Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RETINA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1989

Photoreceptor topography of the retina in the adult pigtail macaque (Macaca nemestrina).

In spite of the crucial role retinal photoreceptors play in mapping optical images into a pattern of neural excitation, there are no complete studies of photoreceptor topography in any primate retina. We have measured the spatial density and inner segment areas of cones and rods across the whole mounted retinas of three adult pigtail macaques (Macaca nemestrina) and constructed maps of photoreceptor density and inner segment diameter. These retinas contain an average of 3.1 million cones (2.8-3.3 million), with an average peak foveal cone density of 210,000 cones/mm2 (190,000-260,000 cones/mm2). Cone density falls steeply with increasing eccentricity, to 100,000 cones/mm2 at 200 microns from the fovea, and to 50,000 cones/mm2 at 750 microns. Imposed on this gradient is a "streak" of higher cone density along the horizontal meridian. At equivalent eccentricities, cone density is higher in nasal and inferior retina. Cone inner segments increase in diameter from 2.3 microns at the foveal center to 11 microns in far temporal retina and 10 microns in far nasal retina. These retinas contain an average of 60.1 million rods (44.9-75.3 million). Rod density is zero within 20 microns of the foveal center, increases to the crest of a "rod ring" at the eccentricity of the optic disk, and then declines. Central rod topography is asymmetric, with higher densities in superior retina. Density along the crest of the rod ring peaks in superior retina at 177,000 rods/mm2, dips as low as 120,000 rods/mm2 along the horizontal meridian, and increases to about 150,000 rods/mm2 in inferior retina. Far peripheral rod topography is relatively symmetric around the fovea. Rod inner segment diameter ranged from 1.5 microns in the fovea to 4 microns at the temporal edge and 3.4 microns at the nasal edge of the retina. At eccentricities exceeding 6 mm, rod inner segment diameter was greater temporally than nasally. Cone inner segments cover 85-90% of the central fovea, with extrareceptor space accounting for the remainder. Cone coverage declines with increasing eccentricity to 20% at the temporal edge and 35% at the nasal edge of the retina. In contrast, rod coverage increases from zero at the foveal center to a maximum of 65% in temporal retina and 50% in nasal retina. The photoreceptor topography of the pigtail macaque is qualitatively similar to that of other macaques and to humans. Photoreceptor topography is formed by a complex interaction between regional changes in cone and rod density and inner segment diameter.

Animals↗
PubMedDate not supplied

Long-term ERG analysis in the partially light-damaged mouse retina reveals regressive and compensatory changes.

Most of the blinding retinopathies are due to progressive photoreceptor degeneration. Treatment paradigms that are currently being investigated include strategies to either halt or slow down photoreceptor cell loss, or to replace useful vision with retinal prosthesis. However, more information is required on the pathophysiological changes of the diseased retina, in particular the inner retina, that occur as a consequence of photoreceptor cell loss. Here we wished to use light damage as a stoppable insult to determine the structural and functional consequences on inner and outer retina, with the overall goal of determining whether survival of a functional inner retina is possible even if the outer retina is damaged. Mice were exposed to a 20-day light-damage period. Electroretinograms (ERG) and morphology were used to assess subsequent recovery. Outer retina was monitored analyzing a-waves, which represent photoreceptor cell responses, and histology. Integrity of the inner retina was monitored, analyzing b-waves and oscillatory potentials (OP1-OP4) and immunohistochemical markers for known proteins of the inner retina. All six ERG components were significantly suppressed with respect to amplitudes and kinetics, but stabilized in a wave-dependent manner within 40-70 days after the end of light exposure. As expected, damage of the outer retina was permanent. However, function of the inner retina was found to recover significantly. While b-wave amplitudes remained suppressed to 60% of their baseline values, OP amplitudes recovered completely, and implicit times of all components of the inner retina (b-wave and OP1-OP4) recovered to a level close to baseline values. Histological analyses confirmed the lack of permanent damage to the inner retina. In summary, these data suggests that the inner retina has the potential for significant recovery as well as plasticity if treatment is available to stop the deterioration of the outer retina.

Animals↗
PubMed2004

Comparative gene expression analysis of murine retina and brain.

