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Journal articles on the topic 'Retinal neurones'
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1
Straznicky, C., and M. Chehade. "The formation of the area centralis of the retinal ganglion cell layer in the chick." Development 100, no. 3 (July 1, 1987): 411–20. http://dx.doi.org/10.1242/dev.100.3.411.
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In adult domestic chickens, the neurones in the retinal ganglion cell layer are very unevenly disposed such that there is a sixfold increase in neurone density from the retinal edge to the retinal centre. The formation of the high ganglion-cell-density area centralis was studied on chick retinal wholemounts from the 8th day of incubation (E8) to 4 weeks after hatching (4WAH). The density of viable neurones and the number and the distribution of pyknotic neurones in the ganglion cell layer were estimated across the whole retina. Between E8 and E10, the distribution of neurones in the ganglion cell layer was anisodensitic with 53,000 mm-2 in the centre compared to 34,000 mm-2 in the periphery of the retina. Thereafter, a progressively steeper gradient of neurone density developed, which decreased from 24,000 mm-2 in the retinal centre to 6000 mm-2 at the retinal periphery by 4WAH. Neuronal pyknosis in the ganglion cell layer was observed between E9 and E17. From E11 onwards, consistently more pyknotic neurones were found in the peripheral than in the central retina. It was estimated that over the period of cell death approximately twice as many neurones died per unit area in the retinal periphery than in the centre. Retinal area measurements and estimation of neurone densities in the ganglion cell layer after the period of neurone generation and neurone death indicated differential retinal expansion, with more expansion in the peripheral than in the central retina. These observations allow us to conclude that the formation of the area centralis of the chick retina involves (1) slightly higher cell generation in the retinal centre, (2) higher rate of cell loss in the retinal periphery and (3) differential retinal expansion.
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BINNS, K. E., and T. E. SALT. "The functional influence of nicotinic cholinergic receptors on the visual responses of neurones in the superficial superior colliculus." Visual Neuroscience 17, no. 2 (March 2000): 283–89. http://dx.doi.org/10.1017/s0952523800172116.
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In the rat, the superficial gray layer (SGS) of the superior colliculus receives glutamatergic projections from the contralateral retina and from the visual cortex. A few fibers from the ipsilateral retina also directly innervate the SGS, but most of the ipsilateral visual input is provided by cholinergic afferents from the opposing parabigeminal nucleus (PBG). Thus, visual input carried by cholinergic afferents may have a functional influence on the responses of SGS neurones. When single neuronal extracellular recording and iontophoretic drug application were employed to examine this possibility, cholinergic agonists were found to depress responses to visual stimulation. Lobeline and 1-acetyl-4-methylpiperazine both depressed visually evoked activity and had a tendency to reduce the background firing rate of the neurones. Carbachol depressed the visual responses without any significant effect on the ongoing activity, while the muscarinic receptor selective agonist methacholine increased the background activity of the neurones and reduced their visual responses. Lobeline was chosen for further studies on the role of nicotinic receptors in SGS. Given that nicotinic receptors are associated with retinal terminals in SGS, and that the activation of presynaptic nicotinic receptors normally facilitates transmitter release (in this case glutamate release), the depressant effects of nicotinic agonists are intriguing. However, many retinal afferents contact inhibitory neurones in SGS; thus it is possible that the increase in glutamate release in turn facilitates the liberation of GABA which goes on to inhibit the visual responses. We therefore attempted to reverse the effects of lobeline with GABA receptor antagonists. The depressant effects of lobeline on the visual response could not be reversed by the GABAA antagonist bicuculline, but the GABAB antagonist CGP 35348 reduced the effects of lobeline. We hypothesize that cholinergic drive from the parabigeminal nucleus may activate presynaptic nicotinic receptors on retinal terminals, thereby facilitating the release of glutamate onto inhibitory neurones. Consequently GABA is released, activating GABAB receptors, and thus the ultimate effect of nicotinic receptor activation is to depress visual responses.
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Galli-Resta, Lucia, Elena Novelli, and Alessandro Viegi. "Dynamic microtubule-dependent interactions position homotypic neurones in regular monolayered arrays during retinal development." Development 129, no. 16 (August 15, 2002): 3803–14. http://dx.doi.org/10.1242/dev.129.16.3803.
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In the vertebrate retina cell layers support serial processing, while monolayered arrays of homotypic neurones tile each layer to allow parallel processing. How neurones form layers and arrays is still largely unknown. We show that monolayered retinal arrays are dynamic structures based on dendritic interactions between the array cells. The analysis of three developing retinal arrays shows that these become regular as a net of dendritic processes links neighbouring array cells. Molecular or pharmacological perturbations of microtubules within dendrites lead to a stereotyped and reversible disruption of array organization: array cells lose their regular spacing and the arrangement in a monolayer. This leads to a micro-mechanical explanation of how monolayers of regularly spaced ‘like-cells’ are formed.
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Gonzalez-Hoyuela, M., J. A. Barbas, and A. Rodriguez-Tebar. "The autoregulation of retinal ganglion cell number." Development 128, no. 1 (January 1, 2001): 117–24. http://dx.doi.org/10.1242/dev.128.1.117.
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The development of the nervous system is dependent on a complex set of signals whose precise co-ordination ensures that the correct number of neurones are generated. This regulation is achieved through a variety of cues that influence both the generation and the maintenance of neurones during development. We show that in the chick embryo, stratified retinal ganglion cells (RGCs) are themselves responsible for providing the signals that control the number of RGCs that are generated, both by inhibiting the generation of new ganglion cells and by killing incoming migratory ganglion cells. Selective toxicological ablation of RGCs in the chick embryo resulted in the achronic generation of ganglion cells, which eventually led to the repopulation of the ganglion cell layer and a large decrease in the physiological cell death affecting postmitotic migratory neurones. Interestingly, the application of exogenous NGF reversed the effects of ganglion cell ablation on ganglion cell death. Because the only source of NGF in the retina is that produced by the stratified ganglion cells, we infer that these differentiated neurones regulate their own cell number by secreting NGF, a neurotrophin that has previously been shown to be responsible for the death of migrating ganglion cells.
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Andressen, Christian, and Jürgen K. Mai. "Localization of the CD15 carbohydrate epitope in the vertebrate retina." Visual Neuroscience 14, no. 2 (March 1997): 253–62. http://dx.doi.org/10.1017/s0952523800011391.
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AbstractThe distribution of the carbohydrate epitope CD 15, a putative cell adhesion molecule, was studied in adult vertebrate retinas by light-microscopic immunohistochemistry. Except for Old World primates, in which no immunoreactivity was detectable, all other species expressed the epitope on retinal interneurones. Subpopulations of stratified amacrine cells were found in all species with the exception of bats and marmoset monkeys, and bipolar cells were immunoreactive in frogs and all amniotic animals. Ganglion cells were labelled in urodelian, in all sauromorphian, as well as in some mammalian species. In some species, the distribution of immunoreactive neurones was correlated to areas of retinal specialization such as the visual streak in frogs and the dorsotemporal field in birds. In these parts of the retina with enhanced visual acuity, more CD 15 glycosylated bipolar cells were found than in other parts. Among mammals, labelled bipolar cells were found exclusively in species with cone-dominated retinas. This comparative study shows that CD 15 expression is consistently membrane associated in morphologically defined subsets of amacrine, bipolar, and ganglion cells throughout the vertebrate phylum. Its distribution pattern was found to depend more on the visual behavior of a given species (cone-dominated or rod-dominated retina) than on phylogenetic proximity between species.
