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At least 1,207 records · Page 67Linked to original sources
PubMed1998

The role of the p53 protein in the selective vulnerability of the inner retina to transient ischemia.

PURPOSE: To determine whether the p53 protein plays a role in the selective vulnerability of the inner retina to transient ischemia. METHODS: Transient retinal ischemia was induced using a high intraocular pressure (HIOP) model in the Sprague-Dawley rat for 60 minutes. Histopathologic outcome was determined 7 days after ischemia. In addition, analysis for evidence for apoptosis (TdT-dUTP terminal nick-end label [TUNEL] staining) and p53 protein expression (immunohistochemistry) was performed at several points during the reperfusion period. In a separate set of experiments, wild-type mice and two groups of transgenic mice, one homozygous and the other heterozygous for the p53 null gene, were also subjected to HIOP for 60 minutes, and histopathology was performed 7 days later. RESULTS: At 7 days subsequent to 60 minutes of ischemia in the rat, there was marked thinning of the inner retinal layers. There were scattered TUNEL-positive cells within the inner retina, peaking at 24 to 48 hours and persisting for at least 7 days. p53 immunochemistry demonstrated elevated protein levels within the inner retina; this finding peaked at 24 to 48 hours but was no longer present at 4 days after ischemia. TUNEL staining of the inner retina of the mouse was most prominent 24 hours subsequent to ischemia but persisted at 48 hours. Seven days subsequent to 60 minutes of ischemia in the wild-type and transgenic mice, histopathologic evaluation demonstrated preservation of the retinal histoarchitecture in the heterozygous group compared with the wild-type or homozygous animals. CONCLUSIONS: These data further support the hypothesis that the delayed cell death that occurs after transient retinal ischemia is, in part, apoptotic. In addition, they suggest a role for the p53 protein in the selective vulnerability of the inner retina to transient ischemia. p53 protein may be a target for future therapeutic agents in the treatment of disorders of the retina where ischemia plays a pathogenetic role.

Animals↗
PubMed1998

Regional expression of disease-related genes in human and monkey retina.

PURPOSE: Although specific genes play a role in regional retinal disease, the correlation of regional gene expression in the disease-affected site has not been previously ascertained. Non-human primates are widely used in models of human retinal function and are theorized to have identical (to human) patterns of expression, but no correlation between primate and human regional retinal gene expression has ever been performed. We wanted to evaluate the pattern of regional gene expression for a number of genes whose dysfunctions are known to selectively affect specific regions of the human retina, and to determine whether patterns of regional gene expression in nonhuman primates correlate with the human. METHODS: Human and rhesus monkey eyes were dissected into retina, retinal pigment epithelium (RPE)/choroid and isolated RPE. Retinal regions were dissected, total RNA was isolated and northern analysis performed. Complementary DNA (cDNA) probes were prepared from genes associated with regional retinal disease. These genes are: rod opsin, the alpha-subunit of rod phosphodiesterase, RDS-peripherin, rod outer membrane (ROM) protein, ornithine aminotransferase (OAT), choroideremia gene product (CHM), tissue specific inhibitor of metalloproteinases-3 (TIMP-3), and red/green photoreceptor pigment protein. We also compared expression of Norrie disease product (NDP), a gene whose mutation is known to globally affect the retina. RESULTS: Rod-specific mRNA expression is highest in the retinal midperiphery, and cone-specific mRNA levels were highest in total RNA from the cone-dominant fovea. mRNA levels for genes coding for proteins expressed in both rod- and cone photoreceptors (RDS-peripherin and ROM-1) are also highest in total RNA from the retinal midperiphery. Regional mRNA levels of CHM and OAT do not directly correlate with their patterns of disease expression. NDP mRNA expression was equivalent in both fovea and midperipheral retina total RNA. Patterns of gene expression were qualitatively similar for both human and rhesus monkey retina. CONCLUSIONS: Regional retinal gene expression is an important factor in regional disease. However, for genes not solely expressed by a single photoreceptor subtype, other factors, such as regional metabolic differences, intra- and intercellular interactions, are also likely to be important in predisposing a single retinal region to disease. The pattern of neural retina OAT mRNA expression may have important implications in determining the appropriate tissue approach in gene therapy for gyrate atrophy. Regional retinal gene expression likely plays a significant, but nonexclusive role in the development of regional retinal disease.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1998

The cloning of GRK7, a candidate cone opsin kinase, from cone- and rod-dominant mammalian retinas.

