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At least 865 records · Page 48Linked to original sources
PubMed2006

Differential effect of dopamine on mitosis in early postnatal albino and pigmented rat retinae.

Insufficient levels of L-DOPA, released from the retinal pigment epithelium (RPE), in albino animals are considered responsible for the abnormal development of the underlying neural retina. L-DOPA normalizes retinal neurogenesis by reducing levels of cell proliferation either by acting on the cells directly or by being converted into dopamine. Here we report the effects of dopamine on mitosis in early postnatal neural retinae from albino and pigmented rats, using 4D (x, y, z and time) confocal microscopy. Exogenous dopamine significantly prolongs mitosis in retinae from albino, but not pigmented, animals. As fewer cells move into and divide in the ventricular zone (VZ) in the presence of dopamine, we conclude that the overall cell cycle is affected. The D1 receptor blocker, SCH 23390, inhibits these effects. Thus, the differential effects of dopamine on neural retinae from pigmented and albino rats in vitro must result from the activation of D1 receptors, which are present in the retina from birth. Immunohistochemical labeling of D1 receptors shows that the pattern of their distribution is similar between pigmentation phenotypes, but levels of expression may be elevated in albinos. Labeling is most intense in the inner plexiform layer but is present throughout the neuroblastic layer. These findings are discussed in light of previous reports of reduced catecholamine levels in the albino retina.

Animals↗
PubMed1993

Changing patterns of the retinoic acid system in the developing retina.

In retinas of embryonic rat and chick, as in the mouse, synthesis of retinoic acid is mediated by different dehydrogenases in dorsal and ventral portions, with the ventral pathways generating higher retinoic acid levels. In the mouse, the dorsal enzyme was previously found to be the aldehyde dehydrogenase class-1 isoform AHD-2 and the ventral enzyme an unknown acidic dehydrogenase activity. This acidic dehydrogenase activity is now shown to consist of an early and a later expressed form, with the early form being indistinguishable from the activity in the early embryonic trunk and heart regions. Expression of the acidic dehydrogenase in the eye is first detected at the optic pit stage (E8.0), a day before the appearance of AHD-2 in the optic vesicle. The acidic dehydrogenase accounts for most of the retinoic acid synthesis in the retina during embryonic and early postnatal stages; during later postnatal stages it disappears and in the adult retina all retinoic acid synthesis is mediated by AHD-2. HPLC measurements in mice show high levels of all-trans- and 13-cis-retinoic acid: at E14 the retina contains a total of about 0.5 microM retinoic acid, and levels in the adult retina are about fourfold lower. The dorso-ventral asymmetry extends also to the cellular retinoic acid binding protein CRABP I, which first appears in the early differentiating ganglion cells in central retina and in the later embryo shows transiently a ventro-dorsally receding pattern of expression.

Aldehyde Dehydrogenase↗
PubMed1996

Intraretinal grafting reveals growth requirements and guidance cues for optic axons in the developing avian retina.

To study environmental factors controlling the growth and navigation of optic axons in the eye, grafts of retinal, optic disc, optic tectum, and floor plate tissue were transplanted into organ-cultured embryonic chick or quail eyes. The growth of axons into and out of the graft was studied in cross sections of the cultured eyes and by DiI tracing in retinal whole mounts. Based on the location and trajectory of axons and based on the quantity of axons that entered and exited the grafts, several requirements for axonal navigation were established: (1) Axonal growth is restricted to an approximately 10-microm-thick layer at the vitreal surface of the retina. (2) The retinal neuroepithelium prior to axogenesis is nonpermissive for neurite outgrowth. This nonpermissive quality is transient and recedes peripherally as the differentiation of the retina progresses. (3) Embryonic axons are able to grow into neonatal and adult retinal grafts, demonstrating that older retina remains permissive for axonal growth. (4) The trajectory of axons into and from retinal grafts that had been rotated in their peripheral-central orientation showed that the retina has an inherent polarity that permits axon growth toward and away from the optic disc, but does not allow axon growth perpendicular to this direction. This centroperipheral cue operates locally rather than by long distance. (5) The optic disc provides an exit for the axons from the retina, but has no detectable neurotropic activity. Finally, optic axons from the host retina readily enter grafts of their target tissue, the optic tectum, but few axons are able to leave tectal transplants.