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Gaucher, David, Emilie Arnault, Zoé Husson, Nicolas Froger, Elisabeth Dubus, Pauline Gondouin, Diane Dherbécourt, et al. "Taurine deficiency damages retinal neurones: cone photoreceptors and retinal ganglion cells." Amino Acids 43, no. 5 (April 4, 2012): 1979–93. http://dx.doi.org/10.1007/s00726-012-1273-3.
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Frade, J. M. "Unscheduled re-entry into the cell cycle induced by NGF precedes cell death in nascent retinal neurones." Journal of Cell Science 113, no. 7 (April 1, 2000): 1139–48. http://dx.doi.org/10.1242/jcs.113.7.1139.
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During their early postmitotic life, a proportion of the nascent retinal ganglion cells (RGCs) are induced to die as a result of the interaction of nerve growth factor (NGF) with the neurotrophin receptor p75. To analyse the mechanisms by which NGF promotes apoptosis, an in vitro culture system consisting of dissociated E5 retinal cells was established. In this system, NGF-induced apoptosis was only observed in the presence of insulin and neurotrophin-3, conditions that favour the birth of RGCs and other neurones expressing the glycoprotein G4. The pro-apoptotic effect of NGF on the G4-positive neurones was evident after 10 hours in vitro and was preceded by a significant upregulation of cyclin B2, but not cyclin D1, and the presence of mitotic nuclei in these cells. Brain-derived neurotrophic factor prevented both the increase of cyclin B2 expression in the G4-positive neurones and the NGF-induced cell death. Finally, pharmacologically blocking cell-cycle progression using the cyclin-dependent kinase inhibitor roscovitine prevented NGF-induced cell death in a dose-dependent manner. These results strongly suggest that the apoptotic signalling initiated by NGF requires a driving stimulus manifested by the neuronal birth and is preceded by the unscheduled re-entry of postmitotic neurones into the cell cycle.
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Hussain, S. T., and E. A. Baydoun. "Cytochemical localization of 5'-nucleotidase in the frog (Rana pipiens) retina. A histochemical and cytochemical study." Journal of Histochemistry & Cytochemistry 33, no. 10 (October 1985): 1067–72. http://dx.doi.org/10.1177/33.10.2995482.
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Localization of 5'-nucleotidase in the frog retina was investigated using histochemical and cytochemical techniques. Light-microscopic observations revealed the presence of this enzyme in the inner retinal layers (the nerve fiber layer, ganglion cell layer, and inner plexiform layer). Ultrastructural investigations revealed that the enzyme activity is associated with the plasma membranes of the Müller cell processes, whereas the Müller cell processes present in the outer retinal layers did not demonstrate any detectable enzyme activity. This observation would appear to confirm our previous findings, that 5'-nucleotidase is an ectoenzyme, but its distribution in frog retina differs from that in rodents and it is only present in the inner layers of the retina. The prominent localization of 5'-nucleotidase on the glial plasma membrane may be viewed in the context of the widely accepted interaction between neurones and glial cells. Since nucleotides do not penetrate the plasma membrane, a mechanism to produce membrane-permeable adenosine, important for neuronal function, is postulated. It is known that 5'-nucleotidase produces adenosine by hydrolyzing adenosine 5'-monophosphate (5'-AMP). Therefore one would expect that the glial membrane-bound enzyme can accomplish the final step in this mechanism by producing the adenosine in the extracellular spaces.
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Uchiyama, Hiroyuki, Hironobu Ito, and Masaki Tauchi. "Retinal neurones specific for centrifugal modulation of vision." NeuroReport 6, no. 6 (April 1995): 889–92. http://dx.doi.org/10.1097/00001756-199504190-00016.
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Sparks, D. L. "The neural encoding of the location of targets for saccadic eye movements." Journal of Experimental Biology 146, no. 1 (September 1, 1989): 195–207. http://dx.doi.org/10.1242/jeb.146.1.195.
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Current models of the saccadic system imply that there are at least three neural representations of a visual target to which a saccade is made: representations in retinal, spatial (head or body) and motor coordinates. This paper presents the evidence supporting these models and summarizes the available neurophysiological data concerning neural representations of target location. In the superior colliculus, neurones in the superficial layers encode target location in retinal coordinates. Neurones in the deeper layers responsive to auditory and visual stimuli carry motor error signals. Evidence is also accumulating that some neurones in the thalamus and the frontal and parietal cortex convey information about target position with respect to the head or body, but these studies are far from complete.
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Osborne, N. N., and G. Quack. "Memantine stimulates inositol phosphates production in neurones and nullifies N- destruction of retinal neurones." Neurochemistry International 21, no. 3 (October 1992): 329–36. http://dx.doi.org/10.1016/0197-0186(92)90183-r.
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Liu, Fang, Alan B. Saul, Prahalathan Pichavaram, Zhimin Xu, Madhuri Rudraraju, Payaningal R. Somanath, Sylvia B. Smith, Ruth B. Caldwell, and S. Priya Narayanan. "Pharmacological Inhibition of Spermine Oxidase Reduces Neurodegeneration and Improves Retinal Function in Diabetic Mice." Journal of Clinical Medicine 9, no. 2 (January 25, 2020): 340. http://dx.doi.org/10.3390/jcm9020340.
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Diabetic retinopathy (DR) is a significant cause of blindness in working-age adults worldwide. Lack of effective strategies to prevent or reduce vision loss is a major problem. Since the degeneration of retinal neurons is an early event in the diabetic retina, studies to characterize the molecular mechanisms of diabetes-induced retinal neuronal damage and dysfunction are of high significance. We have demonstrated that spermine oxidase (SMOX), a mediator of polyamine oxidation is critically involved in causing neurovascular damage in the retina. The involvement of SMOX in diabetes-induced retinal neuronal damage is completely unknown. Utilizing the streptozotocin-induced mouse model of diabetes, the impact of the SMOX inhibitor, MDL 72527, on neuronal damage and dysfunction in the diabetic retina was investigated. Retinal function was assessed by electroretinography (ERG) and retinal architecture was evaluated using spectral domain-optical coherence tomography. Retinal cryosections were prepared for immunolabeling of inner retinal neurons and retinal lysates were used for Western blotting. We observed a marked decrease in retinal function in diabetic mice compared to the non-diabetic controls. Treatment with MDL 72527 significantly improved the ERG responses in diabetic retinas. Diabetes-induced retinal thinning was also inhibited by the MDL 72527 treatment. Our analysis further showed that diabetes-induced retinal ganglion cell damage and neurodegeneration were markedly attenuated by MDL 72527 treatment. These results strongly implicate SMOX in diabetes-induced retinal neurodegeneration and visual dysfunction.
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Ji, Dan, Guang-Yu Li, and Neville N. Osborne. "Nicotinamide attenuates retinal ischemia and light insults to neurones." Neurochemistry International 52, no. 4-5 (March 2008): 786–98. http://dx.doi.org/10.1016/j.neuint.2007.09.012.