PURPOSE: Desensitization in the rod cell of the mammalian retina is initiated when light-activated rhodopsin is phosphorylated by the G protein-coupled receptor kinase (GRK), GRK1, often referred to as rhodopsin kinase. A distinct kinase that specifically phosphorylates cone opsins in a similar manner has not been identified in mammals. To determine the existence of a cone opsin kinase, RNA from the retinas of cone- and rod-dominant mammals was analyzed by PCR. METHODS: RNA prepared from the retinas of two cone-dominant mammals, the thirteen-lined ground squirrel and the eastern chipmunk, and a rod-dominant mammal, the pig, was used to clone a new GRK family member by RT-PCR. The tissue distribution and localization of the kinase in retina were determined by Northern blot hybridization and in situ hybridization. The protein encoded by this cDNA was expressed in human embryonic kidney-293 (HEK-293) cells and compared with bovine GRK1 for its ability to phosphorylate bovine rhodopsin and to undergo autophosphorylation. RESULTS: The cDNA cloned from ground squirrel contains an open reading frame encoding a 548 amino-acid protein. Sequence analysis indicates that this protein is orthologous to GRK7 recently cloned from O. latipes, the medaka fish. Partial cDNA fragments of GRK7 were also cloned from RNA prepared from eastern chipmunk and pig retinas. In situ hybridization demonstrated widespread labeling in the photoreceptor layer of the ground squirrel retina, consistent with expression in cones. Recombinant ground squirrel GRK7 phosphorylates bovine rhodopsin in a light-dependent manner and can be autophosphorylated, similar to bovine GRK1. CONCLUSIONS: These results indicate that cone- and rod-dominant mammals both express GRK7. The presence of this kinase in cones in the ground squirrel and its ability to phosphorylate rhodopsin suggests that it could function in cone cells as a cone opsin kinase.

Amino Acid Sequence↗
PubMed1996

Glutamate metabolic pathways in displaced ganglion cells of the chicken retina.

Glutamate (E) is the putative amino acid neurotransmitter used by ganglion cells, photoreceptors, and bipolar cells. Aspartate (D) and glutamine (Q) are potential precursors of glutamate, and glutamate-utilizing neurons may use one or more of these amino acids to sustain production of glutamate. We used post-embedding immunocytochemistry for several amino acid neurotransmitters to characterize the amino acid signatures for displaced ganglion cells of the avian retina. We found two neurochemical signatures for displaced ganglion cells, EQ and EDQ, in mid-peripheral and far-peripheral retina, respectively. Differences in neurochemical signatures cannot be explained by the existence of two ganglion cell populations, and we propose that the two signature categories for the large-diameter displaced ganglion cells reflect variations in the aspartate precursor pool. The transamination reaction involved in glutamate production, aspartate/oxaloacetate and alpha-ketoglutarate/glutamate, requires an active TCA cycle, since the carbon skeleton of glutamate is derived from alpha-ketoglutarate, a TCA intermediary. We hypothesized that aspartate levels vary in the normal chicken retina because eccentricity-dependent differences in oxygen availability result in changes of alpha-ketoglutarate levels, and hence, alterations in the equilibrium of the transamination reaction. We tested this hypothesis by incubating isolated chicken retinas in anaerobic conditions and found elevated aspartate immunoreactivity in subpopulations of glutamate-utilizing neurons in the central retina. Under aerobic conditions, or in retinas placed directly into fixative, retinal samples from the central edge of the pecten did not show differential cellular staining for aspartate. We have, therefore, identified differences in neurochemical signatures for retinal neurons involving changes in active maintenance of precursor pools.

Aerobiosis↗
PubMed1990

Topography of ganglion cells in human retina.

