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At least 55 records · Page 3Linked to original sources
PubMed1987

Optimum conditions for successful transplantation of immature rat retina to the lesioned adult retina.

We have previously reported the successful transplantation of neonatal rat retina to the lesioned retinas of adult host rats. The current studies provide a much more in-depth evaluation of the optimal conditions under which successful grafting can be achieved. Utilizing the same surgical approach and techniques as in our earlier studies, the variables of host lesion conditioning and donor age were investigated. The grafts were evaluated for survival, location, and degree of achievement of selected histological characteristics. The latter category was organized into an evaluation index (E.I.) which provided a consistent system of scoring for purposes of inter-group comparisons. In order to study the effects of lesion conditioning, neonatal grafts were delivered into fresh (0), 1, 2, 4, and 8 week conditioned lesions. Excellent survival and placement were observed at all conditioning times examined. Even the E.I. failed to reveal any statistically significant differences among the lesion conditioning groups. However, there was the suggestion of reduced scarring in the older, more stable lesion groups. The second portion of the study, dealing with donor age, involved the transplantation of E14, E16, E20, PN1, and PN10 retina into freshly lesioned sites in the host retina. Again the result was excellent overall graft survival and placement in all groups. The E.I. score, however, revealed highly significant differences between PN10 grafts and those from all other groups tested. These differences were revealed for all histological criteria with the exception of non-neuronal barrier formation. These studies show the utility of the current model for the repair of retinal lesions over an extended post-traumatic period as well as revealing the wide developmental window for harvesting retinal tissue for the purpose of intravitreal transplantation.

Aging↗
PubMed1996

QRI, a retina-specific gene, encodes an extracellular matrix protein exclusively expressed during neural retina differentiation.

Neural retina development results from growth arrest of neuroectodermal precursors and differentiation of postmitotic cells. The QRI gene is specifically expressed in Müller retinal glial cells. Its expression coincides with the stage of withdrawal from the cell cycle and establishment of differentiation and is repressed upon induction of retinal cell proliferation by the v-src gene product. In this report, we show that the QR1 gene encodes several glycosylated proteins that are secreted and can either associate with the extracellular matrix or remain diffusible in the medium. By using pulse-chase experiments, the 100-103 kDa forms seem to appear first and are specifically incorporated into the extracellular matrix, whereas the 108 and 60 kDa polypeptides appear later and are detected as soluble forms in the culture medium. We also report that expression of the QR1 gene is developmentally regulated in the chicken. Its mRNA is first detectable at embryonic day 10, reaches a maximal level at embryonic day 15 and is no longer detected at embryonic day 18. Immunolocalization of the QR1 protein in chicken retina sections during development shows that expression of the protein parallels the differentiation pattern of post-miotic cells (in particular Müller cells and rods), corresponding to the two differentiation gradients in the retina: from the ganglion cell layer to the inner nuclear layer and outer nuclear layer, and from the optic nerve to the iris. At embryonic day 10, expression of the QR1 protein(s) is restricted to the optic nerve region and the inner nuclear layer, colocalizing with Müller cell bodies. As development proceeds, QR1 protein localization spreads towards the iris and towards the outer nuclear layer, following Müller cell elongations towards the photoreceptors. Between embryonic days 16 and 18, the QR1 protein is no longer detectable in the optic nerve region and is concentrated around the basal segment of the photoreceptors in the peripheral retina. Our results suggest a role for the QR1 gene product in the process of growth arrest and establishment of photoreceptor differentiation.

Animals↗
PubMed2004

Binding characteristics and daily rhythms of melatonin receptors are distinct in the retina and the brain areas of the European sea bass retina (Dicentrarchus labrax).