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Godement, P., J. Vanselow, S. Thanos, and F. Bonhoeffer. "A study in developing visual systems with a new method of staining neurones and their processes in fixed tissue." Development 101, no. 4 (December 1, 1987): 697–713. http://dx.doi.org/10.1242/dev.101.4.697.
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Carbocyanine dyes, fluorescent lipophilic substances used for optical recordings of membrane voltage and for studies of membrane fluidity, have recently been shown to provide intense and long-lasting staining of neurones in vivo and in vitro (Schwartz & Agranoff, 1981; Honig & Hume, 1985, 1986; Catsicas, Thanos & Clarke, 1986; Landmesser & Honig, 1986; Thanos & Bonhoeffer, 1987). We report here that two of these dyes, diI (1,1′,dioctadecyl-3,3,3′3′-tetramethylindocarbocyanine perchlorate) and diO (3,3′-dioctadecyloxacarbocyanine perchlorate), can also label neurones in embryonic mouse and chicken brain tissue that has been previously fixed in aldehyde fixatives. Neuronal processes and perikarya can be labelled along considerable distances in both anterograde and retrograde directions. The staining of processes and cells, including their finest extensions is smooth and clear, rivalling intracellular injections of HRP or Lucifer Yellow. The appearance and time course of progression of the staining along axons suggest that the staining in fixed tissue occurs due to a process of diffusion of dyes along the plasma membranes of cells. This technique has allowed us to study the first stages in the development of optic fibres in mouse embryos, especially at the optic chiasm. The early retinal projection (E13-E13 1/2) is mainly crossed, but some optic fibres grow to the ipsilateral side of the brain at the outset. Retrogradely labelled ganglion cells from the dorsocentral area of the retina participate in the formation of both the ipsilateral and the contralateral projection. Thus, at early stages, crossed and uncrossed projections arise from identical subregions of the retina and the partition of the retina with respect to the laterality of its projection arises later.
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Acosta, Monica L., Michael Kalloniatis, and David L. Christie. "Creatine transporter localization in developing and adult retina: importance of creatine to retinal function." American Journal of Physiology-Cell Physiology 289, no. 4 (October 2005): C1015—C1023. http://dx.doi.org/10.1152/ajpcell.00137.2005.
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Creatine and phosphocreatine are required to maintain ATP needed for normal retinal function and development. The aim of the present study was to determine the distribution of the creatine transporter (CRT) to gain insight to how creatine is transported into the retina. An affinity-purified antibody raised against the CRT was applied to adult vertebrate retinas and to mouse retina during development. Confocal microscopy was used to identify the localization pattern as well as co-localization patterns with a range of retinal neurochemical markers. Strong labeling of the CRT was seen in the photoreceptor inner segments in all species studied and labeling of a variety of inner neuronal cells (amacrine, bipolar, and ganglion cells), the retinal nerve fibers and sites of creatine transport into the retina (retinal pigment epithelium, inner retinal blood vessels, and perivascular astrocytes). The CRT was not expressed in Müller cells of any of the species studied. The lack of labeling of Müller cells suggests that neurons are independent of this glial cell in accumulating creatine. During mouse retinal development, expression of the CRT progressively increased throughout the retina until approximately postnatal day 10, with a subsequent decrease. Comparison of the distribution patterns of the CRT in vascular and avascular vertebrate retinas and studies of the mouse retina during development indicate that creatine and phosphocreatine are important for ATP homeostasis.
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Kimura, Atsuko, Kazuhiko Namekata, Kohichi Tanaka, and Takayuki Harada. "Dock3 protects retinal neurones from glutamate neurotoxicity and oxidative stress." Neuroscience Research 68 (January 2010): e255. http://dx.doi.org/10.1016/j.neures.2010.07.1132.
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Greenstreet, Elizabeth H., and Mustafa B. A. Djamgoz. "Nitric oxide induces light-adaptive morphological changes in retinal neurones." NeuroReport 6, no. 1 (December 1994): 109–12. http://dx.doi.org/10.1097/00001756-199412300-00029.
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Ikeda, Hisako, Mark W. Hankins, Toshimichi Asai, and Elizabeth A. Dawes. "Electrophysiological properties of neurones following mild and acute retinal ischaemia." Experimental Eye Research 55, no. 3 (September 1992): 435–42. http://dx.doi.org/10.1016/0014-4835(92)90116-a.
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CAMERON, DAVID A. "Cellular proliferation and neurogenesis in the injured retina of adult zebrafish." Visual Neuroscience 17, no. 5 (September 2000): 789–97. http://dx.doi.org/10.1017/s0952523800175121.
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The retinas of adult teleost fish can regenerate neurons following a chemical or mechanical injury. Previous studies have demonstrated that mechanical excision of fish retina induces a hyperplasia within the retinal sheet, including the formation of a proliferative blastema from whence new retinal cells are produced to fill the excision site. The current study was designed to address two issues regarding injury-induced retinal hyperplasia: (1) Retinas of adult zebrafish can regenerate following a surgical excision, but compared to other fish they contain very few proliferative cells: Might retinal injury in adult zebrafish therefore induce minimal, or perhaps no, hyperplasia? (2) The fate of injury-induced, proliferative retinal cells outside surgical excision sites has yet to be determined. Do such cells produce retinal neurons? Evidence is presented that mechanical injury to the adult zebrafish retina induces a dramatic increase in the number of proliferative cells both within and external to the lesion site, and some of these cells apparently migrate within the radial dimension of the retina. Evidence is also presented that injury-induced proliferative cells outside a lesion site can produce retinal neurons—including cone photoreceptors, interplexiform cells, and amacrine cells—that are incorporated into the extant retina. The results suggest that the adult zebrafish retina contains a latent population of cells that is induced to proliferate following retinal injury, and that these cells might represent a novel avenue for pluripotent neurogenesis within the intact adult teleost retina.
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Binns, K. E., and T. E. Salt. "Corticofugal influences on visual responses in cat superior colliculus: The role of NMDA receptors." Visual Neuroscience 13, no. 4 (July 1996): 683–94. http://dx.doi.org/10.1017/s0952523800008579.
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AbstractThe role of N-methyl-D-aspartate (NMDA) receptors in the mediation of cortical inputs to visual neurones in the superficial layers of the superior colliculus (SSC) has been investigated. Extracellular recording with iontophoresis in the SSC of cortically intact cats has demonstrated that visual responses of most neurones were reduced by iontophoretic application of the NMDA receptor antagonist D-2-amino-5-phosphonopentanoate (APS). Following inactivation of areas 17 and 18 of the visual cortex with topical lignocaine, the visual responses of 11, previously AP5-sensitive, neurones were no longer reduced by APS ejection. The cortical input is generally assumed to influence the directional responses of visual neurones in SSC. However, detailed study of the directional bias showed that the degree of directional tuning in SSC neurones was similar to that of retinal ganglion cells, as previously described by others. Moreover, inactivation of the visual cortex with topical lignocaine did not alter the directional bias of SSC neurones. Likewise, the directional bias of SSC neurones was not reduced by iontophoretic ejection of APS in the SSC. These data imply that NMDA receptors have an important role in mediating the cortical input to the SSC. However, cortical input does not appear to be responsible for conferring directional bias upon SSC neurones' visual responsiveness.