We quantified the spatial distribution of presumed ganglion cells and displaced amacrine cells in unstained whole mounts of six young normal human retinas whose photoreceptor distributions had previously been characterized. Cells with large somata compared to their nuclei were considered ganglion cells; cells with small somata relative to their nuclei were considered displaced amacrine cells. Within the central area, ganglion cell densities reach 32,000-38,000 cells/mm2 in a horizontally oriented elliptical ring 0.4-2.0 mm from the foveal center. In peripheral retina, densities in nasal retina exceed those at corresponding eccentricities in temporal retina by more than 300%; superior exceeds inferior by 60%. Displaced amacrine cells represented 3% of the total cells in central retina and nearly 80% in the far periphery. A twofold range in the total number of ganglion cells (0.7 to 1.5 million) was largely explained by a similar range in ganglion cell density in different eyes. Cone and ganglion cell number were not correlated, and the overall cone:ganglion cell ratio ranged from 2.9 to 7.5 in different eyes. Peripheral cones and ganglion cells have different topographies, thus suggesting meridianal differences in convergence onto individual ganglion cells. Low convergence of foveal cones onto individual ganglion cells is an important mechanism for preserving high resolution at later stages of neural processing. Our improved estimates for the density of central ganglion cells allowed us to ask whether there are enough ganglion cells for each cone at the foveal center to have a direct line to the brain. Our calculations indicate that 1) there are so many ganglion cells relative to cones that a ratio of only one ganglion cell per foveal cone would require fibers of Henle radiating toward rather than away from the foveal center; and 2) like the macaque, the human retina may have enough ganglion cells to transmit the information afforded by closely spaced foveal cones to both ON- and OFF-channels. Comparison of ganglion cell topography with the visual field representation in V1 reveals similarities consistent with the idea that cortical magnification is proportional to ganglion cell density throughout the visual field.

Adult↗
PubMed1993

Immunocytochemical staining of AII-amacrine cells in the rat retina with antibodies against parvalbumin.

The rod dominated rodent retina is the preferred tissue for in vitro studies of mammalian retinal physiology and pharmacology. The rod pathway through the rat retina was investigated, therefore, in order to find out whether its organization follows the mammalian "plan." AII-amacrine cells of the rat retina were injected with Lucifer Yellow to characterize the morphology of this bistratified interneuron of the rod pathway. When sections or whole mounts of the rat retina were stained with antibodies against the calcium binding protein parvalbumin (PV), two different amacrine cell types were labeled: the AII-amacrine cell and a widefield amacrine cell. They occur at a ratio of 12:1. Weak label was also observed in ganglion cells. The density of PV-labeled AII-cells decreases from approximately 7,000 cells/mm2 in upper central retina to 2,000 cells/mm2 in peripheral retina. Their cell bodies form a regular mosaic, and the dendritic arbors of three neighbouring AII-amacrine cells overlap (coverage of 3).

Animals↗
PubMed1994

Distribution of Purkinje cell-specific Zebrin-II/aldolase C immunoreactivity in the mouse, rat, rabbit, and human retina.

The developmental, genetic, and biochemical similarities that have been observed between the cerebellum and retina form the basis for ongoing investigations into retinal expression of cerebellar-specific proteins. We have examined the mouse, rat, rabbit, and human retina for expression of a protein that is present in parasagittal Purkinje cell strips and that is recognized by the antibody Zebrin-II. This protein has recently been identified as a member of the aldolase C isoenzymes. Western blotting and immunocytochemistry have been used. The monoclonal antibody Zebrin-II recognized a prominent 36 kDa protein band on immunoblots of both the cerebellum and the retina of the examined species. Immunocytochemistry showed that, in the three nonhuman species, cells were stained in the ganglion cell layer (GCL). In addition, in the mouse and rabbit, cells in the inner nuclear layer (INL) were also labeled. Except for the visual streak, there were more immunopositive cells in the rabbit GCL and INL than in corresponding areas of the mouse retina. In the human, in contrast to the other species, the photoreceptor cell layer was strongly aldolase C immunoreactive. In all species except for the rat, the photoreceptor inner segments also displayed a weak labeling. The results show that this aldolase C isoenzyme is another protein that is selectively expressed by the cerebellum and retina. Furthermore, the retinal expression is species specific, and this pattern seems to show a good correlation with the oxygenation level of the individual compartments. The indication that this aldolase C isoenzyme has specific developmental functions in the retina provides additional clues for our understanding of cerebellar organization.

