[Electroretinogram (ERG)].
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Electroretinography↗
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Multifocal rod electroretinograms.
PURPOSE: To assess the feasibility of obtaining reliable multifocal rod electroretinograms (ERGS) and to compare them to full-field ERGs. METHODS: Multifocal rod ERGs were recorded using a stimulus array of 61 hexagons. The minimum number of dark, blank frames between flashes was varied from 0 (a minimum of 13.3 msec between flashes) to 21 (a minimum of 293 msec between flashes). Full-field ERGs were obtained using trains of flashes designed to simulate the multifocal sequences. Flashes were blue (W47B), except in a few cases in which red (W26) was used to check for cone intrusion. Flash intensities varied from -1 to 1.7 log scot td-s. RESULTS: Dark-adapted, multifocal ERGs to blue flashes had a small, early component followed by a larger, late component. The early component showed little change in amplitude with increasing intensity. Comparisons with the full-field ERGs indicated that the early component was the focal response. The larger, late component was the response to stray light, and it can be suppressed with the addition of a surround. The focal response was from a relatively circumscribed retinal region. This is shown by comparing the multifocal rod responses from a patient with retinitis pigmentosa to her behaviorally measured rod visual field. CONCLUSIONS: By choosing conditions (namely, flashes of moderate intensity with a surround) to minimize the effects of stray light, multifocal rod ERGs can be recorded with sufficient localization to be clinically useful. However, the signal-to-noise ratio of these multifocal rod ERGs was poorer than for multifocal cone responses for comparable recording periods because of the need for blank frames and the slower recovery of the rods to successive presentations.
Adult↗
Intraocular gene transfer of ciliary neurotrophic factor prevents death and increases responsiveness of rod photoreceptors in the retinal degeneration slow mouse.
Several mutations causing both photoreceptor degeneration and malfunction have been identified in humans and animals. Although intraocular injection of trophic factors has been shown to reduce photoreceptor death in a few conditions of rapid photoreceptor loss, it is unclear whether long-term beneficial changes in functional properties of affected photoreceptors can be obtained by treatment with these factors. The rds/rds mouse is a spontaneous mutant bearing a null mutation in the rds/peripherin gene, which is linked to many forms of dominant retinal degenerations in humans. Here, we report that intraocular adenovirus-mediated gene transfer of ciliary neurotrophic factor (CNTF) in this mutant reduces photoreceptor loss, causes a significant increase in the length of photoreceptor segments, and results in a redistribution and an increase in the retinal content of the photopigment rhodopsin. These effects are accompanied by a significant increase in the amplitude of the a- and b-waves of the scotopic electroretinogram. These results suggest that continuous administration of CNTF could potentially be useful for the treatment of some forms of retinal degeneration.
Adenoviridae↗
[Identification of 2 allelic mutations of the gene of the phosphodiesterase beta subunit in a Spanish family with recessive autosomic retinitis pigmentosa].
BACKGROUND: Retinitis pigmentosa (RP) is a group of inherited eye disorders that affect photoreceptor and pigment epithelial function. Mutations in different genes involved in the phototransduction process have been described in patients with autosomal recessive RP. PATIENTS AND METHODS: We examined the gene coding the beta subunit of the phosphodiesterase (PDEB) in a ARRP family with two affected sisters. SSCP (single stand conformational polymorphism) analysis of the coding region of the gene showed abnormal bands in two different exons. PCR products showing SSCP aberrant patterns were subsequently sequenced. RESULTS: The two affected sisters had inherited from their father a PDEB gene with a known mutation (Gln298X) and a rare variant and from their mother a PDEB gene with a new mutation: Asp600Asn. CONCLUSIONS: The nature of the mutations in the PDEB gene and their pattern of inheritance indicate that the lack of activity of the phosphodiesterase (PDE), a key enzyme in the visual phototransduction process, account for the RP phenotype in these patients.