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LIN, BIN, PAUL R. MARTIN, and ULRIKE GRÜNERT. "Expression and distribution of ionotropic glutamate receptor subunits on parasol ganglion cells in the primate retina." Visual Neuroscience 19, no. 4 (July 2002): 453–65. http://dx.doi.org/10.1017/s0952523802194077.
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The response properties of postreceptoral sensory neurones are determined by the properties of their input neurones, by intrinsic membrane properties, and by the properties of neurotransmitter receptors on the soma and dendritic tree. We previously showed that inhibitory neurotransmitter (GABAA and glycine) receptors on a well-characterised sensory neurone, the parasol ganglion cell in the primate retina, are segregated towards the distal part of the dendritic tree. Here we studied the distribution of excitatory ionotropic glutamate receptor subunits on the dendrites of parasol cells in the retina of a New World monkey, the marmoset, Callithrix jacchus. Individual ganglion cells were intracellularly injected in an in vitro retinal wholemount preparation. Ionotropic glutamate receptor subunits, including AMPA (GluR1-4), kainate (GluR6/7), NMDA (NR1C2′) subunits, and the orphan receptors δ1 and δ2 were visualized with immunocytochemical methods. Immunoreactive puncta that colocalized with the dendrites of ganglion cells were analyzed using standard and/or confocal light microscopy. Colocalized puncta were present on parasol dendrites for all subunits studied, but their density was much lower (approximately 1/5) than previously reported for inhibitory (GABA and glycine) receptors. Segregation of the glutamate receptor clusters (GluR1, GluR6/7 subunits) to the peripheral dendrites was less marked than that shown for GABA and glycine receptor clusters. No sign of segregation of colocalized puncta to the peripheral part of the dendritic field was seen with antibodies to the GluR2, GluR2/3, GluR4, δ1/2, or NR1C2′ subunits. The results suggest that although there is diverse expression of glutamate receptor subtypes, the glutamatergic synapses form only a small proportion of the total synaptic input to primate ganglion cells. They further suggest that the processes which control distribution of excitatory and inhibitory synapses on the dendritic field of ganglion cells are, at least to some extent, independent.
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Djamgoz, M. B. A., and H. J. Wagner. "Intracellular staining of retinal neurones: Applications to studies of functional organization." Progress in Retinal Research 6 (January 1987): 85–150. http://dx.doi.org/10.1016/0278-4327(87)90021-6.
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Bray, G. M., M. P. Villegas-Perez, M. Vidal-Sanz, and A. J. Aguayo. "The use of peripheral nerve grafts to enhance neuronal survival, promote growth and permit terminal reconnections in the central nervous system of adult rats." Journal of Experimental Biology 132, no. 1 (September 1, 1987): 5–19. http://dx.doi.org/10.1242/jeb.132.1.5.
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During both development and regeneration, the survival of neurones and the growth of axons are controlled by inherent neuronal properties, conditions in the axonal environment, and the establishment of appropriately timed and specific functional contacts. To study the effects of extrinsic influences on the survival, growth and connectivity of axotomized neurones in the mature mammalian CNS, we replaced the optic nerve in adult rats with segments of autologous peripheral nerve (PN) and used morphometric techniques, neuroanatomical tracer substances and immunological cell markers to examine retinal ganglion cells (RGCs), their axons in the PN grafts and their terminals in the superior colliculi (SC) of these animals. We observed that: (1) the survival of axotomized RGCs was enhanced by the PN grafts; (2) in the PN-grafted eyes, approximately 20% of the surviving RGCs regrew their axons into the grafts and (3) some of the RGC axons that regenerated along the PN grafts bridging the eye and the tectum re-entered the SC, arborized and made synaptic contacts with tectal neurones. It is not known if the terminal connections established between RGCs and cells in the SC are appropriate, functional or capable of influencing the long-term survival of their cells of origin.
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DERRINGTON, ANDREW M., and FATIMA FELISBERTI. "Peripheral shift reduces visual sensitivity in cat geniculate neurones." Visual Neuroscience 15, no. 5 (May 1998): 875–80. http://dx.doi.org/10.1017/s0952523898155128.
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The sudden displacement of the retinal image during a saccade raises the visual threshold of human observers to foveal stimuli. The fall in visual sensitivity observed during this phenomenon, known as saccadic suppression, seems to occur very early in the visual processing chain. The lateral geniculate nucleus (LGN) is a likely locus for the multiple retinal and extraretinal interactions occurring during saccadic eye movements, therefore we used the responses of relay cells of adult cats to simulate a pychophysical experiment. We first measured the responses of X and Y relay cells (27 X and 13 Y) to central spots of optimal size and different contrasts. The spots were presented either alone or time locked with the rapid movement of a large, high-contrast peripheral pattern, referred to as shift. We measured the percentage of trials on which the relay cell fired more spikes when the spot (contrast: 0.03–1.0) was present than when it was absent. In experiments with human observers the task was to indicate, by a keypress, which of two otherwise identical temporal intervals contained the spot. The shift reduces the sensitivity (raises the contrast threshold) of neurones in the cat relay cells to brief, stationary targets presented to the receptive-field center. The suppression of visual sensitivity is significantly greater in Y cells than in X cells (average sensitivity ratios 5.6 ± 5.4 in Y cells, 1.59 ± 0.9 in X cells: P < 0.001, U test). The shift also reduces the sensitivity of human observers to the same target. This suggests that the LGN is a potential locus for the modulation of visual responses that leads to saccadic suppression.
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SHAND, JULIA, MICHAEL A. ARCHER, NICOLE THOMAS, and JENNIFER CLEARY. "Retinal development of West Australian dhufish, Glaucosoma hebraicum." Visual Neuroscience 18, no. 5 (September 2001): 711–24. http://dx.doi.org/10.1017/s0952523801185056.
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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 μm 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 (λmax) located at 522 nm. Single cones were found to possess a visual pigment with λmax at 460 nm and rods with a λmax 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.
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Chen, Jingfei, Qihui Luo, Chao Huang, Wen Zeng, Ping Chen, Qi Gao, Bing Chen, Wentao Liu, Lingzhen Pan, and Zhengli Chen. "Morphology of Inner Retina in Rhesus Monkeys of Various Ages: A Comparative Study." Journal of Ophthalmology 2019 (March 3, 2019): 1–7. http://dx.doi.org/10.1155/2019/7089342.
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Purpose. To investigate the changes of thickness in each layer, the morphology and density of inner neurons in rhesus monkeys’ retina at various growth stages, thus contribute useful data for further biological studies. Methods. The thickness of nerve fiber layer (NFL), the whole retina, inner plexiform layer (IPL), and outer plexiform layer (OPL) of rhesus monkeys at different ages were observed with hematoxylin and eosin (H&E) staining. The morphology and the density of inner neurons of rhesus monkey retina were detected by immunofluorescence. Results. The retina showed the well-known ten layers, the thickness of each retinal layer in rhesus monkeys at various ages increased rapidly after infant, and the retina was the thickest in adulthood, but the retinal thickness stop growing in senescent. Quantitative analysis showed that the maximum density of inner neurons was reached in adolescent, and then, the density of inner neurons decreased in adults and senescent retinas. And some changes in the morphology of rod bipolar cells have occurred in senescent. Conclusions. The structure of retina in rhesus monkeys is relatively immature at infant, and the inner retina of rhesus monkeys is mature in adolescent, while the thickness of each retinal layer was the most developed in the adult group. There was no significant change in senescence for the thickness of each retinal layer, but the number of the neurons in our study has a decreasing trend and the morphological structure has changed.