Animals↗
PubMed1997

Reciprocal expression of the Eph receptor Cek5 and its ligand(s) in the early retina.

Recent evidence suggests that Eph receptor tyrosine kinases and their ligands provide positional information in the developing visual system. We previously found that the Eph receptor Cek5 is more highly expressed in the ventral than dorsal chicken embryonic retina. We now report the identification of a chicken ligand for Cek5 (cCek5-L) that is 75% identical to the ligand LERK2. In situ hybridization experiments do not reveal a dorsoventral gradient of cCek5-L transcripts in the optic tectum at Embryonic Day 8, suggesting that this ligand is not involved in guiding Cek5-expressing axons in the tectum. Surprisingly, it is in the retina that high levels of cCek5-L mRNA are present. In the early retina, cCek5-L is more highly expressed in the dorsal than the ventral aspect. Similarly, a Cek5 Ig chimera labels dorsal but not ventral retina, indicating that even if several Cek5 ligands are present, their overall distribution is complementary to that of Cek5. Hence, Cek5 and cCek5-L may both contribute to define anatomical compartments within the early retina. In contrast, in the 11-day embryonic retina the distributions of Cek5 and its ligand(s) show considerable overlap, suggesting changing functions as development progresses. In dissociated cultures of dorsal or ventral retinal cells seeded on plates coated with either receptor or ligand Ig chimeras, the interaction between Cek5 and its ligand(s) or cCek5-L and its receptor(s) is sufficient to mediate cell adhesion and allows neurite outgrowth.

Amino Acid Sequence↗
PubMed1993

Hydroxyl radical generation in the cat retina during reperfusion following ischemia.

There is increasing evidence that oxygen-derived free radicals are generated during the early phase of reperfusion, and account for part of the damage caused by transient ischemia in various tissues. To study this in the retina, cats were injected intravenously with sodium salicylate (100 mg kg-1), which reacts as a hydroxyl radical trap to form 2,3- and 2,5-dihydroxybenzoic acids (DHBA). Thirty minutes following injection, the retina of one eye of each animal was subjected to ischemia by intraocular pressure elevation via cannulation of the anterior chamber, while the fellow eye served as a sham-operated control. Ischemia was induced for 60 min (six eyes) and 90 min (eight eyes) followed by 5 min of reperfusion. In six other eyes, ischemia was induced for 90 min without reperfusion. After enucleation, the retinas were immediately removed, placed in ice-cold buffer and the retinal levels of 2,3- and 2,5-DHBA were quantitated by high pressure liquid chromatography, coupled with electrochemical detection. Results were normalized and expressed as ng DHBA microgram-1 salicylate mg-1 retinal protein. After 60 min of ischemia followed by reperfusion the normalized levels of 2,3- and 2-5-DHBA were no different in the experimental and control retinas. However, the levels of both 2,3- and 2,5-DHBA were significantly higher in the retinas subjected to 90 min ischemia followed by reperfusion than in the control tissues (P = 0.012 and P = 0.036, n = 8 respectively). Following 90 min ischemia without reperfusion, the normalized dihydroxybenzoate levels in the retinas were no higher than in their controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Regulation of the interphotoreceptor retinoid-binding protein content of the retina by vitamin A.