PURPOSE: Several high-throughput studies have described gene expression in the central nervous system (CNS), and recently there has been increasing interest in analyzing how gene expression compares in different regions of the CNS. As the retina is often used as a model system to study CNS development and function, we compared retina and brain gene expression using microarray analyses. METHODS: Mouse retina, brain and liver RNA was hybridized to a custom cDNA microarray containing 5,376 genes and ESTs, and the data from the quantified scanned images were analyzed using Bioconductor and SAM. Preferential retina expression was confirmed by real-time PCR. The cellular distribution of genes newly identified as retina enriched genes was determined by immunohistochemistry. RESULTS: Using stringent statistical analyses we identified 733 genes that were preferentially expressed in retina and 389 in brain. The retina-liver hybridizations identified an additional 837 retina enriched genes. The cellular distribution in the retina was determined for two genes that had not previously been reported to be expressed in the retina, the transcription regulatory proteins EWS and PCPB1. Both proteins were found primarily in the inner nuclear layer. Finally, a comparison of the microarray data to publicly available SAGE and EST library databases demonstrated only limited overlap of the sets of retina enriched genes identified by the different methodologies. The preferential retinal expression of a subset of genes from the microarray, which were not identified as differentially expressed by other methods, was confirmed by quantitative PCR. CONCLUSIONS: The finding of differences in the groups of identified retina enriched genes from the various profiling techniques supports the use of multiple approaches to obtain a more complete description of retinal gene expression. Characterization of gene expression profiles of retina and brain may facilitate the understanding of the processes that underlie differences between the retina and other parts of the central nervous system.

Animals↗
PubMed1992

Müller cells in vascular and avascular retinae: a survey of seven mammals.

Eight monoclonal antibodies were used to label Müller cells in four mammals that have vascular retinae (cats, dogs, humans, and rats) and in three with avascular retinae (echidnas, guinea pigs, and rabbits). Müller cells were found to have a fairly uniform retinal distribution in seven species, with a mean density of 8,000-13,000 cells mm-2. Müller cells in avascular retinae differ from their vascular counterparts in four respects. First, they are shorter than those in vascular retinae. This difference is mainly due to a reduction in the thickness of the outer nuclear layer. Second, the trunks of Müller cells in avascular retinae tend to be thicker, although those in echidnas are an exception to this trend. Third, Müller cell rootlets in avascular retinae follow a more tortuous course than those in vascular retinae, reflecting the fact that photoreceptor nuclei in the two types of retina have different shapes and stacking patterns. Fourth, due to a reduction in the density of photoreceptors in avascular retinae, there are fewer neurones per Müller cell. Although these four features may enable Müller cells to assist the nutrition of neurones in the inner layers of avascular retinae, they are unlikely to be morphological specializations that have evolved for that purpose. Rather, these features appear to be a direct consequence of the fact that avascular retinae are thinner and have a differently organised outer nuclear layer. These features aside, Müller cells in avascular retinae closely resemble their counterparts in vascular retinae.

Animals↗
PubMed1990

Diffusion of O2 in normal and ischemic retinas of anesthetized miniature pigs in normoxia and hyperoxia.

Transretinal PO2 profiles were recorded with O2-sensitive microelectrodes in the normal retina and in ischemic retinal foci induced by the occlusion of a retinal branch vein with argon laser photocoagulation in anesthetized miniature pigs. In the normal retina there are two PO2 gradients: one from the inner retina and the other from the choroid, both directed toward the middle of the retina. Both PO2 gradients persisted during hyperoxia. Thus, even in hyperoxia, the choroid does not supply the whole thickness of the normal retina with O2. Preretinal and transretinal PO2 measurements in ischemic inner retinal foci showed the existence of two PO2 gradients in steady-state systemic normoxia, as did those in the normal retina. This finding indicates that even in ischemia the choroid does not supply O2 to the inner retina; as a result, tissue hypoxia is maintained. During systemic hyperoxia, the intraretinal PO2 measurements in the ischemic foci showed only one gradient going from the choroid toward the inner retina. This gradient indicates that under these conditions, the choroid can supply O2 to the entire thickness of the ischemic retina. Extending a previously formulated hypothesis, we propose that in the ischemic retina as opposed to the normal retina, hyperoxia does not induce an increase in the O2 consumption of the outer retina. This suggestion could explain the rise in PO2 in the inner ischemic retina during hyperoxia.