Melatonin is synthesized, with a circadian rhythm, in the pineal organ of vertebrates, high levels being produced during the scotophase and low levels during the photophase. The retina also produces melatonin, although in the case of the European sea bass, its secretion pattern appears to be inverted. In the study described here, radioreceptor assay techniques were used to characterize the melatonin binding sites, their regional distribution and their daily variations. Brain and retina membrane preparations were used in all the binding assays and 2-[125I]iodomelatonin ([125I]Mel) as radioligand at 25 degrees C. The specific binding of [125I]Mel was seen to be saturable, reversible, specific and of high affinity. In all the tissues assayed, the power of the ligands to inhibit [125I]Mel binding decreased in the following order: melatonin>>4-P-PDOT>luzindole> or =N-acetylserotonin, which points to the presence of Mel1-like receptors. The inhibition curves of 4-P-PDOT suggested the presence of two different binding sites in the brain areas, but only one type of site of low affinity in the neural retina. No daily variations in [125I]Mel binding capacity (Bmax) or affinity (Kd) were detected in the brain areas, while a clear rhythm in Kd melatonin receptor affinity and Bmax binding capacity was observed in the retina. Kd and Bmax retinal rhythms were out of phase with the lowest Kd and the highest Bmax occurring at scotophase. This result suggests that retinal melatonin is a paracrine factor able to control receptor desensitization during photophase when ocular melatonin is higher in this species.

Animals↗
PubMed1999

RET-RGS, a retina-specific regulator of G-protein signaling, is located in synaptic regions of the rat retina.

RGS (regulators of G protein signaling) proteins negatively regulate the alpha subunit of G proteins by accelerating their intrinsic GTPase activity. In a previous work, we reported the cloning of a cDNA encoding for a new RGS protein, RET-RGS. We showed that it is specifically expressed in the retina, notably by photoreceptor cells and that it has an in vitro GAP activity on transducin. To understand the role of RET-RGS, and in particular to determine whether it regulates the phototransduction cascade in photoreceptor cells, RET-RGS was immunolocalized on rat retina sections. Whereas no labeling was detected in outer nor inner segments of photoreceptors cells, dense immunoreactive products were localized in the outer and inner plexiform layers which correspond to the regions of synaptic interplay between the different neurons of the retina including the photoreceptor cells. These results rule out a role of RET-RGS on the phototransduction cascade and suggest that it may participate in retina specific synaptic transductions.

Animals↗
PubMed1981

Dopaminergic mechanisms in the teleost retina. II. Factors affecting the accumulation of cyclic AMP in pieces of intact carp retina.

The ability of dopamine, dopamine agonists, other proposed retinal neurotransmitters, depolarizing agents and light to stimulate adenylate cyclase activity in pieces of intact carp retina has been examined. The evidence indicates that a dopamine-sensitive adenylate cyclase is the only neurotransmitter activated adenylate cyclase in the carp retina. That is, only dopamine, or agents that activate dopamine receptors, appear to stimulate cyclic AMP synthesis in the retina. Depolarizing agents such as K+ or veratridine also increase retinal cyclic AMP levels, but apparently by releasing endogenous stores of dopamine. For example, the increase of retinal cyclic AMP levels induced by 45 mM-K+ is blocked by 5 mM-Co2+ or 100 microM-haloperidol, a dopamine antagonist. Flashing lights slightly increase cyclic AMP levels in the retina, an effect that is likewise abolished by haloperidol.

1-Methyl-3-isobutylxanthine↗
PubMed1992

Melatonin increases serotonin N-acetyltransferase activity and decreases dopamine synthesis in light-exposed chick retina: in vivo evidence supporting melatonin-dopamine interaction in retina.

The administration of melatonin, either peripherally (0.01-10 mg/kg) or intraocularly (0.001-10 mumol/eye), to light-exposed chicks dose-dependently increased serotonin N-acetyltransferase (NAT) activity in retina but not in pineal gland. The effect of melatonin was slightly but significantly reduced by luzindole (2-benzyl-N-acetyltryptamine), and not affected by two other purported melatonin antagonists, N-acetyltryptamine and N-(2,4-dinitrophenyl)-5-methoxytryptamine (ML-23). The elevation of the enzyme activity induced by melatonin was substantially stronger than that evoked by 5-hydroxytryptamine, N-acetyl-5-hydroxytryptamine, or 5-methoxytryptamine. The melatonin-evoked rise in the retinal NAT activity was counteracted by two dopamine D2 receptor agonists, quinpirole and apomorphine, and prevented by the dopamine D2 receptor blocker spiroperidol, and by an inhibitor of dopamine synthesis, alpha-methyl-p-tyrosine. Melatonin (0.1-10 mg/kg i.p.) dose-dependently decreased the levels of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC), as well as the DOPAC/dopamine ratio, in chick retina but not in forebrain. The results obtained (1) indicate that melatonin in vivo potently inhibits dopamine synthesis selectively in retina, and (2) suggest that the increase in retinal NAT activity evoked by melatonin in light-exposed chicks is an indirect action of the compound, and results from the disinhibition of the NAT induction process from the dopaminergic (inhibitory) signal. The results provide in vivo evidence supporting the idea (derived on the basis of in vitro findings) that a mutually antagonistic interaction between melatonin and dopamine operates in retinas of living animals.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2005

Nutritional manipulation of primate retinas, III: Effects of lutein or zeaxanthin supplementation on adipose tissue and retina of xanthophyll-free monkeys.

