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Results for “Photoreceptor Cells”

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At least 19 recordsLinked to original sources

PubMed1999

Retina-derived microglial cells induce photoreceptor cell death in vitro.

In animals with retinal degeneration, the presence of activated microglial cells in the outer retina during the early stages of injury suggests that they may be involved in the ensuing photoreceptor cell death. In the following study, we investigated the effects of rat retina-derived microglial cells on a photoreceptor cell line (661w) using cell culture techniques. The difficulty of obtaining pure populations of photoreceptor cells necessitated our use of the 661w photoreceptor cells generated from retinas of transgenic mice. 661w Cells were incubated for 24-48 h in basal medium or basal medium conditioned by activated microglial cells (MGCM) or Müller cells (MCCM), and tested for cell death using lactate dehydrogenase (LDH) assay. The induction of apoptosis in the 661w cells by MGCM was investigated using Terminal deoxynucleotidyl Transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) and DNA laddering. Treatment of 661w cells with MGCM for 48 h resulted in approximately 73% of cells dead as compared with 19-20% of cells grown in either basal medium or MCCM. Serum supplementation or pretreatment with heat did not abolish the cytotoxicity of MGCM. More TUNEL-positive cells were observed in MGCM-treated cultures as compared with those in basal medium. Bands in multiples of approximately 180 bp formed DNA ladders in MGCM-treated but not in basal medium-treated samples. Our study shows that microglial cells release soluble product(s) that induce degeneration of cultured photoreceptor cells. Moreover, the mechanism of microglia-induced photoreceptor cell death may involve apoptosis similar to that observed in animals with retinal degeneration.

Animals↗

PubMed2006

Transplantation of bone marrow-derived mesenchymal stem cells rescue photoreceptor cells in the dystrophic retina of the rhodopsin knockout mouse.

BACKGROUND: Retinitis pigmentosa belongs to a large group of degenerative diseases of the retina with a hereditary background. It involves loss of retinal photoreceptor cells and consequently peripheral vision. At present there are no satisfactory therapeutic options for this disease. Just recently the use of mesenchymal stem cells has been discussed as one therapeutical option for retinal degeneration, as they have been shown to differentiate into various cell types, including photoreceptor cells. In this article we wanted to investigate the potency of mesenchymal stem cells to induce rescue effects in an animal model for retinitis pigmentosa, the rhodopsin knockout mouse. METHODS: For the experiments, three experimental groups of 10 animals each were formed. The first group consisted of untreated rhodopsin knockout (rho(-/-)) animals used as controls. The second group consisted of rho(-/-) mice that had received an injection of mouse mesenchymal stem cells, which were transduced using an adenoviral vector containing the sequence for the green fluorescent protein (GFP) prior to transplantation. In the third sham group, animals received an injection of medium only. Thirty-five days after transplantation, GFP-expressing cells were detected in whole-mount preparations of the retinas as well as in cryostat sections. For the detection of rescue effects, semi-thin sections of eyes derived from all experimental groups were produced. Furthermore, rescue effects were also analysed ultrastructurally in ultrathin sections. RESULTS: Histological analysis revealed that after transplantation, cells morphologically integrated not only into the retinal pigment epithelium but also into layers of the neuroretina displaying neuronal and glial morphologies. Furthermore, significant rescue effects, as demonstrated by the occurrence of preserved photoreceptor cells, were detected. CONCLUSIONS: Our data indicate that mesenchymal stem cells can prolong photoreceptor survival in the rhodopsin knockout mouse, also providing evidence of a therapeutical benefit in retinitis pigmentosa.

Adenoviridae↗

PubMed2001

Subretinally transplanted embryonic stem cells rescue photoreceptor cells from degeneration in the RCS rats.