A retinoid-binding protein has been identified in the extracellular space that separates the photoreceptor cells and the retinal pigment epithelium (RPE) of the mammalian retina. This protein (interphotoreceptor retinoid-binding protein, IRBP) appears to be involved in the transport of visual cycle retinoids between the photoreceptors and the RPE. Experiments were conducted to evaluate the possibility that the amount of IRBP in the retina is regulated by the availability of retinoids in the retina. Rats were fed diets containing vitamin A either in the form of retinyl palmitate (+A), which can be metabolically converted into the retinoids involved in vision, or retinoic acid (-A), which does not support visual function. After 23 weeks, when rhodopsin levels had declined by over 90% in the -A rats, some animals in the latter group were given a single intramuscular injection of all-trans retinol. Both 1 day and 1 week later, the IRBP immunoreactivities in the retinas from the treated rats were determined with quantitative immunocytochemistry. IRBP immunolabeling densities were also determined in the +A and -A groups. Retinas of animals that had consumed the -A diet for 23 weeks bound an average of 50% less anti-IRBP antibody in the retina than rats that had been fed the +A diet for the same period. One day after retinol administration, the mean IRBP immunolabeling density had returned to that observed in the +A rats. The restored level of IRBP immunoreactivity was maintained 1 week after injection. The immunocytochemical findings were confirmed by immunoblot analysis of eyecup homogenates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Studies on the mechanism of early onset macular degeneration in cynomolgus monkeys. II. Suppression of metallothionein synthesis in the retina in oxidative stress.

Initial investigations done in this laboratory detected increased albumin and decreased glyceraldehyde 3-phosphate dehydrogenase concentrations in the retina of an animal model manifesting early onset macular degeneration. Both glyceraldehyde 3-phosphate dehydrogenase and albumin are markers of oxidative stress in cells. In this study, we used the same animal model to study further biochemical and physiological processes which may be involved in the pathogenesis of early onset macular degeneration in monkeys. We detected 60% lower catalase and glutathione peroxidase activities in the affected retinas suggesting lower antioxidant activities and oxidative stress. One of the consequences of oxidative stress is the production of metallothionein, a low molecular weight protein also induced by high concentrations of heavy metals such as zinc. Metallothionein was detected by RT-PCR in these monkey retinas. However initial quantitative PCR studies on this protein showed that the synthesis of metallothionein in affected retinas appears to be less than in normal controls. The affected retinas also showed a fourfold lower zinc concentration compared with the normal controls. No significant difference, however, could be detected in the zinc concentrations in plasma samples. Since induction of metallothionein synthesis is mediated by transcription factors which require heavy metals such as zinc for binding to specific sites in the DNA, the lowered zinc concentration may, thus, correlate with the lowered metallothionein expression. And since metallothionein is suggested to function as a free radical scavenger, the lowered metallothionein synthesis may consequently contribute to increased peroxidation reactions in the affected retinas. It appears therefore, that oxidative stress and the decreased metallothionein synthesis may be involved in the pathogenesis of early onset macular degeneration in this animal model.

Amino Acid Sequence↗
PubMed1997

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

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

Animals↗
PubMed1997

In vitro metabolic competence of the frog retina: effects of glucose and oxygen deprivation.

The metabolic competence and histological integrity of the frog retina in vitro were evaluated as a function of the presence/absence of exogenous glucose and of oxygen tension. Dark- and light-adapted frog neural retinas were incubated for 1-8 hr at 23 degrees C in a modified Ringer's-bicarbonate medium under aerobic and anaerobic conditions, in the presence and absence of 10 mM glucose. Control retinas (+glucose, aerobic conditions) maintained ATP levels comparable to those of freshly excised tissue (ave. 17 nmol mg protein-1), produced minimal lactate (ave. 0.12 mumol mg protein-1 hr-1), and exhibited normal histology. In the absence of any exogenous carbon source, retinas incubated aerobically maintained ATP levels, produced lactate, incorporated [3H]acetate into nonsaponifiable lipids, and exhibited histology comparable to controls. In the presence of 1 mM iodoacetate, aerobic ATP levels declined markedly, with or without exogenous glucose. Under anaerobic conditions with glucose present, lactate production increased ca. 8.5-fold, while ATP levels were maintained at control levels, demonstrating a marked Pasteur effect; under these conditions, retinas exhibited only moderate histopathological changes. However, in the absence of both glucose and oxygen, ATP levels declined precipitously, with concomitant massive cytological deterioration. No major differences in the biochemical measurements or histological appearance were observed as a function of light adaptation. These results demonstrate the remarkable resilience of the frog retina to anoxia and hypoglycemic stress. Aerobically, with or without exogenous glucose, ATP production and de novo lipid synthesis are maintained, apparently by recruitment of an endogenous carbohydrate substrate (e.g., glycogen).