Animals↗
PubMed1996

Immunocytochemical colocalization of clusterin in apoptotic photoreceptor cells in retinal degeneration slow rds mutant mouse retinas.

In the rds mutant mouse the photoreceptor cells differentiate normally for the first few postnatal days, with the inner segments projecting an extended cilium. However, outer segments fail to form and only rudimentary disks and opsin-laden vesicles assemble at the tip of the cilium. These are shed into the interphotoreceptor space where they are phagocytosed by the retinal pigment epithelial cells. In this animal model, the photoreceptors undergo a slow degeneration via apoptosis leading to eventual loss of the entire photoreceptor population. Since increased expression of clusterin has been implicated in apoptosis, we studied the expression of clusterin in the rds mutant mouse retina and compared it to normal BALB/ c retinas. Small intestinal microvillus epithelium was used as a positive control tissue for apoptosis. Immunocytochemistry revealed the presence of clusterin in the ganglion cell, inner nuclear and outer plexiform layers and in the retinal pigment epithelium of both the rds and the BALB/c retinas. Interestingly, scattered clusterin-positive cells were observed in the outer nuclear layer (onl) of dystrophic retinas. Since the increased presence of clusterin protein in the onl of dystrophic retina may indicate dying photoreceptor cells due to apoptosis, we utilized a co-localization procedure for apoptotic nuclei and clusterin. For apoptosis we utilized an in situ 3' end labeling of fragmented DNA (TUNEL) and immunohistochemistry for clusterin using brown and red colored substrates respectively. Small intestine tissue sections were also included as positive controls for apoptosis. Our results show that clusterin is co-localized with apoptotic nuclei both in the onl of rds mutant retinas as well as in the small intestine epithelial cells undergoing cell turnover and exfoliation. These results are of interest since overexpression of clusterin is also observed in other neuro-degenerative diseases such as Alzheimer's and Pick's disease.

Animals↗
PubMed2002

Exogenous growth factors stimulate the regeneration of ganglion cells in the chicken retina.

Recent reports have found that the posthatch chicken retina has the capacity for neuronal regeneration. The purpose of this study was to test whether the types of cells destroyed by neurotoxic lesions influence the types of cells that are regenerated, and whether exogenous growth factors stimulate neural regeneration in the chicken retina. N-methyl-D-aspartate (NMDA) was used to destroy amacrine and bipolar cells; kainate was used to destroy bipolar, amacrine, and ganglion cells; colchicine was used to selectively destroy ganglion cells. Following toxin-induced damage, bromo-deoxyuridine was used to label proliferating cells. In some animals, growth factors were injected into the vitreous chamber of the eye. We found that the proliferation of cells within the retina was stimulated by toxin-induced cell loss, and by insulin and FGF2. After either kainate- or colchicine-induced retinal damage, some of the newly generated cells expressed markers and had the morphology of ganglion cells. The combination of insulin and FGF2 stimulated the regeneration of ganglion cells in kainate- and colchicine-treated retinas. We conclude that exogenous growth factors can be used to stimulate neural regeneration in the retina. We propose that the type of neuron destroyed in the retina may allow or promote the regeneration of that neuronal type.

Animals↗
PubMed1992

Beta-like ganglion cells in the South American opossum retina: a Golgi study.