Animals↗
PubMedDate not supplied

The rod circuit in the rabbit retina.

Mammalian retinae have a well-defined neuronal pathway that serves rod vision. In rabbit retina, the different populations of interneurons in the rod pathway can be selectively labeled, either separately or in combination. The rod bipolar cells show protein kinase C immunoreactivity; the rod (AII) amacrine cells can be distinguished in nuclear-yellow labeled retina; the rod reciprocal (S1 & S2) amacrine cells accumulate serotonin; and the dopaminergic amacrine cells show tyrosine-hydroxylase immunoreactivity. Furthermore, intracellular dye injection of the microscopically identified interneurons enables whole-population and single-cell studies to be combined in the same tissue. Using this approach, we have been able to analyze systematically the neuronal architecture of the rod circuit across the rabbit retina and compare its organization with that of the rod circuit in central cat retina. In rabbit retina, the rod interneurons are not organized in a uniform neuronal module that is simply scaled up from central to peripheral retina. Moreover, peripheral fields in superior and inferior retina that have equivalent densities of each neuronal type show markedly different rod bipolar to AII amacrine convergence ratios, with the result that many more rod photoreceptors converge on an AII amacrine cell in superior retina. In rabbit retina, much of the convergence in the rod circuit occurs in the outer retina whereas, in central cat retina, it is more evenly distributed between the inner and outer retina.

Animals↗
PubMed2003

Non-uniform distribution of lesions and biochemical abnormalities within the retina of diabetic humans.

OBJECTIVE: Microaneurysms, acellular capillaries, pericyte ghosts, and thickening of retinal capillary basement membrane are characteristic of diabetic retinopathy, and are believed to be sequelae of excessive blood glucose. Previous studies by us in dogs demonstrated that lesions of diabetic retinopathy were not uniformly distributed across the retina, but were significantly more numerous in the superior/temporal areas of the retina. In the present study, the distribution of these lesions and the biochemical abnormalities postulated to play a role in their pathogenesis have been evaluated in retinas collected at autopsy from diabetic patients. METHODS: Retinas were divided into quadrants (nasal, temporal, superior, inferior), the vasculature exposed by the trypsin-digest method, and the frequency of the lesions compared among the quadrants. Homogenates taken from the mid-retina of nasal and temporal quadrants of retina were used to explore regional differences in expression of Glut1, PKCbeta, and iNOS (Western blots) and caspases (enzymatic activity). RESULTS: Microaneurysms, acellular capillaries and pericyte ghosts were not uniformly distributed across the retina, and were significantly more numerous in the temporal retina than in the nasal retina (P < 0.05). In contrast, the thickness of retinal capillary basement membrane was not found to differ significantly across the retina. In our limited study, activity of the pro-inflammatory protease, caspase 1, was the only biochemical abnormality where there was both a significant diabetes-induced alteration in activity and also a significant difference between retinal quadrants. Expression of the glucose transporter, Glut1, was significanlty decreased in diabetes, but there was no significant difference in expression between the quadrants. Expression of iNOS was increased only in temporal retina in diabetes (but no significant difference between quadrants), and PKCbeta tended to be greater than normal in both temporal and nasal retina. CONCLUSIONS: Retinal microvascular disease does not develop uniformly across the retina of diabetic patients, even though the different regions are exposed to the same level of hyperglycemia.

Aged↗
PubMed1996

Oxygen consumption in the avascular guinea pig retina.