The Royal College of Surgeons (RCS) rat is an animal model for retinal degeneration such as the age-related macular degeneration. The RCS rat undergoes a progressive retinal degeneration during the early postnatal period. A potential treatment to prevent this retinal degeneration is the transplantation into the subretinal space of cells that would replace functions of the degenerating retinal pigment epithelium (RPE) cells or may form neurotrophic factors. In this study we have investigated the potential of subretinally transplanted embryonic stem cells to prevent the genetically determined photoreceptor cell degeneration in the RCS rat. Embryonic stem cells from the inner cell mass of the mouse blastocyst were allowed to differentiate to neural precursor cells in vitro and were then transplanted into the subretinal space of 20-day-old RCS rats. Transplanted and sham-operated rats were sacrificed 2 months following cell transplantation. The eyes were enucleated and photoreceptor degeneration was quantified by analyzing and determining the thickness of the outer nuclear layer by light and electron microscopy. In the eyes transplanted with embryonic cells up to 8 rows of photoreceptor cell nuclei were observed, whereas in nontreated control eyes the outer nuclear layer had degenerated completely. Transplantation of embryonic stem cells appears to delay photoreceptor cell degeneration in RCS rats.

Animals↗

PubMed1985

Response properties of horizontal cells and photoreceptor cells in the retina of the tree squirrel, Sciurus carolinensis.

A new experimental preparation for intracellular recording from mammalian retinal neurons has been established. This is the arterially perfused eyecup preparation of the tree squirrel, Sciurus carolinensis. Two horizontal cell types have been recorded in this preparation. These cell types differ in their response waveforms. Type 1 horizontal cells appear to receive input only from cones, whereas type 2 horizontal cells receive mixed rod-cone input. Sciurus horizontal cells have receptive-field sizes smaller than those of horizontal cells in other mammalian and nonmammalian species. Recordings from a second class of cells in the outer retina of the squirrel reveal receptive-field properties considerably different from those of squirrel horizontal cells and similar to those of photoreceptor cells in other species. On the basis of these receptive-field properties, recording depth, and spectral response characteristics, we conclude that these recordings were from cone-photoreceptor cells. These recordings from squirrel cones are the first demonstration of mammalian photoreceptor response amplitudes and receptive-field interactions comparable with those demonstrated for nonmammalian species.

Animals↗

PubMed1998

Lamprey ganglion cells contact photoreceptor cells.

Lamprey retinal ganglion cells are localized in two separate layers: those close to the vitreous and those at the junction between the inner nuclear and inner plexiform layers, including some others in the inner nuclear layer, close to the photoreceptor cell layer. Whereas most ganglion cell dendrites arborize in the inner plexiform layer and contact amacrine, bipolar and retinopetal cell profiles, some of them, located in the inner nuclear layer, ascend radially through the outer plexiform layer and establish contacts with photoreceptor cells. This ganglion cell type might correspond to the biplexiform ganglion cells already described in gnathostome vertebrate species and could provide a fastforward signal from photoreceptors to ganglion cells, bypassing the usual bipolar cell interneuron.

Animals↗

PubMed1998

Light affects c-fos expression and phospholipid synthesis in both retinal ganglion cells and photoreceptor cells in an opposite way for each cell type.

Retina photoreceptor and ganglion cells isolated from chicks that in vivo were exposed to light have a different phospholipid labeling capacity than those from chicks in the dark. In the light exposed animals, the phospholipid labeling in the ganglion cells is higher (Delta% 45, p<0.005) than in those maintained in the dark, whereas in the photoreceptor cells, the opposite occurs, that is, the phospholipid labeling is higher in the dark than in light. The light-dark differences for phospholipid labeling correlate with the expression of c-fos: when c-fos expression increases (both in mRNA and in c-Fos protein content), phospholipid labeling increases concomitantly. That is, in ganglion cells, c-fos expression and the phospholipid synthesis is higher in light with respect to dark, whereas in photoreceptor cells, c-fos expression and phospholipid synthesis is higher in dark with respect to light. Moreover, when an oligonucleotide antisense to c-fos is administered intraocularly prior to separating the animals into light and dark, no differences in c-fos expression and, consequently, no differences in phospholipid synthesis are found between animals in light and dark. Taken together, these results point to a novel mechanism by which rapid genomic responses to cell stimulation are converted to longer lasting changes in the cell components.