3',5'-Cyclic-GMP Phosphodiesterases↗
Retinal development of West Australian dhufish, Glaucosoma hebraicum.
An investigation of retinal specializations was carried out in larval and juvenile dhufish, Glaucosoma hebraicum (Glaucosomidae, Teleostei). The development of photoreceptors and formation of the retinal mosaic was followed by light and electron microscopy. At hatching the eye was undifferentiated. Cone photoreceptors were present by day 3 posthatch (dph), when exogenous feeding began. Single and multiple cones were present in a row arrangement from 3 dph to 20 dph, when the first rod nuclei were observed. Between 20 dph and approximately 3 months posthatch (mph), the row arrangement was replaced by a square mosaic of four double cones surrounding a single cone, and the cones increased in size, with the outer segments reaching up to 30 microm in length. During the period of spatial rearrangement, triple cones were often observed. From their first appearance, rod photoreceptors were added rapidly. Investigation of ganglion cell topography in 3-mph fish that had attained the adult-like square photoreceptor mosaic was carried out using retinal wholemounts. The highest densities of neurones in the ganglion cell layer were in temporal retina but no well-defined area centralis was observed. Microspectrophotometric measurements of the visual pigments within the outer segments of the photoreceptors of 3-mph fish revealed double cones with identical absorption spectra in each member of the outer segment, and the wavelength of maximum absorption (lambda(max)) located at 522 nm. Single cones were found to possess a visual pigment with lambda(max) at 460 nm and rods with a lambda(max) of 498 nm. The results imply that the larvae and juveniles are adapted for survival in coastal waters and may be active in relatively low light levels from early stages of development.
Animals↗
Putative stem cells and the lineage of rod photoreceptors in the mature retina of the goldfish.
The retinas of teleost fish grow continuously, in part, by neuronal hyperplasia and when lesioned will regenerate. Within the differentiated retina, the growth-associated hyperplasia results in the generation of new rod photoreceptors only, whereas injury-induced neurogenesis results in the regeneration of all retinal cell types. It is believed, however, that both new rod photoreceptors and regenerated neurons originate from the same populations of intrinsic progenitors. Experiments are described here that attempt to identify in the normal retina of goldfish neuronal progenitors intrinsic to the retina, particularly those which have remained cryptic because they divide infrequently. Long-term, systemic exposure to bromodeoxyuridine (BrdU) was used to label these cells. Five populations of proliferative cells were labeled: microglia, which are briefly described but not studied further; retinal progenitors in the circumferential germinal zone (CGZ); and rod precursors in the outer nuclear layer (ONL), both of which have been well characterized previously; and two populations of slowly-dividing cells in the inner nuclear layer (INL). The majority of these cells have a fusiform morphology, whereas the remaining ones are spherical. Longitudinal BrdU labeling suggests that the fusiform cells migrate to the ONL to replenish the pool of rod precursors. A subset of the spherical cells express pax6, although none are stained with markers of differentiated amacrine or bipolar cells. It is hypothesized that these rare, pax6-expressing cells are retinal stem cells, which give rise to the pax6-negative fusiform cells. Based on these data, two models are proposed: the first describes the lineage of rod photoreceptors in goldfish; the second is a consensus model of neurogenesis in the retinas of all teleosts.
Animals↗
A novel signaling pathway from rod photoreceptors to ganglion cells in mammalian retina.
Current understanding suggests that mammalian rod photoreceptors connect only to an ON-type bipolar cell. This rod-specific bipolar cell excites the All amacrine cell, which makes connections to cone-specific bipolar cells of both ON and OFF type; these, in turn, synapse with ganglion cells. Recent work on rabbit retina has shown that rod signals can also reach ganglion cells without passing through the rod bipolar cell. This route was thought to be provided by electrical gap junctions, through which rods signal directly to cones and thence to cone bipolar cells. Here, we show that the mouse retina also provides a rod pathway bypassing the rod bipolar cell, suggesting that this is a common feature in mammals. However, this alternative pathway does not require cone photoreceptors; it is perfectly intact in a transgenic mouse whose retina lacks cones. Instead, the results can be explained if rods connect directly to OFF bipolar cells.