Using the Golgi technique we investigated the morphology of the ganglion cells of the South American opossum retina. We focused our attention on a type of ganglion cell which has a relatively small dendritic field diameter and a medium-sized soma, making it a morphological equivalent of beta ganglion cells of cat retina. Both radial sections of the retina, where the stratification level of ganglion cells dendrites can be observed in the inner plexiform layer (IPL), and flat preparations of the retina, where the whole dendritic field of the ganglion cells can be examined and quantified, have been studied. Usually these cells have one to three primary dendrites, giving rise to short spiny branches. The dendrites of these cells are segregated in two groups, one with dendritic trees arborizing in the inner two thirds and another group arborizing in the outer third of the IPL. The two groups of beta-like cells probably represent the physiological ON- and OFF-center types of ganglion cell as found in cat retina. The mean cell body and dendritic field diameters of 47 cells were 18.5 +/- 1.6 microns, (size range 16-21 microns) and 91.5 +/- 16 microns (range 54-133 microns), respectively. Cell body and dendritic fields sizes were homogeneous across the retina of the opossum. In the opossum the relatively large dendritic fields of the beta-like ganglion cells in the area centralis are consistent with the poor visual acuity of this species.

Animals↗
PubMed1997

Acidic and basic fibroblast growth factor messenger RNA and protein show increased expression in adult compared to developing normal and dystrophic rat retina.

To further elucidate the possible roles of fibroblast growth factors (FGFs) in retinal pathophysiology, messenger RNA levels of acidic and basic FGF (aFGF and bFGF, respectively) were measured throughout embryonic and postnatal development until adulthood in normal and dystrophic (Royal College of Surgeons, RCS) rat retinas using sensitive reverse transcription-coupled polymerase chain reaction (PCR) techniques. In normal rats, both aFGF and bFGF transcript levels remained steadily low throughout embryogenesis and up until 7 d of postnatal age. By 13 d bFGF mRNA had increased 30-fold, and by adulthood (4 mo) levels were 150 times greater than in newborn retina. Dystrophic RCS retinas followed the same basic pattern, except that bFGF expression levels were increased relative to normal rats: By 4 d postnatal RCS retinas contained three times more bFGF mRNA than normal, by 7 d they contained six times more, and by 10 d they contained eight times more. In contrast, aFGF mRNA levels rose only threefold between embryonic and adult stages, and did not show any differences between normal and RCS rats. In parallel, staining of lightly fixed frozen sections of young (< 20 d) normal rat retina with antibodies to bFGF revealed only faint labeling of neural cells, whereas adult retinal sections were labeled strongly, especially within the photoreceptor layer. Twenty-day RCS rat retina showed detectable bFGF-like immunoreactivity. Hence, these data indicate that major aFGF and bFGF expression occurs only late in retinal maturation, suggesting these factors act principally as survival factors, especially for photoreceptors. In addition, the increased expression in a degenerative mutant strain may indicate the early onset of general cellular stress.

Animals↗
PubMedDate not supplied

A case of sectorial benign flecked retina.

PURPOSE: A case of sectorial benign flecked retina not associated with an RDH5 gene mutation is reported. METHODS: A 51-year-old woman showed multiple yellow-white flecks in both eyes similar to those of benign flecked retina but in only the upper half of the retina. We carried out clinical, electrophysiological, and molecular genetic examinations of the patient. RESULTS: Visual acuity was 20/20 OD and 20/20 OS. Fluorescein angiography showed diffuse irregular hypofluorescence that did not correspond to the flecked lesions. A Goldmann-Weeker adaptometer test revealed that the visual threshold of the upper retina was approximately 0.6 to 0.8 log units higher than that of the lower retina. No mutations of the RDH5 gene were detected in exons 2-5 or in the flanking intron sequences. CONCLUSIONS: To our knowledge, this is the first report of sectorial benign flecked retina, and the flecks may not be caused by an RDH5 gene mutation.

Alcohol Oxidoreductases↗
PubMed1991

Dopamine and plasticity of horizontal cell function in the teleost retina: regulation of a spectral mechanism through D1-receptors.