Animals↗

PubMed1995

Müller cell changes precede photoreceptor cell degeneration in the age-related retinal degeneration of the Fischer 344 rat.

Previously, we have used descriptive pathology and histomorphometry, as well as functional testing to characterize the age-related retinal degeneration in the Fischer 344 rat. These studies suggested an association between Müller cells and photoreceptor cells in this process. The purpose of the present study was to further investigate the respective roles of these cell types in the development and progression of the retinal degeneration. Retinas from male Fischer 344 rats aged 3-24 months were first studied by light and electron microscopy. Since Müller cells abundantly express GFAP during pathological states, GFAP content was studied by immunocytochemistry and by immunoblotting following one- and two-dimensional gel electrophoresis. Microscopically, at 12 months, Müller cells showed a gradient of immunoreactivity for GFAP that was minimal in the central retina, positive for their radial processes in the equator, and abundantly expressed in the periphery. At this age, the photoreceptor cells were just beginning to degenerate in the far periphery, while they appeared healthy in the equatorial and central regions. By 24 months, Müller cell hypertrophy was seen in the peripheral regions where photoreceptor cell degeneration was most severe, while the immunoreactivity of the Müller cell processes spread further toward the central regions, ahead of the degeneration of the photoreceptor cells. Thus, Müller cell changes actually preceded photoreceptor degeneration in time and location. This phenomenon was confirmed by measurement of GFAP after one- and two-dimensional PAGE. These findings show that Müller cell changes precede chronic photoreceptor cell degeneration in the aging Fischer 344 rat and are consistent with the hypothesis that Müller cell alteration may be the primary mechanism of this age-related retinal degeneration.

Aging↗

PubMed1996

Apoptotic cell death of photoreceptor cells in mice deficient for the adhesion molecule on glia (AMOG, the beta 2- subunit of the Na, K-ATPase).

Disruption of the gene for the adhesion molecule on glia (AMOG, the beta 2-subunit of the Na, K-ATPase) in mice results in swelling and subsequent degeneration of astrocyte endfeet in the brainstem and in cell death of photoreceptor cells in the retina. In the present study, we demonstrate that photoreceptor cells in the mutant develop normally during the first postnatal week. Compared to wild-type mice, a slightly increased density of degenerating photoreceptor cells became apparent in 9-day-old mutants and numerous degenerating photoreceptor cells were present in the retina of 16-day-old AMOG/beta 2-deficient mice. In situ labelling of degenerating cells by terminal dUTP nick end labelling and electron microscopic analysis revealed apoptotic cell death of photoreceptor cells. Massive degeneration of photoreceptor cells in the mutant at postnatal day 16 correlated with elevated levels of glial fibrillary acidic protein in retinal astrocytes and with expression of this protein by Muller cells. No evidence was found for degeneration of other retinal cell types or for glial cell death in the optic nerve. Our observations demonstrate that the pathological death of cells induced by disruption of the AMOG/beta 2 gene results from activation of an intrinsic death program, similar to what has been shown to occur during normal development.

Adenosine Triphosphatases↗

PubMed1996

Müller and RPE cell response to photoreceptor cell degeneration in aging Fischer rats.

With increasing age, retinas of male Fischer rats gradually lose photoreceptor cells beginning at the ora serrata and extending to the central retina resulting in a pronounced peripheral retinopathy. In this study, we used immunocytochemical methods for glial fibrillary acidic protein (GFAP) and carbonic anhydrase II (CA II) to study the Müller cell response to age-related photoreceptor cell degeneration in the superior retina. Retinas of Fischer rats were also examined by electron microscopy to investigate retinal pigment epithelial (RPE) cell and Bruch's membrane structural changes with advancing age. Our study showed extensive photoreceptor cell loss in the region of the ora serrata beginning by 16 months, while few photoreceptor cells were found at 23 months. Neovascularization also occurred in the area of the peripheral retinopathy at the level of the RPE cells as determined by electron microscopy, as well as a thickening of Bruch's membrane with initial signs of small breaks. Dense areas of GFAP-immunostaining of Müller cell processes were found in the superior peripheral retina of 16-30 month-old rats where photoreceptor cells were degenerating. After 21 months, Müller cell processes extended into the subretinal space. However, in the central retina, where the photoreceptor cell population was more stable, GFAP-immunolabelled Můller cells were not detected. Immunoblots of retinal homogenates confirmed elevated GFAP levels at 18-30 months when compared to homogenates from retinas of 6-month-old Fischer rats. During photoreceptor cell degeneration, Müller cell processes were also prominently immunostained for CA II, which were seen to occupy the subretinal space at 18-30 months. Our results suggest that Müller cells respond to the age-related peripheral retinopathy in Fischer rats by increasing GFAP content and growth of their processes into the subretinal space to form a glial scar, but only in the area of severe photoreceptor cell loss. In addition, RPE and Bruch's membrane of aged retinas exhibit typical early age-related changes as also reported for aged human eyes.