Aminobutyrates↗
Developmental defects in Rb-deficient retinae.
We recently found that the Rb protein is important for the regulation of retinal progenitor cell proliferation and rod photoreceptor development in the mouse retina. These two functions are separate for Rb and in this study we further characterize the role of Rb in retinal development. At postnatal day 12 in the retinae of Chx10-Cre;RbLox/- mice, immature cells are found in the outer nuclear layer where rods normally are differentiating. This results in alternating patches of the outer nuclear layer (ONL) that are lacking rod inputs. At this stage of development, horizontal cell processes at the outer plexiform layer do not mature appropriately and they extend into the outer nuclear layer. These disruptions in horizontal cell differentiation can persist for several weeks into the adult stage. While there are several secondary effects of the loss of Rb on retinal development including, limited cell death in the ONL, Müller glial cell activation, persistence of immature cells in the ONL, and altered nuclear morphology of cells in the ONL, we suggest that the defect in horizontal cell synapse formation at the OPL results from fewer rod inputs. Mice with other developmental defects in photoreceptor cell fate specification or glial cell activation do not exhibit a similar alteration in horizontal cell differentiation. Therefore, the retinae from Chx10-Cre;RbLox/- mice represent a unique model to study the role of rod photoreceptor inputs in horizontal cell differentiation and synapse formation.
Animals↗
Structural specializations of the eye in the vizcacha (Lagostomus maximus maximus).
Vizcachas (Lagostomus maximus maximus, Chinchillidae) are nocturnal rodents living in burrows in many regions of Argentina, Bolivia, and Chile. We have studied the eye of the vizcacha using several light and electron microscopic procedures, with the purpose of understanding the role of vision in the behavior of this species. Our observations demonstrated an avascular, rod-rich retina, with a specialized region spanning through most of the equator of the eye. In this central band, all neural retinal layers exhibited a high cell density, whereas the photoreceptor layer was characterized by the presence of very long rods. In addition, the central region was associated with a distinct pigmentation pattern, including scarce granulation of the pigment epithelium, low pigmentation of the choroid, and the selective attachment of suprachoroidal cells to the inner scleral surface. These central modifications probably form the structural basis of a reflecting tapetum. The eye of the vizcacha received both long and short ciliary vessels, and a specialized cilio-sclero-choroidal vascular network appeared at the equatorial region. Our findings suggest that the equatorial region of the eye of the vizcacha could be a highly sensitive light detector related to foraging behaviors during crepuscular or nocturnal hours.
Animals↗
Impairment of rod cGMP-gated channel alpha-subunit expression leads to photoreceptor and bipolar cell degeneration.
PURPOSE: To determine whether alterations in rod cGMP-gated channel function mediate retinal degeneration, a transgenic approach in which the alpha subunit of the rod cGMP-gated channel is reduced by the expression of an antisense RNA was used. METHODS: A 890-bp fragment of the 5' mouse rod cGMP-gated channel cDNA was cloned in the antisense orientation under the control of the strong bacterial cytomegalovirus promoter. This antisense construct was used to generate transgenic mice in which the expression of the antisense transgene was measured by reverse transcription-polymerase chain reaction. Histologic, immunocytochemical, and TdT-dUTP terminal nick-end labeling (TUNEL) analyses were performed on control and transgenic retina sections to determine the effects of antisense expression on specific cell types. RESULTS: The antisense RNA was able to inhibit the translation of the rod channel protein in an in vitro assay. Three transgenic mouse lines expressing the antisense construct were obtained. Molecular analyses showed that the antisense is expressed in the eye of each transgenic mouse line, where it reduces rod cGMP-gated channel RNA expression. Histologic and immunocytochemical data showed that transgenic retinas have a reduced number of photoreceptors and bipolar cells. TUNEL staining confirmed that photoreceptor and bipolar cells degenerate along an apoptotic pathway. CONCLUSIONS: Impairment of rod cGMP-gated channel alpha subunit expression leads to photoreceptor and bipolar cell degeneration. These transgenic mice are the first model of retinal degeneration caused by an alteration in the expression of the rod cGMP-gated channel. This model system can be used to test therapies designed to slow or stalled retinal degenerations.