The negative feed-back interaction between horizontal cells (HCs) and cones in the cyprinid fish retina is thought to be mediated by horizontal cell spinules. These are "plastic" structures, largely absent from the dark-adapted retina and formed anew during light adaptation. We have previously shown that horizontal cell feed-back is similarly enhanced by light adaptation. The role of the interplexiform cell transmitter dopamine in both processes has been studied in the roach retina. Application of dopamine to dark-adapted retinae induced spinule formation in a dose-dependent way. The effect of dopamine was mimicked by dibutyryl-cAMP and suppressed selectively by D1 receptor antagonists. The effect of light in inducing spinule formation was lost in retinae depleted of endogenous dopamine. However, application of exogenous dopamine to these retinae triggered normal spinule formation. For all pharmacological treatments used, there was a strong correlation between spinule number and degree of feed-back activity in biphasic horizontal cells. Thus, when the spinule content of the cone pedicles was high, biphasic horizontal cell responses exhibited strong depolarizing components and vice versa. It is concluded that light-evoked formation of spinules in HC dendrites involves the action of dopamine upon D1 receptors. Spinules, in turn, are likely to be presynaptic terminals mediating the dynamic negative feed-back effect of horizontal cells upon cones.

Animals↗
PubMed1996

The synaptic complex of cones in the fovea and in the periphery of the macaque monkey retina.

Parallel pathways for visual information processing start at the first synapse of the retina, at the cone pedicle. At least eight different types of bipolar cells receive direct synaptic input from an individual cone. The present study explores whether enough synaptic sites are available at the cone pedicle to supply all these bipolar cells. Monkey retinae were optimally fixed for electron microscopy. Serial horizontal sections were cut through the cone pedicle layer in a piece close to the fovea (eccentricity: 0.75 mm) and in a peripheral piece (eccentricity: 5-6 mm). The ribbon synapses (triads) at the cone pedicle base were analysed. The average number of synaptic ribbons per cone pedicle increased from 21.4 +/- 1.6 (n = 26) in central retina to 41.8 +/- 3 (n = 14) in peripheral retina. Five central and five peripheral pedicles were reconstructed and the invaginating bipolar cell dendrites forming the central elements of the triads were characterized. Close to the fovea an average of 18 invaginating bipolar cell dendrites was found, in peripheral retina the average was 90. Pedicles of foveal cones have one invaginating central process per ribbon, pedicles of peripheral cones have two. It is possible that midget bipolar cell dendrites occupy the majority of triads in the fovea, while in peripheral retina both midget and diffuse bipolar cell dendrites share the triads.

Animals↗
PubMed1995

Distribution of membrane phospholipids in the rabbit neural retina, optic nerve head and optic nerve.

Since diseases of the neural retina and optic nerve can result in alteration of biological membranes, this study determines similarities and differences in the membrane phospholipid content of the neural retina, optic nerve head, and optic nerve to serve as baseline data. Neural retina, optic nerve head, and optic nerve were dissected, isolated as 5 sets from 20 rabbits and frozen in liquid N2. Separate pooled-tissue extracts were prepared for each set of tissues and phosphorus-31 nuclear magnetic resonance (31P NMR) analyses performed. Ten phospholipids were quantified (respective neural retina, optic nerve head, and optic nerve mole % are given for the 5 major phospholipids detected): phosphatidylcholine (PC), 44.61, 27.67, 26.40; PC plasmalogen or alkylacyl PC (CPLIP); phosphatidylinositol (PI); sphingomyelin (SM); phosphatidylserine (PS), 12.63, 14.77, 15.09; phosphatidylethanolamine (PE), 21.21, 9.59, 8.69; PE plasmalogen (EPLAS), 11.07, 30.96, 33.93; an unidentified (unknown) phospholipid (U) at the chemical-shift value of 0.13 ppm; diphosphatidylglycerol (DPG); and phosphatidic acid (PA), 0.46, 2.92, 1.57. Significant differences between the various tissues were determined by the one-way analysis of variance, using a Scheffé range value of P < 0.05. The neural retina in all phospholipids detected except for the uncharacterized (unknown) phospholipid was significantly different from the optic nerve head tissue. The optic nerve head was significantly different from the optic nerve in PC, CPLIP, PE, EPLAS, U, DPG, and PA. The data provide a baseline for studies on pathologically changed neural retina, optic nerve head, and optic nerve.

Animals↗
PubMed2005

Blood-derived macrophages infiltrate the retina and activate Muller glial cells under experimental choroidal neovascularization.

