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At least 703 records · Page 39Linked to original sources
PubMed1985

Isolation of an adhesion-mediating protein from chick neural retina adherons.

Adherons are high molecular weight glycoprotein complexes which are released into the growth medium of cultured cells. They mediate the adhesive interactions of many cell types, including those of embryonic chick neural retina. The cell surface receptor for chick neural retina adherons has been purified, and shown to be a heparan sulfate proteoglycan (Schubert, D., and M. LaCorbiere, 1985, J. Cell Biol., 100:56-63). This paper describes the isolation and characterization of a protein in neural retina adherons which interacts specifically with the cell surface receptor. The 20,000-mol-wt protein, called retinal purpurin (RP), stimulates neural retina cell-substratum adhesion and prolongs the survival of neural retina cells in culture. The RP protein interacts with heparin and heparan sulfate, but not with other glycosaminoglycans. Monovalent antibodies against RP inhibit RP-cell adhesion as well as adheron-cell interactions. The RP protein is found in neural retina, but not in other tissues such as brain and muscle. These data suggest that RP plays a role in both the survival and adhesive interactions of neural retina cells.

Animals↗
PubMed2001

Biochemical and ultrastructural studies in the neural retina and retinal pigment epithelium of STZ-diabetic rats: effect of captopril.

We measured the activities of total Na+, K+-ATPase (Na, K-ATPase), its alpha1 and alpha2/alpha3 isoforms and the angiotensin-converting enzyme (ACE) in the microvascular and neural compartments of the retina, and/or retinal pigment epithelium (RPE) of streptozotocin (STZ)-diabetic rats. The effect of captopril, an ACE inhibitor on Na, K-ATPase activities was also determined and correlated to morphological changes. Insulin-dependent diabetes mellitus was induced by a single intraperitoneal injection of STZ (60 mg/kg) in male Long-Evans rats. ACE activity was inhibited by captopril (10 mg/kg given in the drinking water) for 1 month. Na, K-ATPase activity was measured spectrophotometrically or by a radioassay (32P-labeled ATP). The activity of ACE was determined by a radioassay using tritiated benzoyl-gly-gly-gly as substrate. Both the alpha1 and alpha2/alpha3 isoforms of Na, K-ATPase were present in the microvascular and neural compartments of retinas, whereas only one isoform, the alpha2/alpha3, was found in the RPE. In 2-month diabetic rats, the activity of the alpha2/alpha3 isoform was reduced in both the microvascular and neural compartments of retinas, while the activity of the alpha1 isoform was reduced only in the neural isolates. ACE activity was significantly decreased in the retinal neural compartment and unaltered in the microvascular compartment from 2-month diabetic rats. In 5-month diabetic rats, Na, K-ATPase activity was moderately but not significantly reduced in RPE preparations. Ultrastructural studies revealed a significant deepening of basal infoldings in the RPE and a noticeable increase in the size of the extracellular space between the basal infoldings of 5-month diabetic animals. Captopril stimulated Na, K-ATPase activity in the neural retina, but not in the RPE. Diabetes-induced morphological changes in the RPE were not improved by captopril. An enlargement of intercellular space between the RPE cells was a frequent finding in the treated group. In conclusion, captopril stimulated Na, K-ATPase activity in the neural retina of diabetic rats. This stimulation seems to be beneficial to the neural retina. ACE inhibition, however, did not improve RPE morphological changes. Although the clinical significance of increased intercellular spacing between RPE cells in treated animals is not clearly established, we speculate that it might contribute to an increased alteration of their barrier function. Additional studies are necessary to assess both the desirable and adverse effects of captopril and other ACE inhibitors in the retinas of diabetic patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2004

Comparison of glucose influx and blood flow in retina and brain of diabetic rats.