Oxygen consumption across the retina of a mammal with a naturally avascular retina has not previously been investigated. The oxygen consumption across the avascular retina of the guinea pig was measured in vivo by spatial analysis of the intraretinal oxygen profile. The avascular nature of the guinea pig retina allows the inner retina to be included in the analysis without disrupting the normal physiological state of the retina. Oxygen-sensitive microelectrodes (1-micron tip) were used to make high-resolution measurements of oxygen tension through the retina of anesthetized, mechanically ventilated guinea pigs (n = 10). Oxygen profiles were then analyzed in terms of oxygen tension as a function of distance from the choriocapillaris/Bruch's membrane, and the data were fitted to an established mathematical model of retinal oxygen consumption. The average oxygen consumption of the full thickness of the guinea pig retina was 1.1 +/- 0.09 ml O2.min-1 x 100 g-1 (n = 10). The average oxygen consumption of the outer half of the retina was 2.07 +/- 0.17 ml O2.min-1 x 100 g-1, while that of the inner half was only 0.12 +/- 0.04 ml O2.min-1 x 100 g-1. A localized region of high oxygen consumption was identified in the outer retina in every case, and this region accounted for an average of 93.9 +/- 2.0% of the total retinal oxygen consumption. Only 5.2 +/- 1.4% of the total oxygen consumption was attributable to the inner half of the retina. When choroidal oxygen tension was increased via a combination of systemic hyperoxia and hypercapnia, high oxygen levels could be sustained in all retinal layers. Under these conditions of an excess oxygen supply, the inner retina still consumed only 0.45 +/- 0.11 ml O2.min-1 x 100 g-1, which was 13.8 +/- 2.5% of the total retinal oxygen consumed. The relatively low oxygen consumption in the inner retina of the guinea pig may reflect an interesting adaptation to the constraints imposed by the absence of a retinal circulation in this species.

Animals↗
PubMed2000

Diabetes downregulates GLUT1 expression in the retina and its microvessels but not in the cerebral cortex or its microvessels.

Capillaries in the retina are more susceptible to develop microvascular lesions in diabetes than capillaries in the embryologically similar cerebral cortex. Because available evidence implicates hyperglycemia in the pathogenesis of diabetic retinopathy, differences in glucose transport into the retina and brain might contribute to this observed tissue difference in susceptibility to diabetes-induced microvascular disease. Thus, we compared levels of GLUT1 and GLUT3 expression in the retina, cerebrum, and their respective microvessels by Western blot analysis. In nondiabetic animals, the content of GLUT1 protein in retina and its microvessels was multifold greater than that of cerebral cortex gray matter and its microvessels. Streptozotocin-induced diabetes of a 2-week or 2-month duration reduced GLUT1 expression in the retina and its microvasculature by approximately 50%, but it resulted in no reduction in GLUT1 expression in cerebrum or its microvessels. The density of capillaries in retinas of diabetic animals did not change from normal, and so the observed decrease in GLUT1 expression in the retina and retinal capillaries of diabetic animals cannot be attributed to fewer vessels. Despite the diabetes-induced reduction of GLUT1 expression in retina, neural retina of diabetic rats still possessed more GLUT1 than the cerebrum. Retinal pigment epithelium (RPE) possessed more GLUT1 than neural retina or its microvessels, and expression of the transporter in the RPE was not affected by diabetes. GLUT3 levels were greater in cerebral gray matter than in retina, and they were unaffected by diabetes in either tissue. The effect of diabetes on GLUT1 expression differs between retina and cerebral cortex, suggesting that glucose transport is regulated differently in these embryologically similar tissues. Because diabetes results in downregulation of GLUT1 expression in retinal microvessels, but not in RPE, the fraction of the glucose entering the retina in diabetes is likely to be greater across the RPE than across the retinal vasculature.

Animals↗
PubMed1986

Rabbit ocular and pineal autoimmune response to retina antigens.

Different forms of experimental autoimmune uveitis (EAU) can be produced by varying protocols to present different autoantigens to several species of experimental animal. We have studied the clinical, histological and serological responses of rabbits to footpad injection of various fractions of retina extract. Rabbits injected with retina extract or S antigen developed posterior uveitis. However, rabbits injected with retina extract, also developed an anterior uveitis and pinealitis not seen in rabbits receiving S antigen. The Serological response of rabbits to retina extract was different than that to purified S antigen. Antisera of rabbits receiving retina extract reacted with rabbit retina and pineal gland as well as with guinea pig retina but not with guinea pig pineal gland. In contrast anti-S antigen sera reacted with rabbit retina and guinea pig retina and pineal gland but not with rabbit pineal gland. Gel filtration chromatography of the ammonium sulfate supernate of retina extract was used to differentiate the antigens with which these two sera reacted. An analysis of these experiments gives preliminary evidence of an autoantigen(s) of rabbit retina and pineal gland that is not S antigen. The existence of multiple autoantigens common to retina and pineal gland in various species is significant in that it further underscores the relationship of these tissues. Furthermore, it is not unrealistic to expect more than one autoantigen of retina or uvea to be involved in autoimmune uveitis.

