelic heterogeneity known to be a feature of monogenic RP is complicated further by interactions between unlinked mutations causing digenic RP. Recognition of the inheritance pattern exemplified by these three families might facilitate the identification of other examples of digenic inheritance in human disease.

Alleles↗
PubMed1990

[Prevention of retinal detachment and treatment of retinoschisis].

The necessity for prophylactic treatment for degenerative disease in the peripheral retina cannot be evaluated merely on the basis of the ophthalmoscopic findings. Factors such as the patient's history, refraction, the status of the vitreous, and prospective future cataract extraction all have a major impact on the risk of developing retinal detachment. The latter condition can be classified in to three groups: (1) low risk (patients with no history of retinal detachment, intraocular surgery or posterior vitreous detachment, myopia less than three diopters): treatment of atrophic holes and lattice degeneration is not justified, treatment of flap tears according to the circumstances; (2) medium risk (patients with no history of retinal or posterior vitreous detachment; however, myopia of more than three diopters and/or aphakia): the treatment of lattice degeneration is not justified; treatment of breaks according to the circumstances; (3) high risk: (patients with symptoms of posterior vitreous detachment): the treatment of lattice degeneration and atrophic holes is not justified: treatment of tears is necessary; fellow eyes: the treatment of retinal breaks is necessary; treatment of lattice degeneration seems advisable in cases with bilateral symmetric findings or prior to cataract extraction. Treatment of senile retinoschisis is only justified in cases with large and centrally located holes in the outer wall or in the presence of symptomatic schisis detachment.

Humans↗
PubMed1998

The embryogenesis of rod photoreceptors in the teleost fish retina, Haplochromis burtoni.

Development of the retina, like that of other tissues, occurs via an orderly sequence of cell division and differentiation, producing the functional retina. In teleost fish, however, cell division and differentiation in the retina continue throughout the life of the animal in two distinct ways. Stem cells in a circumferential germinal zone at the periphery of the retina give rise to all retinal cell types and progenitor cells located throughout the retina in the outer nuclear layer (ONL) produce new rod photoreceptors. These processes in adult retina recapitulate in space the embryonic events responsible for forming the retina. Analysis of these events in an African cichlid fish, Haplochromis burtoni, confirmed that cone photoreceptors differentiate first, followed by rod photoreceptors. Correspondingly, at the margin of the eye, cone photoreceptors differentiate nearer to the margin than do rods. Control of photoreceptor production is not understood. Here we present the time of appearance and distribution pattern of GABA and vimentin which are candidates for the control of retinal cell division and differentiation. Antibody staining reveals that both GABA and vimentin exhibit unique patterns of expression during embryonic retinal development. Vimentin immunoreactivity is evident throughout the retina in a spoke-like pattern between developmental Days 4 and 7, as both cone and rod photoreceptors are being formed. GABA is expressed in horizontal cells between Days 5 and 7, corresponding to the onset of rod differentiation in time and in position within the retina. Moreover, the wave of GABAergic staining in the horizontal cells parallels the wave of rod differentiation across the embryonic retina of H. burtoni. Thus, GABA may play a role in the development of rod photoreceptors.

Animals↗
PubMed1995

Retinal haemorrhage in Himalayan mountaineers.

The fundi of 14 climbers were monitored on ascent to 6000 metres over a 15 day period in the Nepal Himalaya. A total of 4 climbers experienced symptomless haemorrhages. These haemorrhages were not secondary to changes in haemoglobin concentration, nor did they appear correlated to the use of acetazolamide. The risk of developing retinal haemorrhage was, however, significantly greater in the better acclimatized individuals. Possible reasons for this relationship are discussed.

Acetazolamide↗
PubMed1987

Developmentally regulated primary glucocorticoid hormone induction of chick retinal glutamine synthetase mRNA.

We have characterized the glucocorticoid hormone induction of glutamine synthetase mRNA in embryonic chick retinal organ cultures by quantitative dot hybridization using a cDNA clone derived from chick retinal RNA. Hydrocortisone (Kapp = 3-4 nM) and dexamethasone (Kapp = 1-2 nM) produce an approximate 30-fold increase in glutamine synthetase mRNA after incubation of organ cultures derived from embryonic day 12 retinae with either hormone for 3 hr. Progesterone is a poor inducer. The glucocorticoid-mediated rise is rapid (t1/2 = 2-3 hr) and occurs in the presence of either of the protein synthesis inhibitors cycloheximide or puromycin, indicating that the induction is a primary or direct response to the hormone. However, the magnitude of the hormonal response observed in culture increases markedly during retinal development. These observations, coupled with the previously reported absence of a hormonal induction in embryonic liver, raise the possibility of a synergistic mechanism, involving tissue-specific regulatory molecules in addition to the glucocorticoid hormone receptor, to explain the retinal-specific primary glucocorticoid hormone induction of glutamine synthetase mRNA.