Adenosine Triphosphate↗
PubMed1998

Immunolocalization of CD44 in the dystrophic rat retina.

The distribution of the cell surface adhesion/receptor molecule CD44 was studied in retinas of the Royal College of Surgeons (RCS) rat which exhibits an inherited retinal dystrophy. In this animal model, the retinal pigment epithelium fails to phagocytize shed photoreceptor outer segment material, a membranous debris layer accumulates in the subretinal space and the photoreceptor cells degenerate. Using immunoperoxidase and immunogold labeling, CD44 was localized to Müller cell apical microvilli in normal rat retinas, as noted in other species. For the RCS rat, immunoperoxidase labeling of 18 day and 1 month retinas showed the typical microvillar labeling pattern. At 2 months postnatal, following degeneration of most of the photoreceptors, a more condensed band of microvillar label was observed. At 3 months, when photoreceptor degeneration was virtually complete, only distinct regions of dense label remained between the neural retina and debris zone. Upon ultrastructural and immunogold analysis, these regions were found to contain closely packed Müller cell microvilli. At all ages studied, labeling for CD44 in the inner retina did not increase, as it does in other forms of retinal degeneration which lack a debris zone. However, by 3 months the debris zone was labeled for CD44 indicating that CD44 molecules remain on Müller cell microvilli and processes which have extended into and become part of the debris zone. This may be caused by an altered distribution of still undetermined ligands for CD44 which are present within the interphotoreceptor matrix of the RCS rat retina.

Animals↗
PubMed1999

Characterization of a novel C-kinesin (KIFC3) abundantly expressed in vertebrate retina and RPE.

Many forms of intracellular transport are mediated by microtubule-dependent motors of the kinesin superfamily (KIFs). To identify kinesins expressed in human retina and RPE, we used degenerate primer RT-PCR to amplify a approximately 440 bp kinesin motor domain fragment from human retinal and RPE messenger RNAs. Four distinct kinesins were detected: one C-kinesin (HsKIFC3); one kinesin from the unc104/KIF1 family [HsKIF1A]; and the ubiquitous and neuronal forms of conventional kinesin heavy chain [HsuKHC and HsnKHC]. The C-kinesin HsKIFC3 comprised 33.3% of the retinal clones and was 60% identical to FKIF2, the most abundant kinesin detected in a previous screen of fish retina and 95% identical to a fragment of MmKifC3 recently amplified from mouse brain. Elsewhere we have reported the sequence of HsKIFC3 and shown that it maps to the same locus on chromosome 16q13-q21 as Bardet-Biedl syndrome Type II, a hereditary retinal degeneration. We describe here the kinesin PCR screen of human retina and RPE and examine the tissue and subcellular distribution of KIFC3 in both fish and human retina using an antibody raised against a peptide conserved between FKIF2 and HsKIFC3. This peptide antibody identified a single approximately 80 kDa band in Western blots of fish and human retina and RPE. In both fish and human retina this antibody strongly labeled photoreceptor terminals in the outer plexiform layer, suggesting that FKIF2/KIFC3 may play some role in the photoreceptor synapse.

Adult↗
PubMed2001

Cellular and subcellular patterns of expression of bFGF and CNTF in the normal and light stressed adult rat retina.