Animals↗
PubMedDate not supplied

[Cell sources, regulatory factors and gene expression in the regeneration of the crystalline lens and retina in vertebrate animals].

Over the past century extensive experimental materials have been accumulated concerning cell sources of lens and retina regeneration, successive transformations of the cells, regulatory factors, and gene expression during restitution of these eye structures. The use of nuclear and cytoplasmic markers provided convincing evidence that the removed lens is restituted from the dorsal iris cells in vivo or from embryonic cells of the pigment epithelium and retina in vitro. The removed or destroyed retina is restituted as a result of transdifferentiation of the pigment epithelium cells in amphibians, fish, birds, and mammals during embryogenesis, in larvae of some anuran amphibians, and in adult newts. Cell precursors of rods are a cell source of retina regeneration in adult fish. A subpopulation of randomly distributed cells, which are a cell source of rod formation during the normal development of the eye was found in the external nuclear layer with the use of electron microscopy and nuclear and cytoplasmic markers. These cells are not only a source of regeneration of rods, but also of cones and cells of the internal nuclear layer after destruction of the corresponding retina layers. There is a peripheral growth area in the retina of vertebrates, where multi- and unipolar cells are localized, which provide for the retina growth during ontogenesis. A paradox of retina regeneration consists in that these little differentiated cells are not a source of complete restitution of the removed or destroyed retina. They make only a small contribution to its regeneration corresponding to the growth potential of cells of this eye region, while restitution of the retina proceeds only at the expense of cells of another type of differentiation. A factor controlling the differentiated state of the cell was found in the dorsal iris during studies of lens regeneration. Removal of this factor in the early stages of cell transformations leads to the initiation of lens regeneration. The factor is not specific and was identified in many cells of vertebrates, including the pigment epithelium and limb tissues, which, as is known, may be fully restituted. Studies of gene expression during lens and retina regeneration are now at the initial stage. The greatest advances were achieved on the model of transdifferentiation of the pigment epithelium cells of chick embryos into lentoids. Expression of genes MMP115 and pP344 was established in the pigment epithelium cells, which characterize the pigmented phenotype of the initial cells. Expression of the alpha-, beta-, and delta-crystallin genes was found in the lentoids, which characterize the phenotype of regenerating structures. The gene activity appears to be switched at an intermediate stage during cell dedifferentiation. Expression of the gamma-crystallin genes during lens regeneration in adult newts is initiated after completion of dedifferentiation and cell proliferation in the dorsal iris. The genes specifically expressed in the dorsal and ventral iris and in the retina rudiment have been identified by the method of gene subtraction. Expression of homeobox-containing genes from the family of PAX genes was found during lens regeneration in adult newts and retina regeneration in adult fish. The role of growth factors (FGF) as morphogenetic factors was proved, which are involved in a yet unknown way of altering the differentiation pathway of the initial cells during formation of the neuroepithelium rudiment in chick embryos, adult newts, and fish.

Animals↗
PubMed1997

Comparative study of astrocytes in human and rabbit retinae.

Immunohistochemical location of Glial Fibrillary Acidic Protein (GFAP) was used to compare the morphology of astrocytes in vascularized and partially vascularized retinae (human and rabbit, respectively). Astrocytes in human and rabbit retinae were found in the same regions as the blood vessels. These cells in partially vascularized retinae differed from those in vascularized retina in several respects. Firstly, there were six morphological types in rabbit retina and only two in human retina. Secondly, in rabbit retinae there were astrocytes only related to blood vessels called "perivascular astrocytes" which were absent in human retinae. Thirdly, the astrocytes were located in the nerve fiber layer and ganglion cell layer in both types of retinae, but in human retinae these cells could also be seen in the internal nuclear layer. These observations demonstrate that there are many differences between astrocytes in human and rabbit retina, suggesting that rabbit retina could be used with caution as an experimental model in comparative studies with human retina.