Animals↗
A combination of CNTF and BDNF rescues rd photoreceptors but changes rod differentiation in the presence of RPE in retinal explants.
PURPOSE: To gather information regarding the combination of ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF), compared with the individual factors when used as a treatment to retard photoreceptor cell loss in rd mouse retina explants and to investigate the observation that the retinal pigment epithelium (RPE) influences rod differentiation by this treatment. METHODS: Postnatal day (PN)2 or PN7 control and rd mouse retinas were grown with attached retinal pigment epithelium (RPE). The explants were kept in culture up to PN28. During this culture period CNTF, BDNF, CNTF+BDNF, or vehicle were continuously administered to the culture medium. The nontrophic factors cyclosporin A and N:-CBZ-aspartic acid-glutamic acid-valine-aspartic acid-fluoromethyl ketone (z-DEVD-fmk) were also used. The number of photoreceptor nuclei remaining in the outer nuclear layer (ONL) was analyzed in hematoxylin and eosin-stained sections. Rod- and cone-specific antibodies were used to determine identity and state of differentiation of the photoreceptors. RESULTS: Compared with vehicle treatment, BDNF or CNTF resulted in 1.4- or 2-fold more surviving cell rows in the ONL, respectively. However, when CNTF and BDNF were applied together, surviving ONL cell counts in the rd explants were approximately 3 times those in vehicle-treated explants. In the presence of CNTF or CNTF+BDNF, opsin and arrestin expression in rods was decreased compared with rods without attached RPE. Cyclosporin A and z-DEVD-fmk did not show rescue of rd photoreceptor cells. CONCLUSIONS: CNTF or BDNF treatment of rd retinal explants delays photoreceptor cell loss to some extent. However, when these agents are combined, photoreceptor rescue is much more effective. The quenching of opsin and arrestin expression caused by treatment suggests that simultaneous with rod rescue, rod differentiation is depressed. Regarding retinal degeneration, the results from the selective inhibitors of apoptosis rank the CNTF+BDNF combination treatment as the most consistent and effective experimental pharmacologic intervention currently available.
Animals↗
Slow-progressing photoreceptor cell degeneration in night blindness c mutant zebrafish.
We describe here the morphological and functional alterations of the retina of mutant zebrafish, night blindness c ( nbc ). The nbc mutant was isolated from the F1 generation of N -ethyl- N -nitrosourea mutagenized founders. Visual sensitivity of wildtype and heterozygous ( nbc (+/-)) mutant fish was determined using a behavioral assay based on visually mediated escape responses. Histology, immunocytochemistry, and electroretinography were used to study structural and functional changes of the outer retina. The behavioral visual response of nbc (+/-) mutants started to deteriorate at 12 months of age. Considerable variations existed between the extents of retinal degeneration of individual fish. In the most severe cases, both rod and cone outer segments were degenerated. In moderate cases, only rod outer segments were affected. Yet in other cases, no degeneration was detected. The retina of homozygous ( nbc (-/-)) larvae had a normal appearance. However, they develop abnormally and died before 9 days post fertilization. In conclusion, nbc causes late-onset and progressive dominant retinal degeneration of both rod and cone photoreceptor cells. However, nbc is not a retina-specific gene, as the homozygous fish displayed extra-retinal defects.
Aging↗
Activation of mislocalized opsin kills rod cells: a novel mechanism for rod cell death in retinal disease.