PURPOSE: Macular pigment (MP) is composed of the xanthophylls lutein (L) and zeaxanthin (Z) and may help to prevent age-related macular degeneration or retard its progression. In this study the effects of L or Z supplementation on carotenoid levels was examined in serum, adipose tissue, and retina in rhesus monkeys with no previous intake of xanthophylls. METHODS: From birth to 7 to 16 years of age, 18 rhesus monkeys were fed semipurified diets containing all essential nutrients but no xanthophylls. Six were supplemented with pure L and 6 with pure Z at 3.9 micromol/kg per day for 24 to 101 weeks. At baseline and at 4- to 12-week intervals, carotenoids in adipose tissue were measured by HPLC. At study completion, carotenoids in serum and retina (central 4 mm, 8-mm annulus, and the periphery) were determined. Results were compared with data from control monkeys fed a standard laboratory diet. RESULTS: Monkeys fed xanthophyll-free diets had no L or Z in serum or tissues. After L or Z supplementation, serum and adipose tissue concentrations significantly increased in the supplemented groups. Both L and 3R,3'S-Z (RSZ or meso-Z, not present in the diet) were incorporated into retinas of monkeys supplemented with L, with RSZ present only in the macula (central 4 mm). All-trans Z, but no RSZ, accumulated in retinas of monkeys supplemented with Z. CONCLUSIONS: L is the precursor of RSZ, a major component of macular pigment. Xanthophyll-free monkeys can accumulate retinal xanthophylls and provide a valuable model for examining their uptake and conversion.

Adipose Tissue↗
PubMedDate not supplied

Effect of visible light on normal and P23H-3 transgenic rat retinas: characterization of a novel retinoic acid derivative present in the P23H-3 retina.

Transgenic rats with the P23H mutation in rhodopsin exhibit increased susceptibility to light damage, compared with normal animals. It is known that light-induced retinal damage requires repetitive bleaching of rhodopsin and that photoreceptor cell loss is by apoptosis; however, the underlying molecular mechanism(s) leading to photoreceptor cell death are still unknown. Photoproducts, such as all-trans retinal or other retinoid metabolites, released by the extensive bleaching of rhodopsin could lead to activation of degenerative processes, especially in animals genetically predisposed to retinal degenerations. Using wild-type and transgenic rats carrying the P23H opsin mutation, we evaluated the effects of acute intense visible light on retinoid content, type and distribution in ocular tissues. Rats were exposed to green light (480-590 nm) for 0, 5, 10, 30 and 120 min. Following light treatment, rats were sacrificed and neural retinas were dissected free of the retinal pigment epithelium. Retinoids were extracted from retinal tissues and then subjected to HPLC and mass spectral analysis. We found that the light exposure affected relative levels of retinoids in the neural retina and retinal pigment epithelium of wild-type and P23H rat eyes similarly. In the P23H rat retina but not the wild-type rat retina, we found a retinoic acid-like compound with an absorbance maximum of 357 nm and a mass of 304 daltons. Production of this retinoic acid-like compound in transgenic rats is influenced by the age of the animals and the duration of light exposure. It is possible that this unique retinoid may be involved in the process of light-induced retinal degeneration.

Animals↗
PubMed2003

Amyloid-beta is found in drusen from some age-related macular degeneration retinas, but not in drusen from normal retinas.