Animals↗
PubMed1980

Development and degeneration of retina in rds mutant mice: light microscopy.

Changes during the development and degeneration of the retina in 020/A mice, which are homozygous for the newly reported rds (retinal degeneration slow), gene were studied by histological and enzyme-histochemical methods with Balb/c mice carrying the normal allele as control. During normal development the total thickness of the retina grows from the time of birth till the age of 21 days and thereafter gradually diminishes, while the thicknesses of the component layers show a characteristic and differential change in course of their histogenesis. In the normal retina the perikarya of the cones are more frequent in the central than in the peripheral areas. The cone frequency in the central retina, but not in the periphery, increases with age and implies selective loss of rod cells in older animals. In the homozygous rds mice, the receptor layer remains rudimentary, but the other retinal layers show a normal trend of growth during the first 2 weeks after birth. Thereafter th morphological layers containing visual cell structures--the receptor, the outer nuclear, and the outer plexiform layers--begin to reduce. The loss of visual cells is readily marked by the reduction of the outer nuclear layer and is first evident at 2 weeks after birth. Degeneration is more rapid up to the age of 2-3 months, when the outer nuclear layer is reduced to half of its original thickness; thereafter degeneration progresses more slowly. The receptor and the outer plexiform layers are also simultaneously reduced. At 9 months, the peripheral parts of the retina, and at 12 months, the entire retina is completely lacking in visual cells. In the central retina of the mutant, rod and cone cell populations are equally affected up to the age of 6 months, as their relative frequency remains similar to the normal. In the peripheral retina, where cell loss is more pronounced, and in the central retina at 9 months an increase in relative frequency of cones is recorded and indicate increased susceptibility of the rods to later degenerative changes. The inner parts of the retina, including inner nuclear, inner plexiform, and ganglion cell layers, remain morphologically unaffected until irregular vascularization follows total loss of visual cells. The pigment epithelium is also affected at this late stage and appears depleted and patchy. In the normal retina, macrophages which are positively stained for the enzyme N-acetyl-beta-glucosaminidase appear in the inner layers with the growth of the retinal vasculature. In the mutant, increased frequency and stainability of the macrophages are discernible in the inner retina at 11 days. The macrophages migrate outwards and are observed in the outer nuclear layer and in the optic ventricle during the period of degeneration. These findings are compared with the observations in the other retinal degeneration mutants in rodents, and in retinitis pigmentosa in humans. The suitability of the rds mice as an animal model system for the human disease is emphasized.

Animals↗
PubMed1992

Ontogeny of somatostatin immunoreactivity in the cat retina.

In the ganglion cell layer of the adult cat retina, subgroups of displaced amacrine cells and alpha ganglion cells are immunoreactive for somatostatin or a somatostatinlike substance. Both types of immunoreactive cells are found preferentially in inferior retina. We studied the development of somatostatin immunoreactivity in the prenatal and postnatal cat retina to determine how such unusual distributions of immunoreactive cells arise. Somatostatin-immunoreactive profiles were first observed at embryonic day (E) 30, within the inner retina in a central region that included the optic disk and the area centralis. By E36, immunoreactivity had virtually disappeared from the central retina but was present throughout the periphery. The immunoreactive profiles could not be classified morphologically because of their immaturity but were most likely retinal ganglion cells, the earliest born cells of the inner retina. Of the two types of immunoreactive cell observed in the adult, the first to be recognized morphologically was the displaced amacrine cell, at E45. These cells were virtually adultlike in morphology and number by E51, two weeks before birth. In contrast, immunoreactive alpha ganglion cells were not apparent until five days after birth and did not achieve their mature numbers and immunoreactive staining characteristics until more than a month later. From the time they could initially be recognized, both immunoreactive displaced amacrine cells and alpha cells were distributed mainly in the inferior retina. A third type of somatostatin-immunoreactive cell was transiently observed in the superior and inferior retina during prenatal and early postnatal development. These cells were characterized by granular staining in irregular shapes and few, if any, faintly stained processes. Injections of retrograde tracers into retinorecipient targets revealed that many of these cells were retinal ganglion cells. They disappeared by postnatal day 38. Our results indicate that somatostatin immunoreactivity initially follows a central-to-peripheral pattern of development, as is typical of other developmental events in the mammalian retina. They also indicate that the two types of somatostatin-immunoreactive neurons present in the adult cat retina (displaced amacrine and alpha ganglion cells) attain their mature immunocytochemical properties with very different timecourses. Finally, the observation that somatostatin immunoreactivity appears transiently in the granular-staining ganglion cells, distributed throughout the superior and inferior retina, suggests that the peptide may play a regulatory role in the development of the retina and/or retinofugal pathways.