This study compared the distributions in the normal and light stressed rat retina of the neuroprotective factors bFGF (basic fibroblast growth factor) and CNTF (ciliary neurotrophic factor). Albino Sprague-Dawley rats were raised in cyclic light and some were exposed to bright continuous light for 48 hr, to induce light damage of photoreceptors. Their retinas were prepared as cryosections, immunolabelled with antibodies to bFGF and CNTF and analysed by confocal microscopy. Both factors were prominent in macroglial cells (astrocytes, Müller cells) and the retinal pigment epithelium (RPE). In the somas of these cells the distributions of the two factors were complementary, with bFGF concentrated in the nuclei and CNTF in the cytoplasm. Both factors were distributed along the processes of macroglial cells, in granular form. CNTF was not detected in neurones, but bFGF was consistently present in the cytoplasm of ganglion cell somas and, in regions of retina subject to stress, in the cytoplasm of photoreceptors. bFGF was not detected in the nuclei or processes of neurones. In retina stressed by light exposure or proximity to the anterior edge of the retina, the levels of bFGF and CNTF were up-regulated, without major changes in localization. Macroglial cells (Müller cells, astrocytes) play a major role in distributing bFGF and CNTF throughout the retina. The different localizations of the two factors within the somas of macroglial, RPE and photoreceptor cells, suggest that their protective actions are exerted by distinctive mechanisms.

Animals↗
PubMed1996

Cyclosporine treatment promotes survival of human fetal neural retina transplanted to the subretinal space of the light-damaged Fischer 344 rat.

We have reported that xenografts of human fetal neural retina survive in the subretinal space of cyclosporine-immunosuppressed rats. In view of the current controversy regarding the role of cyclosporine, we wished to determine if cyclosporine immunosuppression was an absolute requirement for retinal xenograft survival. Neural retinas from human fetal eyes obtained within 1 h of termination of pregnancy were stored in Optisol medium (Chiron Vision, Irvine, CA) at 4 degrees C for 2 and 7 days. Retinas were then transplanted to the subretinal space of either cyclosporine-treated (10 mg/kg/day) light-damaged Fischer 344 rat eyes (17 animals, 28 eyes) or to the subretinal space of light-damaged Fischer 344 rat eyes (9 animals, 15 eyes) receiving no cyclosporine treatment. Grafted eyes were observed clinically at 10, 20, and 30 days posttransplantation. At 30 days, the animals were sacrificed and the grafts observed histologically. Human fetal retina xenografted to the subretinal space of immunosuppressed rats survived (9/17 animals, 12/28 eyes), showed good integration with the host retina and initial photoreceptor differentiation. Tissue xenografted to the subretinal space of non-cyclosporine-treated rats was not observed to survive (0/9 animals, 0/15 eyes). A low level cellular reaction was seen around three of the injection sites within the nonimmunosuppressed rats. We conclude that immunosuppression is necessary for the survival of human fetal neural retina xenografted to the subretinal space.

Animals↗
PubMed2001

Neuroprotective effects of lamotrigine and remacemide on excitotoxicity induced by glutamate agonists in isolated chick retina.

The possible neuroprotective effects of two recently developed antiepileptic compounds, lamotrigine (LTG) and remacemide (REMA), against glutamate agonist-induced excitotoxicity have been investigated in the isolated chick embryo retina model. Retina segments from 15- or 16-day-old embryos were incubated in 1 ml of balanced salt solution, at 25 degrees C for 30 min, in the presence or absence of N-methyl-d-aspartate (NMDA), kainic acid (KA), or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) (10 to 200 microM). LTG, REMA, and the active desglycinyl metabolite of REMA (d-REMA) (10-200 microM) were added separately 5 min before glutamate agonists. Retina damage was assessed after 24 h (i) by measuring LDH activity present in the medium, expressed as percentage of total retina LDH activity, and (ii) by histological analysis of retina specimens through scoring for the presence or absence of edema, necrosis, nuclear pyknosis, and cell layer damage. LTG, REMA, and d-REMA reduced LDH release produced by NMDA 58-70% in a dose-dependent manner, with d-REMA being the most potent (EC(50): d-REMA, 25.75 +/- 3.27 microM; REMA, 64.75 +/- 7.75 microM; LTG, 60.50 +/- 6.80 microM; P < 0.001). The drugs had less effect on the LDH release produced by AMPA and KA. Histological analysis confirmed these biochemical results, with all three compounds reducing edema and the number of necrotic and pyknotic nuclei in the ganglion layer. d-REMA provided almost complete protection of the ganglion cell layer against damage produced by NMDA. Combinations of d-REMA and LTG showed additive rather than potentiative effects against NMDA-induced cell injury. The present data provide pharmacological evidence that LTG, REMA, and d-REMA decrease glutamate agonist-induced excitotoxicity in isolated chick retina, findings that might have therapeutic implications for various neurological disorders.