PURPOSE: Age-related macular degeneration (AMD) is the most common cause of irreversible vision loss in the elderly. Increased understanding of the pathogenesis is necessary. Amyloid-beta (Abeta), a major extracellular deposit in Alzheimer's disease plaques, has recently been found in drusen, the hallmark extracellular deposit in AMD. The goal of this study was to characterize the distribution and frequency of Abeta deposits in drusen from AMD and normal post mortem human retinas to gain additional insight about the potential role of Abeta in AMD patho genesis. METHODS: Immunocytochemistry was performed with three Abeta antibodies on sections from 9 normal and 9 AMD (3 early, 3 geographic atrophy, 3 exudative AMD) retinas. Five sections from each eye were evaluated. Abeta positive deposits in drusen were identified using epifluorescence and confocal microscopy. Antibodies were pre-adsorbed with Abeta peptide to verify specificity. Some sections were stained with PAS-hematoxylin to aid in evaluation of morphology. RESULTS: To test and optimize immunocytochemistry, Abeta was detected in amyloid plaques from Alzheimer's brains. Abeta label was blocked by pre-adsorption of antibody with Abeta peptide, verifying specificity. Four of the 9 AMD retinas and none of the 9 normal retinas had Abeta positive drusen. Two of the early AMD eyes had a few A[beta] positive drusen, each with a few Abeta-containing vesicles, and 2 of the geographic atrophy (GA) eyes had many Abeta positive drusen with many Abeta containing vesicles. CONCLUSIONS: Abeta was present in 4 of 9 AMD eyes. Within these eyes, Abeta localized to a subset of drusen. None of the 9 normal eyes surveyed, some of which had small drusen, were A beta positive. Abetapositive vesicles were most numerous in GA eyes at the edges of atrophy, the region at risk for further degeneration. These results suggest that Abeta in drusen correlates with the location of degenerating photoreceptors and retinal pigment epithelium (RPE) cells. Further work will be necessary to determine whether Abeta deposition in drusen may contribute to or result from retinal degeneration.

Aged↗
PubMed1978

Studies on the retina and the pigment epithelium in hereditary canine ceroid lipofuscinosis, I. The distribution of enzymes in the whole retina and pigment epithelium.

The massive accumulation of autofluorescent lipopigments, representative of autoxidation, is a key morphological feature in canine ceroid lipofuscinosis (CCL). In the eye peroxidase, catalase, and four acid hydrolases were compared with regard to aged and clinical condition in a series of English setters affected with CCL. In unaffected English setters "soluble" peroxidase increased in the RPE to adult levels at 2 yr of age. Affected dogs had higher RPE peroxidase activity earlier in life, which then decline with age. The soluble retinal peroxidase of both unaffected and CCL dogs increased steadily with age, but the latter group of dogs were much lower in activity. By 2 yr of age, RPE and retinal peroxidase values were only 25% and 47% of unaffected dog levels. Although the soluble enzyme of unaffected dogs exhibited a maturational profile, membrane-bound RPE peroxidase showed a hyperbolic curve reaching a maximum at 10 mo of age. By 2 yr of age, the "bound" enzyme in affected dogs was below unaffected levels in the RPE and retina. Three acid hydrolases were slightly increased in the RPE and retina of affected dogs. Acid lipase activity, however, was similar in both unaffected and CCL dogs. Catalase was not found in the RPE of either group of dogs. The catalase activity in the retina of both affected and unaffected dogs was at similar levels. Since catalase is not present in the RPE, the major defense against peroxidase accumulation and peroxide toxicity probably depends upon peroxidase. The present study indicates that a decrease in this key regulating enzyme may be related to the formation of lipopigments in the retina and RPE of dogs with CCL.

Age Factors↗
PubMed1997

Dopamine D4-like receptors in vertebrate retina: does the retina offer a model for the D4-receptor analysis?

Dopamine is a major catecholamine in vertebrate retina. The amine is localized, depending on the species, in a subset of amacrine and/or interplexiform cells. The dopamine-containing cells in retina are activated upon light exposure, with resulting increase in the amine synthesis and release. Dopamine, acting as a light-adaptive signal, controls many aspects of retinal physiology; among its diverse effects is modulation of the night-driven melatonin biosynthesis, which occurs in photoreceptors. Activation of dopamine receptors belonging to D2-family, localized on photoreceptors, rapidly suppresses the nocturnal cyclic AMP-dependent activity of serotonin N-acetyltransferase (NAT), a key regulatory enzyme in melatonin biosynthesis. Convincing evidence indicates that these NAT activity-modulating receptors represent the D4-subtype dopamine receptors, which--most probably indirectly--control in a negative manner the activity of intraphotoreceptor Ca2+/calmodulin-dependent adenylyl cyclase. This article reviews current knowledge on dopamine D4-subtype receptors, with a special emphasis to their function in vertebrate retina. In addition, some findings resulting from our recent experiments with newly synthesized D4-receptor-selective ligands are presented and discussed. It is proposed that the avian retina, with its ability to synthesize melatonin in a dopamine-sensitive manner (via D4-like dopamine receptor), may offer a suitable specific in vivo model which allows to study potential ligands (both agonists and antagonists) of the D4-subtype dopamine receptor.