Animals↗
PubMed1983

The enzymatic estimation of organic hydroperoxides in the rat retina.

An enzymatic procedure for the estimation of organic hydroperoxides has been adapted to biological tissues and applied to the measurement of hydroperoxides in the rat retina. Hydroperoxides are determined from the coupled activities of glutathione peroxidase and glutathione reductase as measured by the loss of NADPH absorbance. To minimize the effects of tissue catalyzed peroxide degradation, incubations were performed in the presence of 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU); which inhibited the activity of retinal tissue glutathione reductase by 85%. For comparisons to the enzymatic technique, retinal tissue hydroperoxides were also estimated by the absorption of tissue extracts at 232 nm. Using the enzymatic procedure the hydroperoxide concentration in whole retina homogenates was significantly higher in 19-day-old rats than in either 35-day or adult animals. Hydroperoxides in the retina of young rats exposed to light for one hour were significantly lower than in non-exposed controls, while in adult rats, following light, hydroperoxides increased 13%. Fractionation of rat retinas into crude ROS and retina minus ROS components revealed that the ROS fractions contain at least twice the hydroperoxide concentration of the remaining retina. The concentration of hydroperoxides in the ROS fractions from dark-reared rats were significantly lower than in cyclic-light-reared animals. In both types of rats, one hour intense light exposure resulted in an increase in ROS hydroperoxides but the increases were not significant. ROS hydroperoxides were also found to be 85-90% water soluble. Estimates of the retinal hydroperoxide content obtained by absorption at 232 nm gave similar results to the enzymatic technique, but the levels were significantly lower. When retinas were maintained in vitro for one hour before analysis, hydroperoxides determined by either technique were significantly higher than in retinas assayed immediately, but A232 hydroperoxides were still significantly lower than hydroperoxides measured by the enzymatic procedure. It is concluded: (1) that the observed retinal hydroperoxide concentration depends upon animal age and the method of measurement; (2) that within the retina the photoreceptor cell contains at least a two-fold higher concentration of hydroperoxides than the remaining retina and that prior light history can affect those hydroperoxide levels (it appears that the photoreceptor cell is also a major site of hydroperoxide formation in the retina); (3) that during intense light exposure of short duration significant levels of hydroperoxides do not accumulate in the retinas of rats.

Animals↗
PubMed1988

Opsin, G-protein and 48-kDa protein in normal and rd mouse retinas: developmental expression of mRNAs and proteins and light/dark cycling of mRNAs.

Retinal degeneration in rd mice is manifested during the most rapid period of postnatal photoreceptor differentiation and is hypothesized to be caused by a lesion in cGMP metabolism. We have studied the sequence of developmental expression of three proteins involved in the cGMP cascade and the mRNAs from which they are translated, in rd and control mouse retinas. Slot blot analysis of retinal RNAs indicates that the mRNAs coding for opsin, the alpha, beta and gamma subunits of G-protein and 48-kDa protein each has the same time for onset of expression in normal and diseased retinas. G beta and 48-kDa protein mRNAs are already detectable at birth, opsin mRNA appears by postnatal day 5 (P5), G gamma mRNA at P6 and G alpha mRNA by P8. The levels of all these mRNAs decrease in the diseased retinas after P11-P12, correlating with the reduction in photoreceptor cell number that characterizes the rd disease. Immunocytochemistry indicates that the 48-kDa protein is present at birth, G gamma and opsin are detectable at P4 and G alpha at P7. After P7, opsin and G-protein immunoreactivity are localized throughout the photoreceptor cell in the rd retinas but they are found only in the outer segment in control retinas. The 48-kDa protein immunoreactivity, which is observed in the whole photoreceptor layer both in rd and control retinas throughout development, is the only one of all immunoreactivities analysed that remains at 2 months of age in the rd retina and is probably localized in cones. However, at 6 months of age, 48-kDa protein immunoreactive cells are no longer present in the rd retina. We have also investigated whether there is a daily rhythm for the levels of mRNA present at different times during the light/dark periods in developing rd/rd and rd/+ retinas and in adult normal (+/+) retinas. We find that the levels of each mRNA analysed appear to cycle in the +/+ adult retina, with the greatest amount of opsin and the three subunits of G-protein mRNAs occurring just before light onset and the greatest amount of 48-kDa protein mRNA occurring just before lights off. Cycling in the developing diseased or control retinas (P0-P12) is not observed and may be masked by the pronounced cell growth that occurs during this period.