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Silverman, Sean M., and Wai T. Wong. "Microglia in the Retina: Roles in Development, Maturity, and Disease." Annual Review of Vision Science 4, no. 1 (September 15, 2018): 45–77. http://dx.doi.org/10.1146/annurev-vision-091517-034425.
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Microglia, the primary resident immune cell type, constitute a key population of glia in the retina. Recent evidence indicates that microglia play significant functional roles in the retina at different life stages. During development, retinal microglia regulate neuronal survival by exerting trophic influences and influencing programmed cell death. During adulthood, ramified microglia in the plexiform layers interact closely with synapses to maintain synaptic structure and function that underlie the retina's electrophysiological response to light. Under pathological conditions, retinal microglia participate in potentiating neurodegeneration in diseases such as glaucoma, retinitis pigmentosa, and age-related neurodegeneration by producing proinflammatory neurotoxic cytokines and removing living neurons via phagocytosis. Modulation of pathogenic microglial activation states and effector mechanisms has been linked to neuroprotection in animal models of retinal diseases. These findings have led to the design of early proof-of-concept clinical trials with microglial modulation as a therapeutic strategy.
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Cervia, Catalani, and Casini. "Neuroprotective Peptides in Retinal Disease." Journal of Clinical Medicine 8, no. 8 (August 1, 2019): 1146. http://dx.doi.org/10.3390/jcm8081146.
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In the pathogenesis of many disorders, neuronal death plays a key role. It is now assumed that neurodegeneration is caused by multiple and somewhat converging/overlapping death mechanisms, and that neurons are sensitive to unique death styles. In this respect, major advances in the knowledge of different types, mechanisms, and roles of neurodegeneration are crucial to restore the neuronal functions involved in neuroprotection. Several novel concepts have emerged recently, suggesting that the modulation of the neuropeptide system may provide an entirely new set of pharmacological approaches. Neuropeptides and their receptors are expressed widely in mammalian retinas, where they exert neuromodulatory functions including the processing of visual information. In multiple models of retinal diseases, different peptidergic substances play neuroprotective actions. Herein, we describe the novel advances on the protective roles of neuropeptides in the retina. In particular, we focus on the mechanisms by which peptides affect neuronal death/survival and the vascular lesions commonly associated with retinal neurodegenerative pathologies. The goal is to highlight the therapeutic potential of neuropeptide systems as neuroprotectants in retinal diseases.
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MÖLLER, ANNA, and THOR EYSTEINSSON. "Modulation of the components of the rat dark-adapted electroretinogram by the three subtypes of GABA receptors." Visual Neuroscience 20, no. 5 (September 2003): 535–42. http://dx.doi.org/10.1017/s0952523803205071.
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The separate components of the dark-adapted electroretinogram (ERG) are believed to reflect the electric activity of neurones in both the inner and the outer layers of the retina, although their precise origin still remains unclear. The purpose of this study was to examine whether selective blockage or stimulation of the different subtypes of GABA receptors might help further elucidate the cellular origin of the components of the dark-adapted ERG. The rat retina is of interest since the localization and physiology of GABA receptors in that retina have been examined in great detail. GABA agonists and antagonists, known to affect the responses of neurons in the inner plexiform layer, were injected into the vitreous of one eye while ERG responses evoked by flashes of white light were recorded. GABA and the GABAa agonist isoguvacine completely removed the oscillatory potentials (OPs) and reduced the amplitude of the a- and b-waves. TPMPA, a GABAc antagonist, reduced the a- and b-waves but had no significant effect on the OPs. Baclofen, a GABAb agonist, reduced the amplitude of the a- and b-waves, without having any effects on the amplitude of the OPs. The GABAb antagonist CGP35348 increased the amplitudes of the a- and b-wave without having an effect on the amplitudes of the OPs. The GABAb receptor ligands had significant and opposite effect on the latency of the OPs. These results indicate that retinal neurons, presumably a subpopulation of amacrine cells, that have GABAb receptors are not the source of the OPs of the ERG, although they may modulate these wavelets in some manner, while contributing to the generation of the dark-adapted a- and b-waves. OPs are modified by stimulation of GABAa receptors, and the a- and b-waves by stimulation of all GABA receptor subtypes.
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CAMERON, DAVID A., and MAUREEN K. POWERS. "Morphology and visual pigment content of photoreceptors from injured goldfish retina." Visual Neuroscience 17, no. 4 (July 2000): 623–30. http://dx.doi.org/10.1017/s0952523800174115.
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Adult teleost fish retinas can regenerate neurons following either surgical or pharmacological injury. The cellular milieu of the damaged retina within which regenerated neurons are produced might be different in these two model systems of retinal injury, and thus the phenotypic attributes of regenerated neurons in the two model systems might also differ. To determine if the phenotypic attributes of photoreceptors, and by extension the recovery of vision, are different between these two model systems, we compared the visual pigment content and morphology of photoreceptors derived from goldfish retinas of both models with control retina. Visual pigments—which consist of a protein moiety (opsin) and a chromophore—were analyzed in single, isolated photoreceptors using microspectrophotometric techniques. We report that visual pigments and photoreceptor morphologies in the surgical model closely matched those of native retina. In contrast, neither photoreceptor morphology nor visual pigment content matched closely in the pharmacological model. The results indicate that phenotypic attributes of photoreceptors can differ significantly between the two model systems of retinal regeneration, but that in both systems, rod- and cone-mediated visual functions can potentially be reestablished.
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Zhdankina, A. A., G. A. Kon, M. B. Plotnikov, Ye Yu Varakuta, S. V. Logvinov, A. Ye Prosenko, and N. G. Kolosova. "INVESTIGATION OF NEUROPROTECTIVE ACTIVITY THIOPHANE INVOLUTIONAL CHORIORETINAL DEGENERATION IN RATS OXYS." Bulletin of Siberian Medicine 12, no. 3 (June 28, 2013): 24–32. http://dx.doi.org/10.20538/1682-0363-2013-3-24-32.
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The method of spontaneous and induced luminol -dependent chemiluminescence in homogenates of rat retinas OXYS registered increase in the generation of free radicals against decrease in total antioxidant activity. With the ultra-microscopic and quantitative analysis revealed degenerative retinal neurons rats OXYS: the percentage increase in neurosensory cells with pyknosis of nuclei, hyperchromatic piknomorfnyh associative neurons and ganglion n eurons that have been modified on a light and dark type. Thiophane, limiting free radical reactions in the retina and protects retinal neurons from damage.
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Jeon, C. J., and R. H. Masland. "Selective accumulation of diamidino yellow and chromomycin A3 by retinal glial cells." Journal of Histochemistry & Cytochemistry 41, no. 11 (November 1993): 1651–58. http://dx.doi.org/10.1177/41.11.8409373.