Aging↗

PubMed1991

Effects of macrophage and retinal pigment epithelial cell transplants on photoreceptor cell rescue in RCS rats.

The effects of macrophage transplants on photoreceptor cell survival in retinas of Royal College of Surgeons (RCS) dystrophic rats were contrasted with RPE-cell transplants, sham-injection and surgical controls. The effects of these different treatments on the thickness and total area of the outer nuclear layer (ONL) were evaluated by light and electron microscopy at 1, 2 and 5 months after transplantation or surgical manipulations. Macrophage transplants into dystrophic retinas, although significantly reducing the debris zone thickness (p less than 0.01), had little effect on photoreceptor cell survival (2-3 cells thick ONL) after two months. In contrast, two months after RPE-cell transplantation, retinas exhibited an 8-10 cell thick ONL. Also, inner and outer segments of rescued photoreceptor cells were present, especially in areas directly beneath RPE-cell transplants. At the same time period, retinas injected with saline had a 2-3 cell thick ONL with no organized inner or outer segments. Furthermore, the affected ONL area in macrophage-transplanted or saline-injected retinas was significantly smaller than that seen in RPE-cell transplanted retinas (p less than 0.0001). Surviving photoreceptor cells were found only in the RPE-cell transplanted retinas five months after treatment. No effect on photoreceptor cell survival was seen in saline-injected, needle-inserted or incision-only retinas. Thus, transplantation of healthy RPE cells is an effective long-term therapeutic approach to correct the genetic defect in retinas of RCS dystrophic rats.

Animals↗

PubMed1990

A method for measuring the oxygen consumption of photoreceptor cells in the steady state and after a brief stimulation by light.

The rate of oxygen consumption (QO2) in living tissue cannot be directly measured but may be estimated by mathematically modelling the diffusion of oxygen in the tissue and measuring the local partial pressure of oxygen (PO2). The retina of arthropods contains only two types of cells, photoreceptor and glial cells, which are regularly distributed. Because of this simple structure, simple models of diffusion can be used to estimate the QO2 of the tissue, both in steady state and after a brief stimulation by light. We used a model of diffusion in a plane sheet to calculate the QO2 in a slice of honeybee drone retina, which contains a few thousand cells. We then modified the method slightly and used a model with spherical symmetry to calculate the QO2 in the cluster of three photoreceptor cells of the barnacle and in the single ventral photoreceptor cells of Limulus.

Animals↗

PubMed1987

Characterization of photoreceptor cell differentiation in the rat retinal cell culture.