Diabetes is associated with extensive microvascular pathology and decreased expression of the glucose transporter (GLUT-1) in retina, but not brain. To explore the basis of these differences, the authors simultaneously measured glucose influx (micromol x g(-1) x min(-1)) and blood flow (mL x g(-1) x min(-1)) in retina and brain cortex of nondiabetic control rats (normoglycemic and acute-hyperglycemic) and in rats with streptozotocin-induced diabetes (with or without aminoguanidine (AMG) treatment) using a single-pass, dual-label indicator method. In addition, tissue glucose and adenosine triphosphate (nmol/mg dry weight) levels were measured. Glucose influx in retina exceeded that of cortex by about threefold for both the nondiabetic and diabetic groups. In contrast, blood flow in retina was significantly lower than in cortex by about threefold for each group. Retinal and cortical glucose influx in the diabetic rats was lower than in the nondiabetic acute-hyperglycemic group, but not in the normoglycemic group. Blood flow in these tissues remained relatively unchanged with glycemic conditions. The glucose levels in the diabetic retina (aminoguanidine untreated and aminoguanidine treated) were fourfold to sixfold greater than the nondiabetic retina. The cortical glucose levels remained unchanged in all groups. These data suggest that the accumulation of glucose in the diabetic retina cannot be explained by increased endothelial-glucose uptake or increased vascular membrane permeability.

Animals↗
PubMed2000

Histopathologic abnormalities in rabbit retina after intravitreous injection of expansive gases and air.

PURPOSE: To evaluate histopathologic retinal changes in rabbit eyes after injection of pure perfluoropropane (C3F8) gas, pure sulfur hexafluoride (SF6) gas, or air into the vitreous cavity. METHODS: Air, C3F8 gas, or SF6 gas (0.4 mL each) were injected into rabbit vitreous cavities. Two, 4, and 6 weeks later, light and electron microscopic examinations were conducted, and the immunohistochemical localization of glutamate in the retina was studied. Noninjected eyes served as controls. RESULTS: At all time points, thinning or disappearance of the outer plexiform layer in the superior retina in eyes that received C3F8 gas was found; the inferior retina was the same as in controls. In eyes that received SF6 gas or air, light and electron microscopy showed that the superior and inferior retina were the same as in controls at all time points. Immunohistochemical examination showed abnormal glutamate distribution of the superior retina in eyes injected with C3F8 gas, SF6 gas, or air. However, glutamate distribution was the same as in controls in the inferior retina in eyes injected with C3F8 gas, SF6 gas, or air. CONCLUSIONS: Retinal tamponade using intraocular gases induces histopathologic retinal changes in the superior retina of the rabbit eye, where the gases are in continuous contact with the eye.

Air↗
PubMed2004

Structural features of attached retina in rhegmatogenous retinal detachments.

PURPOSE: To examine the thickness and structural features of the ophthalmoscopically normal-appearing, attached retina in rhegmatogenous retinal detachments by optical coherence tomography (OCT) and compare them with those of the fellow eye. METHODS: Seventy eyes of 35 patients with rhegmatogenous retinal detachments were included in this study. The retinal detachments were not total. None of the patients had pathologic myopia or a history of ocular surgery. The fellow eyes were ophthalmoscopically normal and used as controls. Attached retinal sites of the eyes with a retinal detachment and the corresponding retinal sites of the fellow eyes were examined by OCT. Three OCT sections were taken from each eye, and thicknesses of three reflective zones corresponding to the inner part of the neurosensory retina (partial neurosensory retina), photoreceptor-photoreceptor outer segment, and total retinal thickness on each OCT section were measured and compared with those of the fellow eye. These three measurements were taken as the main outcome measures and performed on five different sites of each OCT section taken from each eye. RESULTS: The mean partial neurosensory retinal thickness of the attached retina in the eyes with a retinal detachment and the corresponding retinal sites in the fellow eyes was 172.74 +/- 14.23 microm and 170.60 +/- 16.51 microm, respectively. There was no statistically significant difference between these two values. The mean photoreceptor outer segment thickness of the attached retina in the eyes with a retinal detachment and the corresponding retinal sites in the fellow eyes was 62.74 +/- 12.02 microm and 58.23 +/- 15.14 microm, respectively. There was a statistically significant difference between these two values. The mean total retinal thickness of the still-attached retina in the eyes with a retinal detachment and the corresponding retinal sites in the fellow eyes were 293.23 +/- 27.87 microm and 277.06 +/- 19.12 microm, respectively. There was a statistically significant difference between these two values. CONCLUSIONS: The main difference between the two groups of eyes was at the level of the thickness of the black hyporeflective zone, corresponding anatomically to the photoreceptor and photoreceptor outer segment that enlarges in the retinal detachments. Therefore, there may be a subclinical retinal detachment or a global retinal relaxation even in the ophthalmoscopically normal-appearing, still-attached retina. This may be the underlying cause of preoperative and postoperative signs and symptoms. Additional studies are required to confirm these findings.