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We applied the fluorescent DNA stains diamidino yellow (DY) and chromomycin A3 to rat and rabbit retinas in vivo and in vitro. They accumulated in the nuclei of a subpopulation of cells of the inner nuclear layer. The number and distribution of the fluorochrome-accumulating cells were similar to those of the Müller glia, and double-labeling experiments showed that the cells accumulating DY or chromomycin A3 contained oriented filaments of vimentin. The fluorochromes also accumulated in the sparse astrocytes and oligodendrocytes located among the myelinated fibers of the rabbit central retina. Specific accumulation in retinal glia occurred only when the fluorochromes were applied to living retinas. If the plasma membranes were disrupted by fixation or exposure to detergent, most retinal cells were stained. This indicates that the locus of specificity is the entry of the molecules into the cells. When applied to living retinas, other DNA stains selectively accumulate in subclasses of retinal neurons. Why DNA-binding molecules should selectively cross the membranes of either retinal neurons or retinal glia remains an unsolved problem.
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YURCO, PATRICK, and DAVID A. CAMERON. "Cellular correlates of proneural and notch-delta gene expression in the regenerating zebrafish retina." Visual Neuroscience 24, no. 3 (May 2007): 437–43. http://dx.doi.org/10.1017/s0952523807070496.
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Fish can regenerate retinal neurons following ocular injury. Evidence is mounting that astrocytic glia function as inducible, regenerative stem cells in this process, but the underlying molecular events that enable neuronal regeneration are comparatively unclear. In the current study gene array, quantitative real-time PCR, in situ hybridization, and immunohistochemical approaches were used to identify, in the damaged retina of adult zebrafish, correlations between transcriptional events and entry into the cell cycle by Müller cells, a type of astrocytic cell present in all vertebrate retinas that is a candidate ‘stem cell’ of regenerated neurons. A proneural gene (achaete-scute homolog 1a, ash1a) and neurogenic components of the Notch signaling pathway, including notch3 and deltaA, were implicated. An injury-induced, enhanced expression of ash1a was observed in Müller cells, which is hypothesized to contribute to the transition of these cells, or their cellular progeny, into a notch3-expressing, regenerative progenitor. A model of vertebrate retinal repair is suggested in which damage-induced expression of proneural genes, plus canonical Notch-Delta signaling, could contribute to retinal stem cell promotion and subsequent regenerative neurogenesis.
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Vlasiuk, Anastasiia, and Hiroki Asari. "Feedback from retinal ganglion cells to the inner retina." PLOS ONE 16, no. 7 (July 22, 2021): e0254611. http://dx.doi.org/10.1371/journal.pone.0254611.
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Retinal ganglion cells (RGCs) are thought to be strictly postsynaptic within the retina. They carry visual signals from the eye to the brain, but do not make chemical synapses onto other retinal neurons. Nevertheless, they form gap junctions with other RGCs and amacrine cells, providing possibilities for RGC signals to feed back into the inner retina. Here we identified such feedback circuitry in the salamander and mouse retinas. First, using biologically inspired circuit models, we found mutual inhibition among RGCs of the same type. We then experimentally determined that this effect is mediated by gap junctions with amacrine cells. Finally, we found that this negative feedback lowers RGC visual response gain without affecting feature selectivity. The principal neurons of the retina therefore participate in a recurrent circuit much as those in other brain areas, not being a mere collector of retinal signals, but are actively involved in visual computations.
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Mitrofanis, John, and Barbara L. Finlay. "Developmental changes in the distribution of retinal catecholaminergic neurones in hamsters and gerbils." Journal of Comparative Neurology 292, no. 3 (February 15, 1990): 480–94. http://dx.doi.org/10.1002/cne.902920312.
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Rörig, Birgit, and Rosemarie Grantyn. "Ligand- and voltage-gated ion channels are expressed by embryonic mouse retinal neurones." NeuroReport 5, no. 10 (June 1994): 1197–200. http://dx.doi.org/10.1097/00001756-199406020-00009.
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LASCARATOS, G., and NN OSBORNE. "Indocyanine green-induced toxicity to retinal neurones in cultures is enhanced by light." Acta Ophthalmologica 86 (September 4, 2008): 0. http://dx.doi.org/10.1111/j.1755-3768.2008.653.x.
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Razafsky, David, Candace Ward, Chloe Potter, Wanqiu Zhu, Yunlu Xue, Vladimir J. Kefalov, Loren G. Fong, Stephen G. Young, and Didier Hodzic. "Lamin B1 and lamin B2 are long-lived proteins with distinct functions in retinal development." Molecular Biology of the Cell 27, no. 12 (June 15, 2016): 1928–37. http://dx.doi.org/10.1091/mbc.e16-03-0143.
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Lamin B1 and lamin B2 are essential building blocks of the nuclear lamina, a filamentous meshwork lining the nucleoplasmic side of the inner nuclear membrane. Deficiencies in lamin B1 and lamin B2 impair neurodevelopment, but distinct functions for the two proteins in the development and homeostasis of the CNS have been elusive. Here we show that embryonic depletion of lamin B1 in retinal progenitors and postmitotic neurons affects nuclear integrity, leads to the collapse of the laminB2 meshwork, impairs neuronal survival, and markedly reduces the cellularity of adult retinas. In stark contrast, a deficiency of lamin B2 in the embryonic retina has no obvious effect on lamin B1 localization or nuclear integrity in embryonic retinas, suggesting that lamin B1, but not lamin B2, is strictly required for nucleokinesis during embryonic neurogenesis. However, the absence of lamin B2 prevents proper lamination of adult retinal neurons, impairs synaptogenesis, and reduces cone photoreceptor survival. We also show that lamin B1 and lamin B2 are extremely long-lived proteins in rod and cone photoreceptors. OF interest, a complete absence of both proteins during postnatal life has little or no effect on the survival and function of cone photoreceptors.
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Sanyal, S., R. K. Hawkins, H. G. Jansen, and G. H. Zeilmaker. "Compensatory synaptic growth in the rod terminals as a sequel to partial photoreceptor cell loss in the retina of chimaeric mice." Development 114, no. 3 (March 1, 1992): 797–803. http://dx.doi.org/10.1242/dev.114.3.797.
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In the retina of chimaeric mice of rd and wild-type genotypic combination, selective loss of rd/rd photoreceptor cells, after initial development, leads to a mosaic retina with variable amounts of normal photoreceptor cells present over the retinal surface. In some of the rod terminals of these retinas the synaptic complexes with the second order retinal neurons are seen to contain multiple synaptic ribbons and an increased number of profiles of the postsynaptic elements. These changes are observed only in the rod terminals and not in the cone pedicles. Computer aided three-dimensional reconstruction of the altered synapses shows that these changes result from an increase in the number of synaptic sites, characterized by multiplication of the synaptic ribbons and enlargement of the second order neuronal processes. A quantitative analysis of such synapses, based on serial electron micrographs, shows that these are most frequently located in the retinal regions of the chimaeric individuals that have suffered maximum photoreceptor cell loss. Thus synaptic growth appears to take place as a reaction to the reduction of afferent input to the postsynaptic components. These findings demonstrate persistent synaptic plasticity in the rod terminals of mammalian retina during the maturational phase of late postnatal development. Compensatory synaptic growth in the rod terminals, as recorded here, can have important implications for the maintenance of visual sensitivity in the diseased or ageing retina.