Rod photoreceptors are highly compartmentalized sensory neurons that maintain strict ultrastructural and molecular polarity. Structural subdivisions include the outer segment, inner segment, cell body, and synaptic terminal. The visual pigment rhodopsin is found predominantly in membranes of the rod cell outer segment but becomes mislocalized, appearing throughout the plasma membrane of the cell in many retinal diseases and injuries. Currently, there is no known link between rhodopsin redistribution and rod cell death. We propose that activation of mislocalized rhodopsin kills rod cells by stimulating normally inaccessible signaling pathways. This hypothesis was tested in primary retinal cell cultures, which contain photoreceptors. In rod photoreceptors, opsin immunofluorescence occurred throughout the rod cell plasma membrane. Activation of this mislocalized opsin by photostimulation after formation of isorhodopsin or by incubation with beta-ionone (opsin agonist) killed 19-30% of rod cells. Rod cell death was apoptotic, as indicated by marked chromatin condensation and the requirement for caspase-3 activation. Rod cell death could be induced by forskolin (adenylate cyclase agonist), and conversely, beta-ionone-induced cell death could be blocked by cotreatment with SQ22536 (an adenylate cyclase inhibitor). Pertussis toxin (a G protein inhibitor) also blocked beta-ionone-induced cell death. The data support a mechanism by which activation of mislocalized opsin initiates apoptotic rod cell death through G protein stimulation of adenylate cyclase.
Adenine↗
Spatiotemporal gradients of cell genesis in the primate retina.
A cardinal event in the development of all brain structures is the time at which progenitor cells leave the cell cycle and begin to differentiate. We examined cell genesis in the retina of the macaque monkey (Macaca mulatta) by labeling dividing cells with radioactive thymidine ([3H]TdR) and following their fate at terminal division by virtue of their remaining radiolabeled after a long survival period. A number of distinct patterns of cell genesis were observed. The two tissues generated by the optic vesicle, the retinal pigment epithelium and neuroretina, share closely coincident temporal and spatial patterns of cell genesis, indicating that this process may be controlled by a common mechanism. Although overlapping to varying degrees, a clear sequence of genesis was revealed between specific cell types within the neuroretina: ganglion cells are generated first, followed by horizontal cells, cone photoreceptors, amacrine cells, Müller cells, bipolar cells, and, finally, rod photoreceptors. Retinal ganglion cells of differing soma diameter are born at different times-the smallest cells are generated early, the largest late, suggesting a further refined sequence of the functional classes of monkey retinal ganglion cells (first P gamma, then P beta, last P alpha). In addition, at sites where a homogeneous population of cells are crowded and stacked on top of each other (the foveola and perifovea for cones and ganglion cells, respectively) there is a vitreal-to-scleral intralaminar pattern of [3H]TdR labeled cell placement, which reflects both time of genesis and pattern of movement during foveation. These gradients suggest several scenarios for cell fate specification in the retina, many of which might not be obvious in mammals that develop more quickly and have less specialized retinal structure. Thus, data from the highly specialized and slowly developing macaque retina can help to understand visual development in humans and indicate useful avenues for future experimental studies in other species.
Animals↗
Rb regulates proliferation and rod photoreceptor development in the mouse retina.
The retinoblastoma protein (Rb) regulates proliferation, cell fate specification and differentiation in the developing central nervous system (CNS), but the role of Rb in the developing mouse retina has not been studied, because Rb-deficient embryos die before the retinas are fully formed. We combined several genetic approaches to explore the role of Rb in the mouse retina. During postnatal development, Rb is expressed in proliferating retinal progenitor cells and differentiating rod photoreceptors. In the absence of Rb, progenitor cells continue to divide, and rods do not mature. To determine whether Rb functions in these processes in a cell-autonomous manner, we used a replication-incompetent retrovirus encoding Cre recombinase to inactivate the Rb1(lox) allele in individual retinal progenitor cells in vivo. Combined with data from studies of conditional inactivation of Rb1 using a combination of Cre transgenic mouse lines, these results show that Rb is required in a cell-autonomous manner for appropriate exit from the cell cycle of retinal progenitor cells and for rod development.