Animals↗
PubMed1993

Pathophysiology and treatment of clinically resistant cytomegalovirus retinitis.

PURPOSE: To determine the incidence, pathophysiology, clinical outcome, and survival in patients with clinically resistant retinitis. METHODS: Cytomegalovirus (CMV) retinitis was prospectively studied in 100 patients with acquired immune deficiency syndrome (AIDS). In 11 of these patients, clinically resistant retinitis developed, defined as new activity or progression, despite at least 8 consecutive weeks of induction doses of either foscarnet or ganciclovir. Fundus photography, pharmacokinetics, CMV cultures and sensitivities, and survival analyses were studied. The therapeutic interventions attempted after clinically resistant retinitis was identified included continuing a high dose (induction level) of the same antiviral drug, changing the antiviral drug, and combining antiviral therapy with foscarnet and ganciclovir. RESULTS: Clinically resistant retinitis occurred in 11 (11%) of 100 patients with CMV retinitis and appeared to be a manifestation of acquired CMV antiviral drug resistance. Drug metabolism and pharmacokinetics in these patients were normal. The use of combination therapy with foscarnet and ganciclovir was effective in halting the progression of retinitis in three (75%) of four patients (6 of 7 eyes able to be evaluated) receiving combination therapy. CONCLUSION: Clinically resistant retinitis is a manifestation of infection by CMV that has acquired drug resistance. In these patients, combination antiviral drug treatment should be considered. It is likely that clinically resistant retinitis will become more frequent as patients with CMV retinitis and AIDS survive longer.

AIDS-Related Opportunistic Infections↗
PubMed1998

neuroD induces photoreceptor cell overproduction in vivo and de novo generation in vitro.

The molecular mechanisms underlying the generation of the various types of cells in the vertebrate retina are largely unknown. We investigated the possibility that genes belonging to the basic helix-loop-helix (bHLH) family of transcriptional factors participate in cell-type specification during retinal neurogenesis. Chick neuroD was isolated from an embryonic cDNA library and its deduced amino acid sequence showed 75% identity with mouse neuroD. In situ hybridization showed that neuroD was expressed in cells located at the outer portion of the developing retinal neuroepithelium, the location where prospective photoreceptors reside. Misexpression of neuroD in retinal neuroepithelium through replication-competent, transformation-deficient retroviruses produced a retina with three, instead of two, layers of photoreceptor cells; the number of cells that express visinin, a marker for cone photoreceptors, increased over 50% compared to control embryos misexpressing the green fluorescent protein. No significant changes were observed in the number of other retinal neurons, including those that express RA4 (ganglion cells), pax6 (ganglion cells and amacrine cells), and chx10 (bipolar cells). Retroviral-driven misexpression of neuroD in monolayer cultures of retinal pigment epithelium yielded de novo production of photoreceptor cells with no other types of retinal neurons detected. We propose that neuroD is important for photoreceptor cell production in the vertebrate retina.

Amino Acid Sequence↗
PubMed2002

Zebrafish mutagenesis yields eye morphological mutants with retinal and lens defects.

A chemical mutagenesis to identify zebrafish eye morphological mutants was performed by screening F(3) larvae at 5 and 7 days post-fertilization (dpf) for changes in eye or pupil size. Based on histological analysis, four different phenotypic classes were obtained. The two Class I and three Class II mutants are all characterized by small eyes and exhibit defects in early retinal development or unregulated cell death, respectively. The single Class III mutant has reduced ocular pigmentation. The three Class IV mutants display defects in the ocular lens, including one mutant line with normal sized eyes and pupils that develops lens opacity at 7 dpf.

Animals↗
PubMed1984

Retinal oxygen tension and oxygen reactivity in retinopathy of prematurity in kittens.

In the first series of experiments, preretinal oxygen tensions were measured using microelectrodes in newborn kittens, at 6 +/- 2 days of age, following their placement in an atmosphere of 80 to 90% oxygen for 5 +/- 1 day. The oxygen exposure caused an obliteration of the normally developing retinal vasculature. Preretinal oxygen tensions in the resultant avascular retina were close to zero while those in the vascular retina were near normal. The avascular retina was a "sink" for ocular oxygen. Oxygen breathing resulted in expected increases in preretinal oxygen tension, but, surprisingly, the preretinal oxygen tension decreased with continued oxygen administration. Because the oxygen tension in the avascular retinal area is determined primarily by the choroidal circulation, we speculated that increased oxygen caused a decreased choroidal blood flow. In the second series of experiments, however, choroidal blood flow was measured in the kittens by applying a temperature probe to the sclera and oxygen breathing did not appear to have an effect. These results did not support the initial speculation. It may be that the decrease in preretinal oxygen tension observed with continued oxygen administration resulted from progressive increase in utilization.

Animals↗