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Stutzki, Henrike, Florian Helmhold, Max Eickenscheidt, and Günther Zeck. "Subretinal electrical stimulation reveals intact network activity in the blind mouse retina." Journal of Neurophysiology 116, no. 4 (October 1, 2016): 1684–93. http://dx.doi.org/10.1152/jn.01095.2015.
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Retinal degeneration ( rd) leads to progressive photoreceptor cell death, resulting in vision loss. Stimulation of the inner-retinal neurons by neuroprosthetic implants is one of the clinically approved vision-restoration strategies, providing basic visual percepts to blind patients. However, little is understood as to what degree the degenerating retinal circuitry and the resulting aberrant hyperactivity may prevent the stimulation of physiological electrical activity. Therefore, we electrically stimulated ex vivo retinas from wild-type ( wt; C57BL/6J) and blind ( rd10 and rd1) mice using an implantable subretinal microchip and simultaneously recorded and analyzed the retinal ganglion cell (RGC) output with a flexible microelectrode array. We found that subretinal anodal stimulation of the rd10 retina and wt retina evoked similar spatiotemporal RGC-spiking patterns. In both retinas, electrically stimulated ON and a small percentage of OFF RGC responses were detected. The spatial selectivity of the retinal network to electrical stimuli reveals an intact underlying network with a median receptive-field center of 350 μm in both retinas. An antagonistic surround is activated by stimulation with large electrode fields. However, in rd10 and to a higher percentage, in rd1 retinas, rhythmic and spatially unconfined RGC patterns were evoked by anodal or by cathodal electrical stimuli. Our findings demonstrate that the surviving retinal circuitry in photoreceptor-degenerated retinas is preserved in a way allowing for the stimulation of temporally diverse and spatially confined RGC activity. Future vision restoration strategies can build on these results but need to avoid evoking the easily inducible rhythmic activity in some retinal circuits.
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Pfister, Delaney, Chuanjiang Yu, Da Som Kim, Jingling Li, Audrey Drewing, and Lei Li. "Zebrafish Olfacto-Retinal Centrifugal Axon Projection and Distribution: Effects of Gonadotropin-Releasing Hormone and Dopaminergic Signaling." Developmental Neuroscience 38, no. 1 (October 28, 2015): 27–33. http://dx.doi.org/10.1159/000439524.
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The terminalis neurons (TNs) have been described in teleost species. In zebrafish, the TNs are located in the olfactory bulb. The TNs synthesize and release gonadotropin-releasing hormone (GnRH) as one of the major neurotransmitters. The TNs project axons to many brain areas, which include the neural retina. In the retina, the TN axons synapse with dopaminergic interplexiform cells (DA-IPCs) and retinal ganglion cells (RGCs). In this research, we examine the role of GnRH and dopaminergic signaling in TN axon projection to the retina using the transgenic zebrafish Tg(GnRH-3::GFP). While the TNs developed at 34 h postfertilization (hpf), the first TN axons were not detected in the retina until 48-50 hpf, when the first DA-IPCs were differentiated. In developing embryos, inhibition of retinal GnRH signaling pathways severely interrupted the projection of TN axons to the retina. However, inhibition of retinal dopaminergic signaling produced little effect on TN axon projection. In adult retinas, inactivation of GnRH receptors disrupted the patterns of TN axon distribution, and depletion of DA-IPCs abolished the TN axons. When DA-IPCs regenerated, the TN axons reappeared. Together, the data suggest that in developing zebrafish retinas GnRH signaling is required for TN axon projection, whereas in adult retinas activation of GnRH and dopaminergic signaling transduction is required for normal distribution of the TN axons.
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Braisted, J. E., T. F. Essman, and P. A. Raymond. "Selective regeneration of photoreceptors in goldfish retina." Development 120, no. 9 (September 1, 1994): 2409–19. http://dx.doi.org/10.1242/dev.120.9.2409.
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Previous work has shown that the neural retina in adult goldfish can regenerate. Following retinal damage elicited by surgical or cytotoxic lesions, missing neurons are replaced by foci of proliferating neuroepithelial cells, which previous studies have suggested are derived from rod precursors. In the intact retina, rod precursors proliferate but produce only new rods. The regenerative responses observed previously have involved replacement of neurons in all retinal layers; selective regeneration of specific neuronal types (except for rod photoreceptors) has not been reported. In the experiments described here, we specifically destroyed either cones alone or cones and rods with an argon laser, and we found that both types of photoreceptors regenerated within a few weeks. The amount of cone regeneration varied in proportion to the degree of rod loss. This is the first demonstration of selective regeneration of a specific class of neuron (i.e., cones) in a region of central nervous tissue where developmental production of that class of neuron has ceased. Selective regeneration may be limited to photoreceptors, however, because when dopaminergic neurons in the inner retina were ablated with intraocular injections of 6-hydroxydopamine, in combination with laser lesions that destroyed photoreceptors, the dopaminergic neurons did not regenerate, but the photoreceptors did. These data support previous studies which showed that substantial cell loss is required to trigger regeneration of inner retinal neurons, including dopaminergic neurons. New observations here bring into question the presumption that rod precursors are the only source of neuronal progenitors during the regenerative response. Finally, a model is presented which suggests a possible mechanism for regulating the phenotypic fate of retinal progenitor cells during retinal regeneration.
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Sarthy, P. V., and M. Fu. "Localization of laminin B1 mRNA in retinal ganglion cells by in situ hybridization." Journal of Cell Biology 110, no. 6 (June 1, 1990): 2099–108. http://dx.doi.org/10.1083/jcb.110.6.2099.
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In the nervous system, neuronal migration and axonal growth are dependent on specific interactions with extracellular matrix proteins. During development of the vertebrate retina, ganglion cell axons extend along the internal limiting (basement) membrane and form the optic nerve. Laminin, a major component of basement membranes, is known to be present in the internal limiting membrane, and might be involved in the growth of ganglion cell axons. The identity of the cells that produce retinal laminin, however, has not been established. In the present study, we have used in situ hybridization to localize the sites of laminin B1 mRNA synthesis in the developing mouse retina. Our results show that there are at least two principal sites of laminin B1 mRNA synthesis: (a) the hyaloid vessels and the lens during the period of major axonal outgrowth, and (b) the retinal ganglion cells at later development stages. Müller (glial) cells, the major class of nonneuronal cells in the retina, do not appear to express laminin B1 mRNA either during development or in the adult retina. In Northern blots, we found a single transcript of approximately 6-kb size that encodes the laminin B1 chain in the retina. Moreover, laminin B1 mRNA level was four- to fivefold higher in the postnatal retina compared to that in the adult. Our results show that in addition to nonneuronal cells, retinal ganglion cells also synthesize laminin. The function of laminin in postnatal retinas, however, remains to be elucidated. Nevertheless, our findings raise the possibility that neurons in other parts of the nervous system might also synthesize extracellular matrix proteins.
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Tadmor, Y., and D. J. Tolhurst. "Calculating the contrasts that retinal ganglion cells and LGN neurones encounter in natural scenes." Vision Research 40, no. 22 (October 2000): 3145–57. http://dx.doi.org/10.1016/s0042-6989(00)00166-8.