Acetamides↗
PubMed1987

Mathematical model and simulation of retina and tectum opticum of lower vertebrates.

The processing of information within the retino-tectal visual system of amphibians is decomposed into five major operational stages, three of them taking place in the retina and two in the optic tectum. The stages in the retina involve (i) a spatially local high-pass filtering in connection to the perception of moving objects, (ii) separation of the receptor activity into ON- and OFF-channels regarding the distinction of objects on both light and dark backgrounds, (iii) spatial integration via near excitation and far-reaching inhibition. Variation of the spatial range of excitation and inhibition allows to account for typical activities observed in a variety of classes of retina ganglion cells. Mathematical description of the operations in the tectum opticum include (i) spatial summation of retinal output (mainly of class-2 and class-3 retina ganglion cells), and (ii) direct or indirect lateral inhibition between tectal cells. In the computer simulation, first the output of the mathematical retina model is computed which, then, is used as the input to the tectum model. The full spatio-temporal dynamics is taken into account. The simulations show that different combinations of strength of lateral inhibition on the one side and the response properties of the retina ganglion cells on the other side determine the response properties of tectal cell types involved in object recognition.

Amphibians↗
PubMedDate not supplied

Alterations in rabbit retina lipid metabolism induced by detachment. Decreased incorporation of [3H]DHA into phospholipids.

BACKGROUND: Docosahexaenoic acid (22:6n-3, DHA) is found in high concentration in phospholipids from retinal membranes, and is essential for their function. This study investigated the effect of in vivo retinal detachment on in vitro lipid metabolism using [3H]DHA. METHODS: Rabbit retina was detached from the retinal pigment epithelium by injecting physiological saline into the subretinal space of the eye. Retinal samples from control (non-operated) and sham (operated, no detachment) animals, and from attached and detached retinal areas from the same eye, were incubated in vitro with [3H]DHA for 4 hours, and then prepared for biochemical and autoradiographic analysis. RESULTS: In control and sham retinas, [3H]DHA was preferentially esterified into phospholipids (82%) with low labeling of free fatty acids (FFA) (5%). In samples from detached areas of the retina, a higher proportion of [3H]DHA was recovered in the FFA pool (up to 30%) and its esterification was shunted into triacylglycerol, thereby reducing the formation of [3H]DHA-phospholipids. Changes were sustained through 48 hours of postdetachment. High labeling of inner segments and synaptic terminals was observed autoradiographically in control retinas, while in detached retinas, clusters of labeling were detected in the neural retina, and eventually within the photoreceptor layer. CONCLUSION: Retinal detachment induces longlasting changes in lipid metabolism which are reflected in lower labeling of [3H]DHA-phospholipids. Metabolic changes, sustained through 48 hours, may lead to inadequate synthesis/turnover of phospholipids, among them, those containing DHA, possibly resulting in defective disc membrane assembly with subsequent deterioration of visual cells.

Animals↗
PubMed1976

[Cavity structures in the peripheral retina].