Adolescent↗
PubMed2005

Ultrastructural analysis of rabbit retina irradiated with a new 670-nm diode red laser at different powers.

PURPOSE: Diode lasers have compact dimensions, efficient electric-optical conversion, absence of major cooling requirements, long useful life, and minimal maintenance. We verified the structural and ultrastructural effects of diode red laser emissions at 670 nm on pigmented rabbit retina. METHODS: Transpupillary laser pulses were applied to rabbit retinas at variable powers with a spot size of 500 microm ( approximately 1,000 microm at the retina level) and duration of 200 milliseconds. Light and electron microscopic analyses were performed. RESULTS: Subthreshold non-visible lesions were produced using a power of 200 mW. Ophthalmoscopically visible lesions were produced using a power of 400 mW. More prominent lesions were obtained using a higher power (600 mW). Structural and peculiar ultrastructural changes correlated with the power used. In general, damage was incurred by the retinal pigment epithelium with extension into the superficial choroid posteriorly and into the outer retina anteriorly. The inner retina was involved at higher power levels. CONCLUSIONS: Ultrastructural analysis of rabbit retina treated with the 670-nm diode laser adds newer insights on tissue changes after thermal irradiation. The effects observed are consistent with those reported for the krypton red laser. The 670-nm diode laser is an economic small-size photocoagulator that appears to be a promising modality for transpupillary laser photocoagulation of the retina.

Animals↗
PubMed2004

Ca(2+) signalling and gap junction coupling within and between pigment epithelium and neural retina in the developing chick.

Development of the neural retina is controlled in part by the adjacent retinal pigment epithelium (RPE). To understand better the mechanisms involved, we investigated calcium signalling and gap junctional coupling within and between the RPE and the neural retina in embryonic day (E) 5 chick. We show that the RPE and the ventricular zone (VZ) of the neural retina display spontaneous Ca(2+) transients. In the RPE, these often spread as waves between neighbouring cells. In the VZ, the frequency of both Ca(2+) transients and waves was lower than in RPE, but increased two-fold in its presence. Ca(2+) signals occasionally crossed the boundary between the RPE and VZ in either direction. In both tissues, the frequency of propagating Ca(2+) waves, but not of individual cell transients, was reduced by gap junction blockers. Use of the gap junction permeant tracer Neurobiotin showed that neural retina cells are coupled into clusters that span the thickness of the retina, and that RPE cells are both coupled together and to clusters of cells in the neural retina. Immunolabelling for Cx43 showed this gap junction protein is present at the junction between the RPE and VZ and thus could potentially mediate the coupling of the two tissues. Immunolabelling for beta-tubulin and vimentin showed that clusters of coupled cells in the neural retina comprised mainly progenitor cells. We conclude that gap junctions between progenitor cells, and between these cells and the RPE, may orchestrate retinal proliferation/differentiation, via the propagation of Ca(2+) or other signalling molecules.

Aniline Compounds↗
PubMed1996

Unique distribution of somatostatin-immunoreactive cells in the retina of the tree shrew (Tupaia belangeri).