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Neal, M. J., J. R. Cunningham, S. J. Paterson, and A. T. Mcknight. "Inhibition by nociceptin of the light-evoked release of ACh from retinal cholinergic neurones." British Journal of Pharmacology 120, no. 8 (April 1997): 1399–400. http://dx.doi.org/10.1038/sj.bjp.0701135.
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Hitchcock, Peter F., and Jeff T. Vanderyt. "Regeneration of the dopamine-cell mosaic in the retina of the goldfish." Visual Neuroscience 11, no. 2 (March 1994): 209–17. http://dx.doi.org/10.1017/s0952523800001577.
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AbstractA fundamental anatomical feature of retinal neurons is that they form planar mosaics. Each mosaic can be described by its density, pattern, and regularity (non-randomness). As part of ongoing studies to quantitatively describe the anatomy of regenerated retina in the goldfish, we determined the planimetric density and regularity of the mosaic of dopaminergic interplexiform cells in patches of regenerated retina and compared this to the mosaic generated de novo. In addition, we selectively ablated dopaminergic neurons with the neurotoxin 6–hydroxydopamine (6–OHDA) before inducing local regeneration and determined whether or not the absence of the extant dopaminergic neurons modulated the planimetric density or number of regenerated ones. The results showed that dopaminergic neurons are regenerated at higher planimetric densities and in less orderly arrays than normal. Furthermore, there was no statistical difference in the density or number of regenerated cells in normal retinas and retinas treated with 6–OHDA.
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SARTHY, VIJAY P., V. JOSEPH DUDLEY, and KOHICHI TANAKA. "Retinal glucose metabolism in mice lacking the L-glutamate/aspartate transporter." Visual Neuroscience 21, no. 4 (July 2004): 637–43. http://dx.doi.org/10.1017/s0952523804214122.
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The conventional view that glucose is the substrate for neuronal energy metabolism has been recently challenged by the “lactate shuttle” hypothesis in which glutamate cycling in glial cells drives all neuronal glucose metabolism. According to this view, glutamate released by activated retinal neurons is transported into Müller (glial) cells where it triggers glycolysis. The lactate released by Müller cells serves as the energy substrate for neuronal metabolism. Because the L-Glutamate/aspartate transporter (GLAST) is the predominant, Na+-dependent, glutamate transporter expressed by Müller cells, we have used GLAST-knockout (GLAST−/−) mice to examine the relationship between lactate release and GLAST activity in the retina. We found that glucose uptake and lactate production by the GLAST−/− mouse retina was similar to that observed in the wild type mouse retina. Furthermore, addition of 1 mM glutamate and NH4Cl to the incubation medium did not further stimulate glucose uptake in either case. When lactate release was measured in the presence of the lactate uptake inhibitor, α-cyano-4-hydroxycinnamate, there was no significant change in the amount of lactate released by retinas from GLAST−/− mice compared to the wild type. Finally, lactate release was similar under both dark and light conditions. These results show that lactate production and release is not altered in retinas of GLAST−/− mice, which suggests that metabolic coupling between photoreceptors and Müller cells is not mediated by the glial glutamate transporter, GLAST.
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Someya, Akagawa, Mori, Morita, Yui, Asano, Sakamoto, and Nakahara. "Role of Neuron–Glia Signaling in Regulation of Retinal Vascular Tone in Rats." International Journal of Molecular Sciences 20, no. 8 (April 20, 2019): 1952. http://dx.doi.org/10.3390/ijms20081952.
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The interactions between neuronal, glial, and vascular cells play a key role in regulating blood flow in the retina. In the present study, we examined the role of the interactions between neuronal and glial cells in regulating the retinal vascular tone in rats upon stimulation of retinal neuronal cells by intravitreal injection of N-methyl-d-aspartic acid (NMDA). The retinal vascular response was assessed by measuring the diameter of the retinal arterioles in the in vivo fundus images. Intravitreal injection of NMDA produced retinal vasodilation that was significantly diminished following the pharmacological inhibition of nitric oxide (NO) synthase (nNOS), loss of inner retinal neurons, or intravitreal injection of glial toxins. Immunohistochemistry revealed the expression of nNOS in ganglion and calretinin-positive amacrine cells. Moreover, glial toxins significantly prevented the retinal vasodilator response induced by intravitreal injection of NOR3, an NO donor. Mechanistic analysis revealed that NO enhanced the production of vasodilatory prostanoids and epoxyeicosatrienoic acids in glial cells in a ryanodine receptor type 1-dependent manner, subsequently inducing the retinal vasodilator response. These results suggest that the NO released from stimulated neuronal cells acts as a key messenger in neuron–glia signaling, thereby causing neuronal activity-dependent and glial cell-mediated vasodilation in the retina.
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Fu, Zhongjie, Ye Sun, Bertan Cakir, Yohei Tomita, Shuo Huang, Zhongxiao Wang, Chi-Hsiu Liu, et al. "Targeting Neurovascular Interaction in Retinal Disorders." International Journal of Molecular Sciences 21, no. 4 (February 22, 2020): 1503. http://dx.doi.org/10.3390/ijms21041503.
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The tightly structured neural retina has a unique vascular network comprised of three interconnected plexuses in the inner retina (and choroid for outer retina), which provide oxygen and nutrients to neurons to maintain normal function. Clinical and experimental evidence suggests that neuronal metabolic needs control both normal retinal vascular development and pathological aberrant vascular growth. Particularly, photoreceptors, with the highest density of mitochondria in the body, regulate retinal vascular development by modulating angiogenic and inflammatory factors. Photoreceptor metabolic dysfunction, oxidative stress, and inflammation may cause adaptive but ultimately pathological retinal vascular responses, leading to blindness. Here we focus on the factors involved in neurovascular interactions, which are potential therapeutic targets to decrease energy demand and/or to increase energy production for neovascular retinal disorders.
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Beach, Krista M., Jianbo Wang, and Deborah C. Otteson. "Regulation of Stem Cell Properties of Müller Glia by JAK/STAT and MAPK Signaling in the Mammalian Retina." Stem Cells International 2017 (2017): 1–15. http://dx.doi.org/10.1155/2017/1610691.
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In humans and other mammals, the neural retina does not spontaneously regenerate, and damage to the retina that kills retinal neurons results in permanent blindness. In contrast to embryonic stem cells, induced pluripotent stem cells, and embryonic/fetal retinal stem cells, Müller glia offer an intrinsic cellular source for regenerative strategies in the retina. Müller glia are radial glial cells within the retina that maintain retinal homeostasis, buffer ion flux associated with phototransduction, and form the blood/retinal barrier within the retina proper. In injured or degenerating retinas, Müller glia contribute to gliotic responses and scar formation but also show regenerative capabilities that vary across species. In the mammalian retina, regenerative responses achieved to date remain insufficient for potential clinical applications. Activation of JAK/STAT and MAPK signaling by CNTF, EGF, and FGFs can promote proliferation and modulate the glial/neurogenic switch. However, to achieve clinical relevance, additional intrinsic and extrinsic factors that restrict or promote regenerative responses of Müller glia in the mammalian retina must be identified. This review focuses on Müller glia and Müller glial-derived stem cells in the retina and phylogenetic differences among model vertebrate species and highlights some of the current progress towards understanding the cellular mechanisms regulating their regenerative response.