Animals↗
Scotopic sensitivity of central retina in early age-related macular degeneration.
PURPOSE: To test scotopic sensitivity and investigate whether there is rod system dysfunction in the central retina in early age-related macular degeneration (AMD). METHODS: Scotopic (450 nm stimulus) and photopic (white light stimulus) sensitivity in 24 patients with early AMD was measured at 81 loci in central 25 degrees of retina, and compared with the age-match normal controls. RESULTS: Mean scotopic sensitivity of AMD patients was significantly lower than that of the normal controls. The patients of reduced scotopic sensitivity were more than those of reduced photopic sensitivity. Scotopic sensitivity deficit decreased with increasing eccentricity with the greatest deficit was 2.5 degrees to 5.0 degrees. CONCLUSIONS: Scotopic sensitivity was decreased in the early stage of AMD. The parafoveal rod cells were selectively damaged in AMD. Scotopic sensitivity testing in macula may be a useful tool to diagnose and measure the fundus dysfunction of AMD.
Dark Adaptation↗
Pre- and post-synaptic effects of manipulating surface charge with divalent cations at the photoreceptor synapse.
Persistence of horizontal cell (HC) light responses in extracellular solutions containing low Ca2+ plus divalent cations to block Ca2+ currents (ICa) has been attributed to Ca2+-independent neurotransmission. Using a retinal slice preparation to record both ICa and light responses, we demonstrate that persistence of HC responses in low [Ca2+]o can instead be explained by a paradoxical increase of Ca2+ influx into photoreceptor terminals arising from surface charge-mediated shifts in ICa activation. Consistent with this explanation, application of Zn2+ or Ni2+ caused a hyperpolarizing block of HC light responses that was relieved by lowering [Ca2+]o. The same concentrations of Zn2+ and Ni2+ reduced the amplitude of ICa at the rod dark potential and this reduction was relieved by a hyperpolarizing shift in voltage dependence induced by lowering [Ca2+]o. Block of ICa by Mg2+, which has weak surface charge effects, was not relieved by low [Ca2+]o. Recovery of HC responses in low [Ca2+]o was assisted by enhancement of rod light responses. To bypass light stimulation, OFF bipolar cells were stimulated by steps to -40 mV applied to presynaptic rods during simultaneous paired recordings. Consistent with surface charge theory, the post-synaptic current was inhibited by Zn2+ and this inhibition was relieved by lowering [Ca2+]o. Nominally divalent-free media produced inversion of HC light responses even though rod light responses remained hyperpolarizing; HC response inversion can be explained by surface charge-mediated shifts in ICa. In summary, HC light responses modifications induced by low divalent cation solutions can be explained by effects on photoreceptor light responses and membrane surface charge without necessitating Ca2+-independent neurotransmission. Furthermore, these results suggest that surface charge effects accompanying physiological changing divalent cation levels in the synaptic cleft may provide a means for modulating synaptic output from photoreceptors.
Animals↗
Regulation of cell division and rod differentiation in the teleost retina.
We tested the effects of several growth factors on the proliferation and differentiation of cells in the teleost retina which typically become rod photoreceptors to understand their regulation. Using organotypic slice cultures of differentiated teleost fish retinal tissue, we found that insulin and insulin-like growth factor I (IGF-I) stimulate proliferation of rod precursor cells whereas basic fibroblast growth factor (bFGF) does not. In the presence of bFGF, however, a greater proportion of the cells that had divided expressed a rod photoreceptor-specific phenotype than did control slices. This suggests insulin and the related IGF-I can influence the regulation of neuronal cell division whereas bFGF promotes the differentiation of neuronal stem cells into rod photoreceptors in retinal slice culture. These results support the idea that cell division and differentiation are differentially regulated and diffusible factors play a role in this process.
Animals↗