Somatostatin-like immunoreactive cells in the tree shrew retina were studied with the monoclonal antibody S8 against the neuropeptide somatostatin 14. As in some other mammals, immunoreactive somata are exclusively found in the ganglion cell layer. Immunoreactive processes form a sparse main plexus in the inner plexiform layer near the border of the inner nuclear layer; fewer additional processes are found closer to the ganglion cell layer. With retrograde labelling of retinal ganglion cells by injections of the tracer Fast Blue into the superior colliculus and lateral geniculate body and counterstaining of the retinae with S8, approximately 5% of the immunoreactive somata were double-labelled at any retinal location. The vast majority of somatostatin-like immunoreactive cells are thus displaced amacrine cells. Their somata are distributed over the entire retina. Their population density is highest in the temporal retina, with peak densities of approximately 5000 cells/mm2 near the central area and a steep density gradient. In the remaining retina densities are 200-400 cells/mm2, falling to approximately 100 cells/mm2 at the retinal margins. This is in stark contrast to the somatostatin-like immunoreactive cells in other mammalian retinae which have densities of 10-40 cells/mm2 and are confined to restricted retinal regions (inferior retina and/or retinal margin).

Amidines↗
PubMed2006

Dark-rearing-induced reduction of GABA and GAD and prevention of the effect by BDNF in the mouse retina.

Gamma-aminobutyric acid (GABA) is an important retinal neurotransmitter. We studied the expression of GABA, glutamate decarboxylase 65 (GAD65) and GAD67 by immunocytochemistry and Western blot, in the retinas of control and dark-reared C57BL/6J black mice. This study asked three questions. First, is visual input necessary for the normal expression of GABA, GAD65 and GAD67? Second, can the retina recover from the effects of dark-rearing if returned to a normal light-dark cycle? Third, does BDNF prevent the influence of dark-rearing on the expression of GABA and GAD? At postnatal day 10 (P10), before eye opening, GABA immunoreactivity was present in the ganglion cell layer (GCL), in the innermost rows of the inner nuclear layer (INL) and throughout the inner plexiform layer (IPL) of control and dark-reared retinas. In P30 control retinas, GABA immunoreactivity showed similar patterns to those at P10. However, in P30 dark-reared retinas, the density of GABA-immunoreactive cells was lower in both the INL and GCL than in control retinas. In addition, visual deprivation retarded GABA immunoreactivity in the IPL. Western blot analysis showed corresponding differences in the levels of GAD65 but not of GAD67 expression between control and dark-rearing conditions. In our study, dark-rearing effects were reversed when the mice were put in normal cyclic light-dark conditions for 2 weeks. Moreover, dark-reared retinas treated with BDNF showed normal expression of both GABA and GAD65. Our data indicate that normal expression of GABA and GAD65 is dependent on visual input. Furthermore, the data suggest that BDNF controls this dependence.

Animals↗
PubMed1982

Glycerol phosphate dehydrogenase in developing chick retina and brain.

The development of cytoplasmic glycerol phosphate dehydrogenase (GPDH) activity in chick neural retina is compared with that in brain. GPDH converts dihydroxyacetone phosphate to glycerol 3-phosphate, an intermediate in phospholipid synthesis. The enzyme is known to be under corticosteroid control in rat brain and spinal cord (but not muscle or liver) and in primary oligodendrocyte cultures. It has not been previously studied in the eye. In chick brain the GDPH specific activity rises fivefold from the early embryo to the adult, with nearly all the increase occurring between embryonic day 14 and hatching. This time course correlates well with the known maturation of chick adrenal cortex (which produces corticosteroids). On the other hand, in chick retina the GPDH specific activity remains at a low basal level throughout development. Furthermore, adult rat and beef retinas show much lower enzyme activity than do the corresponding brain tissues. GPDH can be induced precociously by hydrocortisone in embryonic chick brain from days 12 through 16, both in the intact embryo and in tissue culture; however, GPDH is not at all inducible in chick retina. The developmental increase in chick brain GPDH can be correlated qualitatively with myelin formation, as shown by luxol fast blue staining, whereas no myelin is seen in retina at any age. Our results are consistent with recent immunocytochemical studies demonstrating that GPDH in rat brain is associated with myelin-producing oligodendroglial cells, absent in retina. In comparison, another glial enzyme, glutamine synthetase (GS), known to be inducible in both chick brain and retina, is localized in brain astrocytes and retinal Müller cells.

Aging↗
PubMed1982

Serotonin-containing neurones in vertebrate retinas.