Amino Acid Sequence↗
PubMed1995

[Constitutional release of nitrogen monoxide (NO) by the retina of the minipig is a major determinant of arteriolar basic tonus in the internal retina].

PURPOSE: NO is a nonpolar gas, which diffuses across cell membranes in an isotropic fashion. In relatively large arteries NO has been identified as the endothelium-derived releasing factor and the current hypothesis is that NO controls the vascular tone. We are investigating an alternative hypothesis proposing that the retinal tissues surrounding the arterioles contribute in the process of NO production. METHODS: We performed flicker light stimulation in anesthetized minipigs (hypnodyl 100 mg/hr, tubocurarine 0.1 mg/hr und N2O) in steady-state of normoxia-normocapnia. An NO-microprobe mounted on a micromanipulator was introduced into the eye through the pars plana and positioned on the preretinal space in a zone free of visible vessels. Preretinal NO gradient and recording of NO release variations in response to flicker light stimulation were performed so as periarteriolar microinjections of nitro-L-arginine. RESULTS: When advancing the NO-probe from the vitreous towards the retina we recorded an NO-gradient corresponding to an efflux of 7.1 pMol x min-1 x cm-2 (N = 9). With the microprobe positioned close to the retina and after 60 min dark adaptation we recorded a mean increase in NO release of 1.59 muMol +/- 0.13 SE. After periarteriolar microinjection of nitro-Larginine we recorded a transitory reversible vasoconstriction. CONCLUSIONS: These results indicate that a process occurring in the extravascular tissue of the retina modulates the production of NO and that constitutional NO release by the retina is a major determinant of the basal retinal arteriolar tone.

Animals↗
PubMed1986

Morphologic findings in the rabbit retina following irradiation with the free-running neodymium-YAG laser. Disruption of Bruch's membrane and its effect on the scarring process in the retina and choroid.

The scarring process induced within the retina and choroid of pigmented rabbits' eyes following irradiation with the neodymium-YAG laser (working in the free-running mode) was examined at the ultrastructural level. Scarring of the sensory retina proceeded rapidly and was well advanced two weeks after irradiation, whereas in the choroid, signs of repair were apparent only after six weeks. This difference in the rate of repair between the two tissues has a bearing on the scarring pattern in the retinochoroid as a whole. The severity of damage to the elastic component of Bruch's membrane also has important consequences in relation to the repair processes in the retina and choroid. Microfractures within this layer, while enabling migrating cells of various kinds to penetrate into the inner collagenous zone, did not prevent complete regeneration of the retinal pigment epithelium (RPE). In instances of greater rupture, however, RPE regeneration was found to stop at the border of the break, and the discontinuity produced within Bruch's membrane and the RPE allowed the glial scar to expand into the choroid. In this region, new formation of vessels was not found.

Animals↗
PubMed1984

Dopaminergic neurones in various retinas and the postnatal development of tyrosine-hydroxylase immunoreactivity in the rabbit retina.

The localisation of tyrosine-hydroxylase immunoreactive neurones in retinas of a variety of animals were examined. Immunoreactivity was associated with specific populations of amacrine neurones in all species examined, viz; rabbit, guinea pig, monkey, cow, frog, pigeon and goldfish. Only in the goldfish was immunoreactivity also associated with processes situated in the outer plexiform layer showing that in this species catecholamine interplexiform cells exist. The development of tyrosine-hydroxylase immunoreactive neurones in the rabbit retina was also analysed. The first immunoreactive positive cells were observed by the third postnatal day. The immunoreactive positive neurones at this stage are weak and lack processes. The intensity of the immunoreactivity increases with development, but processes are lacking, until the 10th postnatal day. The immunoreactive neurones only appear fully developed by the 22nd to 28th postnatal day. Autoradiographical analysis of 3H-dopamine uptake strongly suggests that neurones containing tyrosine-hydroxylase immunoreactivity in the different retinas have the capacity to take up exogenous dopamine. It is therefore concluded that localisation of either 3H-dopamine uptake or tyrosine-hydroxylase provides a means of locating catecholamine neurones.