Photoreceptor cell differentiation in the rat retina was studied in vivo and in vitro, using an immunohistochemical method to demonstrate opsin-like immunoreactivity. Cells in a dissociated monolayer culture expressed some properties characteristic of rat rod cells developing in vivo, including a ciliary structure and opsin-like immunoreactivity. Immunoblot analysis revealed that cultured retinal cells synthesize a polypeptide with the same molecular weight as that synthesized by the intact retina. Although the outer segment (OS) was not present in the culture, immunoreactive cells possessed a ciliary structure. Opsin-like immunoreactivity was found on the plasma membrane, including the cilia. The neuritic extensions were also intensely stained. In mature rod cells of the intact rat retina, opsin was detected only on the OS but, during development, it was found both in the somatic region of the rod cells and on the differentiating OS. During maturation of rod cells opsin immunoreactivity seemed to shift to the OS from other locations. However, some "displaced" photoreceptor cells, found in the inner nuclear layer and extending fibers bipolarly, retained immunoreactivity throughout their structure. The absence of polarized distribution of opsin in these cells is considered to be due to an abnormal environment, which may also be the case with cultured retinal cells. The present culture conditions will offer a useful model system to understand the cellular mechanism of the hereditary retinal dystrophy of rodent animals in which photoreceptor cells selectively degenerate.

Animals↗

PubMed1975

Light dependence of osmium reactivity in mouse photoreceptor cells.

Mouse photoreceptor cells exhibit local accumulations of osmium deposits after prolonged osmic staining at slightly elevated temperatures. Deposits were evident along the membranes of outer segment lamellae, Golgi cisternae and vesicles, nuclear envelopes, and synaptic vesicles. Other membranes within the photoreceptor cells were unreactive. No osmium reactivity was seen in other cells of the retina except for osmiophilic outer segment material which had been phagocytized by the pigment epithelium. In the outer segments, inner segments, and synaptic regions of the photoreceptor cells, the amount of osmium reactivity was increased by light stimulation and decreased following extended dark adaptation. The possible significance of the localized osmium reactivity is discussed.

Animals↗

PubMed1981

Synaptic vesicle exocytosis in goldfish photoreceptor cells.

The photoreceptor cell endings of goldfish retinas were examined using ultrathin and freeze-fracture techniques. The synaptic vesicles could be seen lying closely packed in rows on each side of the synaptic ribbon, and the vesicles nearest to the end of the ribbon could be seen to be in direct contact with the presynaptic membrane. The openings of the synaptic vesicles to the synaptic cleft could also be observed at the presynaptic membrane nearest to the end of the ribbon, that is, 100 nm distant from the center of the apex. In the freeze-fractured replicas of the presynaptic membrane, the band-shaped membrane particle aggregation was seen at the apex and a row of the crater-like or circular protuberances were observed at each side of the apex. These structures were considered to be changes of the presynaptic membrane organizations according to the synaptic vesicle exocytosis. It may be possible that the synaptic vesicle exocytosis in the photoreceptor cells occurs at the sites of the presynaptic membrane nearest to the apical end of the synaptic ribbon, and that the exocytotic sites form a line on each side of the apex.

Animals↗

PubMed1994

Detection of estrogen receptor mRNA in trout pineal and retina: estradiol-17 beta modulates melatonin production by cultured pineal photoreceptor cells.

Pineal photoreceptor cells produce the neurohormone melatonin, a major "Zeitgeber" of the organism. This compound is involved in the control of development, growth, sexual maturation, and seasonal reproductive cycles. The present study reports that the photosensitive pineal organ and the retina of the trout express a 3.5-kb mRNA corresponding to the estradiol-17 beta receptor. The effects of estradiol-17 beta on melatonin production by cultured pineal photoreceptor cells were also studied. Under a light/dark (LD:12/12) cycle, these cells maintained a rhythmic secretion of melatonin, with higher amounts being released during the dark phase. The amplitude of the rhythm tended to increase with time in culture. Application of estradiol-17 beta during the dark phase of an LD cycle (i.e., for 12 hr) affected melatonin release in a dose-dependent manner; low concentrations (10(-10) to 10(-8) mol/liter) were inhibitory, whereas high concentrations (over 10(-7) mol/liter) were stimulatory (when compared to the values obtained at 10(-9) mol/liter). When estradiol-17 beta was given continuously for several 24-hr LD cycles, the inhibitory effect observed during the first dark phase disappeared in subsequent dark periods. In the presence of estradiol-17 beta, at concentrations ranging from 10(-10) to 10(-5) mol/liter, a high amplitude rhythm in melatonin secretion returned more rapidly than in controls. The present results suggest that estradiol-17 beta receptors are expressed in the fish pineal and retina and that estradiol-17 beta modulates melatonin secretion by cultured pineal photoreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Study on the aging changes of DNA and protein synthesis of bipolar and photoreceptor cells of mouse retina by light and electron microscopic radioautography.