It has been established by a combination of HPLC and electrochemical detection that frog, lizard, goldfish, rabbit, and bovine retinas contain both dopamine and serotonin. Immunohistological and immunoradiographical methods show that serotonin is localised in amacrine perikarya and processes situated in the inner plexiform layers of frog, lizard, and goldfish retinas. The amount of serotonin in the mammalian retina appears to be too low for detection in neurones. The serotonin in the bovine retina is located mainly in the inner nuclear and plexiform layers, suggesting that the amine is present in the same types of cells as found for frog, lizard, and goldfish retinas. Retinas incubated in [3H]serotonin showed that radioactivity is associated with processes in the inner plexiform layer and amacrine perikarya. These results suggest that the neuronal elements that contain endogenous serotonin also have the capacity to accumulate exogenous amine and are consistent with the opinion that serotonin has a neuronal function in retinas of a variety of vertebrates.

Animals↗
PubMed1982

Biosynthesis of somatostatin-like immunoreactivity by frog retinas in vitro.

Somatostatin-like immunoreactivity has been localized to a wide variety of central nervous system neurons, including the retina. We utilized the unique advantages the retina provides for in vitro studies of nerves to examine the biosynthesis of somatostatin. Extracts of frog retinas pulse-labeled with [35S]cysteine for various time periods revealed uptake of radioactivity into material adsorbable by anti-somatostatin antibody linked to affinity beads. This uptake increased in a curvilinear fashion for 4 h and was inhibited by cycloheximide (0.2 mM) or by boiling the retinas prior to labeling. Pulse-chase experiments revealed that affinity-adsorbable radioactivity from retinal extracts decreased with time of incubation in chase medium; 89% of this decrease could be accounted for by increased in the affinity-adsorbable radioactivity of the chase medium. Chromatography of the retinal extracts on Sephadex G50 (superfine) revealed four elution peaks, whereas only one peak, co-eluted with somatostatin-14, could be identified in the medium. Chromatographic elution patterns of affinity-adsorbable radioactivity from extracts of pulse-labeled retinas incubated in chase medium for various times showed a gradual shift of radioactivity from the earlier-eluting peaks to the later ones. These studies indicate that biosynthesis of somatostatin occurs in frog retinas in vitro. The retina may be a useful model for further study of peptidergic neurons.

Animals↗
PubMed1982

Increased levels of 3',5'-cyclic adenosine monophosphate induced by cobaltous ion or 3-isobutylmethylxanthine in the incubated mouse retina: evidence concerning location and response to ions and light.

Dark levels of 3',5'-cyclic adenosine monophosphate (cyclic AMP) of mouse retinas incubated in Earle's medium were elevated by 3-isobutyl-methylxanthine (IBMX) and/or Co2+ or Mn2+, but not by Cd2+, methylverapamil, or excess Mg2+ of Ca2+. Light reduced elevated dark levels of cyclic AMP in the presence of agents known to block the light modulation of post-receptoral neurons (aspartate, Co2+, high Mg2+), a finding consistent with a cyclic AMP metabolism in photoreceptors. Co2+-elevated cyclic AMP levels were not less light-sensitive than cyclic GMP levels. Ouabain substantially increased IBMX-elevated cyclic AMP with a persistent light response, but reduced the dark action of Co2+. IBMX, but not Co2+, also increased cyclic AMP in receptorless (rd/rd) retinas; haloperidol partly reduced this IBMX effect. In normal retinas in Co2+ medium, progressively replacing Na+ by K+ (but not choline+) from 1--50 mM caused a progressive fall in dark, light-sensitive cyclic AMP levels, but from 50 to 100 mM-K+ there appeared haloperidol-preventable increases in both the dark- and light-insensitive levels of cyclic AMP. In IBMX-aspartate medium a haloperidol-preventable, light-insensitive increase in cyclic AMP appeared from 20 mM-K+ upwards. Haloperidol-preventable increases in cyclic AMP as induced by high K+ required Co2+ in normal retinas, but not in receptorless retinas, and 5 nM-Co2+ greatly increased the response to dopamine in receptorless retinas. The post-dopaminergic neurons, which are 4th-order neurons, may have become hypersensitive to dopamine in receptorless retinas consequent to the absent signal from the 1st-order photoreceptors, or directly, as an effect of the same gene underlying the dystrophy.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Dopaminergic receptors in bovine retina and their interaction with thyrotropin-releasing hormone.