Aging↗
PubMed1995

Oxygen consumption in the isolated toad retina.

Retinal O2 utilization was studied to identify the O2 consuming processes in the retina and the spatial distribution of those processes. Neural retina, retinal pigment epithelium and choroid were dissected from the toad eye and superfused with an oxygenated Ringer's solution. Double-barreled microelectrodes were used to measure O2 and local voltage simultaneously within the retina in both light and dark adaptation. The profile of PO2 was measured during a withdrawal of the electrode tip across the retinal pigment epithelium and through the neural retina. The PO2 decreased through the distal retina, reaching a minimum in the inner segment or outer nuclear layer, and then increased steadily through the proximal retina. From fitting PO2 profiles measured in the dark-adapted retina to a three-layer diffusion model, O2 consumption was found to be 1.0 +/- 0.4 and 0.4 +/- 0.3 ml O2 (100 g min)-1 in the outer and inner halves of the retina, respectively. Light decreased consumption in both halves of the retina. In steady illumination (500 nm) that saturated the ERG b- and c-waves, O2 utilization decreased significantly to 48% and 68% of the dark values in the outer and inner retina, respectively. When Na+ was removed from the superfusate to inhibit the photoreceptor Na+/K+ pump, O2 consumption in the outer retina decreased by about the same amount as in light, but O2 consumption in the inner retina was not significantly affected.

Adaptation, Ocular↗
PubMed1989

Light-evoked increases in [K+]o in proximal portion of the dark-adapted cat retina.

1. The scotopic threshold response (STR) and slow negative response are negative-going potentials in the dark-adapted electroretinogram (ERG) of the cat eye that originate proximal to the photoreceptors and are present at threshold and with dim illuminations. The present paper examines the hypothesis that these events are associated with Müller cell responses to potassium released by proximal retinal neurons by measuring light-dependent changes in extracellular K+ concentration [( K+]o, in proximal retina. 2. Extracellular field potentials and changes in [K+]o, evoked in response to diffuse illumination of the dark-adapted retina, were recorded with a double-barreled K+-sensitive microelectrode placed in the retina at different depths. The vitreal ERG was recorded at the same time. 3. The dynamic range of the light-evoked increases in [K+]o, recorded in proximal retina from threshold to saturation, was strikingly similar to that of the STR and slow negative response. The threshold for the [K+]o increase was near that of the most sensitive ganglion cells, and the response saturated approximately 2.4 log units below rod saturation. Also, onset latencies and rates of rise for the increases in [K+]o and the field potentials in proximal retina followed similar functions of intensity. 4. The depth distribution of the light-evoked [K+]o increases resembled that of the STR. The increases in [K+]o were largest and fastest in proximal retina where the STR was largest. This was true both for very low intensity stimuli, below the threshold for PII (DC-component and b-wave) in distal retina, and for stimulus intensities near STR saturation, where PII (DC-component) was present. For stimuli of intensities near rod saturation, when the b-wave was present in distal retina, there was a small fast increase in [K+]o at light onset in distal retina and a slower increase in proximal retina. Both increases were truncated by spread of the large light-evoked decrease in [K+]o in subretinal space that is known to cause the c-wave in the ERG and slow PIII in neural retina. 5. The duration of the increases in [K+]o in proximal retina was more sustained than the proximal field potentials. In response to stimuli of 2-4 s, the field potential began to recover toward base line after about 300 ms, whereas the increases in [K+]o remained at maximal levels until stimulus offset.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