Animals↗
PubMed1992

A factor derived from chick embryo retina which inhibits DNA synthesis of retina itself.

Chick embryo retinas contain a peptide factor that inhibits DNA synthesis in explants of chick embryo retina. The inhibitory factor, obtained by acid/ethanol extraction from 15-day-old chick embryo retinas, was partially purified by affinity chromatography on heparin-sepharose CL-6B and gel filtration on Sephadex G-100. The inhibitor reduced DNA synthesis with maximal effects observed in retinal explants from 7 to 8-day-old chick embryos. The inhibitory effect became apparent after 10 h of incubation and reached the maximum levels after 16 h. DNA-inhibiting activity was heat and acid-stable and was destroyed by trypsin and alkaline treatments. The inhibitory effect was observed in retinal explants incubated in a medium free from L-glutamine, and the addition of this compound to the medium reduced the inhibitory effect in a concentration-dependent manner.

Animals↗
PubMed1990

Cell commitment and differentiation in explants of embryonic rat neural retina. Comparison with the developmental potential of dissociated retina.

The differentiation of presumptive neural retina following its isolation from rat embryos and growth in explant and monolayer culture has been studied to obtain information regarding the extent to which factors extrinsic and intrinsic to the retina participate in determining molecular and cytological differentiation. Explanted retinal epithelium retained the capacity for mitosis, as shown by [3H]thymidine incorporation, and from the undifferentiated neuroepithelium, retinal cell-types emerged and acquired a laminar organization resembling that in vivo. Characterization of rod photoreceptor cells at both the light and electron microscopic level showed that these cells exhibit differentiated structural features including inner segments, connecting cilia and membranous expansions suggestive of forming outer segments. Immunofluorescent labeling with an antibody to a synaptic vesicle protein, and electron microscopic identification of synaptic elements showed formation of synapses by the photoreceptor cells within the explant. Neurites extending from the explants exhibited growth on laminin, fibronectin and collagen substrates. Since the neurites immunolabeled with antibodies to the 140 kDa subunit of neurofilament and with antibodies to Thy-1, they could be identified as axons of ganglion cells. Antibodies to a variety of cell-type specific antigens showed that the cells expressed molecules associated with the fully differentiated cell. Furthermore, since our approach has been to explant embryonic retina at an age when the antigens are not yet expressed in vivo, the appearance of the antigens in culture represented de novo expression. In contrast, neural retinal cells in dissociated cultures did not exhibit de novo expression of differentiated molecular properties.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The marker for nitric oxide synthase, NADPH-diaphorase, co-localizes with GABA in horizontal cells and cells of the inner retina in the carp retina.

NADPH-diaphorase histochemistry selectively stained discrete populations of neurons contributing to the inner plexiform layer of the carp retina. In addition H1 horizontal cells contributing to the outer plexiform layer were labeled. In these cells as in a subpopulation of the labeled cells in the inner retina, NADPH-activity co-localized with GABA immunoreactivity. NADPH-activity is a direct marker for NO synthesis and it is concluded that NO might be an important mediator of light-dependent adaptational processes in the outer retina.

Amino Acid Oxidoreductases↗
PubMedDate not supplied

The origin of slow PIII in frog retina: current source density analysis in the eyecup and isolated retina.

The objective of this research was to determine the sources and sinks of current underlying the slow PIII component of the electroretinogram. Current source density analysis of the ERG evoked by diffuse light flashes was performed in eyecup and isolated retinas of frog. Blockade of synaptic transmission with aminophosphonobutyric + kynurenic acids simplified the CSD profiles through the retina. In addition to the photoreceptor source/sink pair, there was evidence for a major slow PIII source near the outer limiting membrane, a major sink near the inner limiting membrane, and a small source near the inner plexiform layer. Addition of Ba2+ abolished the slow PIII source/sinks, and it left only the photoreceptor source and sink. The results support the idea that slow PIII originates through K+ spatial buffering by Müller cells. Specifically, the light-evoked decrease in [K+]o in the subretinal space causes a primary K+ efflux from Müller cells (current source) and a primary K+ influx at the Müller cell endfeet (current sink). A decrease in [K+]zero in the proximal retina, caused by diffusion of K+ to the subretinal space, results in K+ efflux (the current source) at the inner plexiform layer.

Animals↗