A superfusion technique was employed to study the release of [3H]dopamine from isolated bovine retina. Only K+-stimulated release was observed from both light- and dark-adapted retina; release by other stimuli was from dark-adapted retina only. Light-evoked release of [3H]dopamine from dark-adapted retina was blocked by thyrotropin-releasing hormone (TRH), which has previously been identified as a retinal neuropeptide. TRH itself released small amounts of [3H]dopamine from dark-adapted retina. These results are interpreted as indicating that TRH acts as a modulator of dopaminergic activity in retina through the agency of presynaptic autoreceptors. Evidence of the existence of a feedback inhibition system, probably mediated by dopaminergic autoreceptors, was found by the inclusion of sulpiride, a dopaminergic D2 receptor antagonist in the perfusate, which, in a stereoselective manner, enhanced spontaneous and light-evoked release of [3H]dopamine. On the other hand, dopamine (1 microM) reduced these effects. TRH did not affect the high-affinity uptake system for dopamine in retina; this, then, could not account for the effects on release. Radioligand binding showed a specific, saturable high-affinity binding system for [3H]TRH, with an apparent KD of 2.2 nM and a Bmax of 23 fmol/mg protein in bovine retinal membranes. Displacement experiments showed that specific [3H]TRH binding was displaced in the nanomolar range by spiperone and in the micromolar range by dopamine, whereas L-(--)-sulpiride was virtually inactive in displacing [3H]TRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Differences and similarities in muscarinic receptors of rat heart and retina: effects of agonists, guanine nucleotides, and N-ethylmaleimide.

Muscarinic receptor stimulation inhibits cyclic AMP formation in rat atria but not in retina. We compared the properties of the muscarinic receptors in rat atrial and retinal membranes using the antagonist [3H]quinuclidinyl benzilate. In both atria and retina there is a single binding site for antagonists, while agonists appear to interact at two classes of binding sites. Muscarinic receptors in atria and retina have the same apparent affinities for several antagonists and for a series of muscarinic agonists. In both tissues N-ethylmaleimide decreases agonist affinity for the high-affinity binding sites. Muscarinic receptors in atria and retina differ, however, in several properties relating to the proportions of high- and low-affinity agonist sites. First, guanine nucleotides markedly increase the proportion of low-affinity binding sites in atria, but not in retina. Second, for all agonists there are fewer high-affinity binding sites in retina. Third, the "partial agonist" pilocarpine appears to interact with two classes of binding sites in atria, but with only a single class of sites in retina. Our data suggest that muscarinic receptors that inhibit cyclic AMP formation and those that do not share common properties that determine receptor affinity for agonists and classic antagonists. The differences between these receptors are manifest, however, in the effects of guanine nucleotides and the ability of agonists, especially those of low efficacy, to affect the proportion of high- and low-affinity sites and to effect a biological response.

Animals↗
PubMed1988

Muscarinic acetylcholine receptors from avian retina and heart undergo different patterns of molecular maturation.

Muscarinic acetylcholine receptors (mAChRs) from the avian CNS exist in two molecular weight forms whose concentrations change during development. Here, we have compared the development of mAChRs from embryonic hearts with those of the CNS. Analysis of [3H]-propylbenzilylcholine mustard (PrBCM)-labeled retina and heart mAChRs by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed two atropine-sensitive peaks for each tissue. Apparent molecular masses of retina mAChRs, 86 +/- 0.7 kilodaltons (kDa) and 72 +/- 0.7 kDa, were different from those of heart mAChRs, 77 +/- 1.0 kDa and 52 +/- 0.9 kDa. During retina development, the major receptor type changed from 86 kDa to 72 kDa. No such change occurred during heart development. Furthermore, the 52-kDa species appeared to be generated by endogenous proteolysis, as prolonged incubation of heart membranes at 37 degrees C increased the amount of 52-kDa peptide with a decrease of 77-kDa peptide. Protease inhibitors blocked this conversion. Incubation of retina membranes at 37 degrees C did not result in a conversion of the 86-kDa peptide into the 72-kDa peptide, but it did cause the appearance of a minor amount of 52-kDa peptide. The proteolysis of retina mAChRs was not enhanced by cohomogenizing them with heart tissue, arguing against the presence of releasable proteases in heart. Membrane-bound retina and heart mAChRs displayed similar sensitivity to exogenous (Staphylococcus aureus V8) protease, indicating that heart receptors were not unusually susceptible to proteolytic attack; analysis of the labeled polypeptides with the V8 protease showed different patterns of digestion for the retina and heart receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