The DNA and protein synthesis of the bipolar cells and photoreceptor cells of aging mouse retina from fetal to postnatal 1 year were studied by light and electron microscopic radioautography. Meanwhile the ultrastructure of these cells was observed by electron microscopy. The bipolar and photoreceptor cells incorporated 3H-thymidine from embryonic day 19 until 1 week after birth, while 3H-leucine from embryonic day 19 to postnatal 1 year. The 3H-thymidine labelled cells had undeveloped cell organelles in their cytoplasm. On the contrary, the unlabelled cells had well developed cell organelles, mainly mitochondria and endoplasmic reticulum in their cytoplasm. The mitochondria became elongated when the outer segments were well developed. The protein synthesis of the bipolar cells and photoreceptor cells as demonstrated with 3H-leucine labeling was vigorous at embryonic day 19 and early postnatal days when the inner and outer segments were formed. The peak of this phenomenon was observed at 1 day after birth. The activity of protein synthesis was also detected at the adult stage. However there was no significant fluctuation in any stages from 14 days after birth to 1 year.

Aging↗

PubMed2005

Expression of aquaporin-1 immunoreactivity by photoreceptor cells in the mouse retina.

Aquaporin water channels play a crucial role in the maintenance of ionic and osmotic homeostasis in the neural tissue. In the sensory retina, aquaporin-4 is expressed by Müller glial cells, predominantly in the inner retina, while aquaporin-1 is expressed mainly in the outer retina. However, it is unknown whether aquaporin-1 expression occurs in Müller cells or photoreceptor cells. By using immunohistochemical staining of retinal slices from rds mice, we show that the immunoreactivity for aquaporin-1 disappears along with the photoreceptor cell degeneration. In suspensions of dissociated retinal cells from control mice, photoreceptor cells expressed aquaporin-1 immunoreactivity while Müller cells were largely devoid of staining. The data suggest that photoreceptor cells, but not Müller cells, express aquaporin-1 in the murine retina.

Animals↗

PubMed1990

Amino acid and cDNA sequence of bovine phosducin, a soluble phosphoprotein from photoreceptor cells.

Vertebrate photoreceptor cells contain a soluble phosphoprotein, phosducin, which complexes with the beta, gamma subunits of the GTP-binding protein, transducin. Light-induced changes in cyclic nucleotide levels modulate the phosphorylation of phosducin by protein kinase A. The complete amino acid sequence of purified phosducin from bovine retinas was determined by Edman degradation from overlapping polypeptides derived from enzymatic digestion by trypsin and Staphylococcus aureus V8 protease or from chemical degradation by cyanogen bromide. Excluding the unidentified group which blocks the NH2 terminus, phosducin contains 245 amino acids with a calculated molecular weight of 28,185 and isoelectric point of pH 4.5. Phosducin is enriched with acidic and sulfur-containing amino acids, having 32 glutamic acid, 16 aspartic acid, 9 methionine, and 5 cysteine residues. It also contains 24 serine and 8 threonine residues, of which only serine 73 is located within a consensus phosphorylation sequence (-RKMS(P)QV-) for cyclic nucleotide-dependent protein kinase. Secondary structure analysis predicts the presence of 62% alpha-helix, 22% beta-sheet, and 16% random coil, with eight turns. Computer-aided searches of protein data banks revealed no apparent homology to any sequenced protein except that coded by a MEKA cDNA clone (Kuo, C-H., Akiyama, M., and Miki, N. (1989) Mol. Brain Res. 6, 1-10) which deviates from the confirmed phosducin sequence in the last 15 amino acids. Sequence analysis of a cDNA clone for bovine retinal phosducin confirmed that the MEKA clone deviation resulted from an unidentified cDNA guanosine nucleotide, a shifted reading frame and a premature stop codon.

Amino Acid Sequence↗