1. Lange's fold of the ora frequently found at autopsy in fetuses and infants is a purely postmortal change. 2. The 'honeycomb ora' occurring in infants and small children may sometimes be present in vivo. The extensive and larger cavities however may well have appeared only postmortally here too (they are not seen in older children). 3. Both the typical or external and the reticular or internal cystoid degeneration of the peripheral retina increase in frequency and extent with increasing age. Both occur in vivo. Biomicroscopically cystoid degenerations apparently can be demonstrated in any living eye after indentation of the ora. Basal membrane fragments and microfibrils have sometimes been shown by staining in the cyst walls (when cyst and vitreous body are connected) and mucopolysaccharides in the cystoid cavities. But there are also cystoid degenerations occurring postmortally. The picture of internal cystoid degeneration can also be seen as a fixation artefact (only) in fetuses in not yet vascularised sections of the retina. In the cystoid cavities one finds histologically sometimes reaction-free cell debris, torn fibres and isolated cell nuclei of the granular layers. Whereas the biomicroscopically found cystoid degenerations almost always end (well) in front of the equator of the eyeball, the histologically found cystoid degenerations are seen relatively often considerably behind the equator. Scotomas to be expected in vivo in these cases have not been observed so far. The periphery of the retina is histologically often torn off the ora without any reaction and displaced far forward. The picture of cystoid degeneration can also be produced quite artificially by bulging of the retina due to fixation in histology (different treatment of the two halves of the eyeball). Even without any tissue participation a picture like cystoid degeneration below the peripheral retina, between it and the pigmented epithelium, may develop in celloidin itself if too quickly hardened. 4. Retinal cysts found relatively often histologically are predominantly extensive cystoid degenerations. Exceptionally these are apparently identical with the rare cysts or retinoschisis cases visible ophthalmoscopically. 5. Small to large-cystic retinal degenerations are mostly secondary reactive changes. The situation of Lange's fold, honeycomb ora and especially cystoid degenerations depends postmortally (but also apparently in vivo) on the pull of the zonule and vitreous body fibrils as regards extent and direction. The intravitally present cavities in (honeycomb ora and) cystoid degeneration are considerably increased postmortally and apparently still more by histological preparation. In addition there seems to be an age-specific alteration in the ratio of the pull of zonule-vitreous body fibrils on the one hand and the (age-dependent) tearability of the retina on the other: in fetuses and infants we get Lange's fold, in infants and small children honeycomb ora and in later childhood increasingly extensive cystoid degenerations.

Cysts↗
PubMed1990

The changing distribution of neurons in the inner nuclear layer from metamorphosis to adult: a morphometric analysis of the anuran retina.

The generation and changing distribution of neurons of the inner nuclear layer (INL) in the retina of two anuran species, Bufo marinus and Xenopus laevis, were studied from metamorphosis to adult. Morphometric studies were undertaken at six developmental stages in Bufo and four in Xenopus. The number and thickness of neurons in the INL were established in 29 predetermined retinal locations from serial sections of the eyes cut vertically or horizontally. The total number of neurons in the INL increased from metamorphosis to adult from 826,000 +/- 185 to 18,760,000 +/- 562 (mean +/- SD) in Bufo and from 308,000 +/- 25 to 877,000 +/- 31 in Xenopus. Over the same period the surface area of the INL increased about 50-fold from 2 mm2 to 96 mm2 in Bufo and 5-fold from 2.5 mm2 to 13 mm2 in Xenopus. In Bufo the difference between the highest cell number (central-temporal retina) and the lowest cell number in a sample area (dorsal and ventral peripheral retina) was 2.1:1 at metamorphosis. This ratio increased to 3.4:1 in the adult. Both the cell number and cell density per sample area in the INL was found to be higher along the nasotemporal meridian of the eye overlying the visual streak of the ganglion cell layer (GCL) of the retina. The retinal distribution of neurons in the INL did not change significantly during postmetamorphic growth in Xenopus. At metamorphosis a 1.7:1 difference was found between the highest neuron number (retinal ciliary margin) and lowest neuron number (retinal centre) decreasing to 1.5:1 in the adult. Retinae were labelled with 3H-thymidine in 15 mm Bufos and examined 2, 6, 12 and 18 weeks later. Higher rates of cell addition to the nasal and temporal poles of the INL were found compared with that at the dorsal and ventral poles. The retinal radial growth at the ciliary margin of the dorsal, ventral, nasal and temporal poles between the time of isotope injection and 18 weeks survival was found to be uneven; more radial elongation occurred at the nasal, dorsal and ventral poles and less at the temporal pole. These observations suggest that (a) the neuron distribution of the INL in adult animals approximates that of the GCL and (b) the visual streak-like area of the INL in Bufo develops by a sustained differential cell addition at the temporal and nasal poles of the retina.

Animals↗