GD3 prevalence in adult rat retina correlates with the maintenance of a high GD3-/GM2-synthase activity ratio throughout development.

Unlike neurons from avian retina and other regions of avian and mammalian brain, neurons from mammalian retina not only contain gangliosides of the gangliotetraosyl ceramide series but also maintain a prevalence of GD3, a ganglioside of the lactosylceramide series characteristic of proliferative neural cells, when they are fully differentiated. We show here that GD3 is prevalent at all developmental periods of the rat retina from birth [50% of total gangliosidic N-acetylneuraminic acid (NeuNAc)] to adult (30% of total gangliosidic NeuNAc). GD3-synthase specific activity increased about 1.5-fold from birth to day 7 and essentially plateaued thereafter. The GD3-/GM2-synthase specific activity ratio was compared in rat and chicken retina at early and late developmental stages. In chicken retina the ratio was about 0.7 at early (when GD3 is prevalent) and decreased to 0.07 at late (when GD1a is prevalent) developmental stages. In rat retina the ratio was about 13 and 6 at, respectively, early and late developmental stages. These findings suggest that the prevalence of GD3 and of other "b" pathway gangliosides in adult rat retina neurons could be due in part to the maintenance of a high GD3-/GM2-synthase activity ratio throughout development of the tissue.

Aging↗
PubMed1991

The relationship between light, dopamine release and horizontal cell coupling in the mudpuppy retina.

1. The effect of different experimental conditions on electrical coupling between horizontal cells in the mudpuppy retina was studied by comparing the changes in responses to illumination of the central and peripheral portions of the receptive field, using centred spot and annulus stimuli. An increase in the amplitude of the response to a centred spot stimulus and a decrease in the amplitude of the response to a concentric annulus indicated a decrease in coupling, and vice versa. 2. Dopamine (10-250 microM) caused a decrease in coupling between horizontal cells. The uncoupling effect of dopamine was much greater in dark-adapted than in light-adapted retinas. The effect of the D1-receptor agonist SKF38393 was similar to that of dopamine. The effect of the D2-receptor agonist LY171555 on coupling was opposite to that of dopamine; this was attributed to a reduction in endogenous dopamine release. 3. The D1 antagonist SCH23390 (15 microM) caused an increase in coupling between horizontal cells. This effect was much greater in light-adapted than in dark-adapted retinas. 4. The glutamate analogue 2-amino-4-phosphonobutyrate (APB), which hyperpolarizes on-centre bipolar cells and blocks their responses to light, caused an increase in coupling between horizontal cells. This effect of APB was greater in light-adapted retinas than in dark-adapted retinas. The effect of APB on coupling could be reversed by the addition of dopamine, but the effect of dopamine on coupling could not be reversed by the addition of APB. These results suggest that APB increases horizontal cell coupling by causing a decrease in dopamine release. 5. In dark-adapted retinas, 2.5 min exposure to an adapting light caused a decrease in coupling between horizontal cells; the uncoupling effect of the adapting light was blocked in the presence of either SCH23390 or APB. 6. The results suggest that coupling between horizontal cells in the mudpuppy retina is decreased by dopamine acting at D1 receptors, that the release of dopamine affecting horizontal cells is greater under light-adapted conditions, and that the pathway by which exposure to light increases this dopamine release is mainly via on-centre bipolar cells.

Adaptation, Ocular↗