Inflammation is a major mechanism in the pathogenesis of age-related macular degeneration, the most important cause of blindness in the elderly. Previous studies have focused on the role of macrophages in regulating the growth of pathological new vessels over the retina, called choroidal neovascularization (CNV). However, no research has been done to evaluate the role of inflammation as a mechanism of vision loss and retinal degeneration in the retina underlying CNV. In other neuropathological conditions, hematogenous macrophages and/or resident microglia contribute to neurodegeneration. We have combined laser-induced CNV in mice and bone marrow transplantation with GFP-labeled bone marrow to determine the relative role of recruited blood-derived macrophages versus resident microglia in the retina associated with CNV. Using these chimeric mice, we have found that many GFP-labeled cells infiltrated the retina underlying CNV but not the retina unaffected by CNV. Immunostaining for the cell adhesion molecules VCAM 1, ICAM 1, and PECAM was strongly upregulated in retinal blood vessels under CNV. All GFP-labeled cells were immunoreactive for the macrophage marker F4/80. Most (70%) of the F4/80 immunoreactive cells were GFP-labeled under CNV. The density of resident microglia did not increase. Most GFP-labeled cells were found in close proximity to activated Muller cells. Depleting circulating macrophages with clodronic acid diminished the density of F4/80 immunoreactive cells as well as the density of pERK immunoreactive Muller cells in the retina under CNV. Thus, recruitment of blood-derived macrophages more than resident microglia seems to be associated with CNV.

Animals↗
PubMed2005

Two major tachykinins, substance P and substance K, are localized to distinct subsets of amacrine cells in the anuran retina.

Tachykinins are known to be major excitatory neuromodulators in neural systems, including the retina of many vertebrate species. Among them substance P has been detected in several species, including anurans. However, none of the other major tachykinins has been sought for in the anuran retina. The aim of this study was to identify another major tachykinin, substance K (neurokinin A) in the frog retina and compare its distribution to that of substance P. Since one of the synthetic pathways of the above mentioned tachykinins make it possible to produce both peptides from one large precursor RNA, we also investigated possible colocalization with double-label immunocytochemistry. Our results show that both substance P and substance K are localized to wide-field amacrine cells in the retina of a terrestrial frog (Pelobates fuscus). Preabsorption and double-label studies provided evidence that the populations of substance P- and substance K-immunoreactive cells are clearly distinct and their dendritic arbor do not overlap in the inner plexiform layer of the retina. These findings provide evidence for the presence of (i) a novel anatomically/neurochemically identifiable amacrine cell type and (ii) predict distinct synthetic pathways for substance P and substance K in the anuran retina.

Amacrine Cells↗
PubMed1991

Rod bipolar cells in the cone-dominated retina of the tree shrew Tupaia belangeri.

The tree shrew has a cone-dominated retina with a rod proportion of 5%, in contrast to the common mammalian pattern of rod-dominated retinae. As a first step to elucidate the rod pathway in the tree shrew retina, we have demonstrated the presence of rod bipolar cells and studied their morphology and distribution by light and electron microscopy. Rod bipolar cells were labeled with an antiserum against the protein kinase C (PKC), a phosphorylating enzyme. Intense PKC immunoreactivity was found in perikarya, axons, and dendrites of rod bipolar cells. The cell bodies are located in the sclerad part of the inner nuclear layer, the dendrites ascend to the outer plexiform layer where they are postsynaptic to rod spherules, and an axon descends towards the inner plexiform layer (IPL). The axons branch, and terminate in the vitread third of the IPL where mammalian rod bipolar cells are known to terminate. Two amacrine cell processes are always seen as the postsynaptic elements (dyads). Dendritic and axonal arbors of rod bipolar cells are rather large, up to 100 microns in diameter. The topographical distribution of the rod bipolar cells was analyzed quantitatively in tangential sections. Their density ranges from 300 cells/mm2 in peripheral retina to 900 cells/mm2 more centrally. The distribution is rather flat with no local extremes. Consistent with the low rod proportion in tree shrew, the rod bipolar cell density is low compared to the rod-dominated cat retina for example (36,000-47,000 rod bipolar cells/mm2). Rod-to-rod bipolar cell ratios in the tree shrew retina range from smaller than 1 to about 7, and thus are also lower than in cat.

Animals↗