An immunocytochemical comparison of Müller cells and astrocytes in the cat retina

Lewis, Geoffrey P.; Erickson, Page A.; Kaska, Deborah D.; Fisher, Steven K.

doi:10.1016/0014-4835(88)90067-x

Cited by 92 publications

(45 citation statements)

References 49 publications

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“…Our data are, however, at variance with the only other systematic investigation of GS in (cat) retinal astrocytes (Lewis et al, 1988), where immunoreactivity could not be detected. Also, , applying the same antiserum as Lewis et al ( 1988) in a light microscopical investigation of the mouse retina, state that "'GS is always confined exclusively to the Muller glial cells."…”

Section: Astrocytescontrasting

confidence: 95%

Coincidence of L‐glutamate/L‐aspartate transporter (GLAST) and glutamine synthetase (GS) immunoreactions in retinal glia: Evidence for coupling of GLAST and GS in transmitter clearance

Derouiche

Rauen

1995

J of Neuroscience Research

239

155

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Our aim was to identify proteins that mediate the uptake and degradation of synaptically released glutamate, focusing on the rat retina with its well-defined glutamatergic pathways. Immunoreactivity against the L-glutamate/L-aspartate transporter (GLAST) is present in Müller cells. Ultrastructurally, even the finest glial processes, particularly those ensheathing identified structures of glutamatergic transmission (rod spherules), are immunoreactive for GLAST. Further light and electron microscopic observations revealed that also retinal astrocytes and pigment epithelial cells are immunoreactive for GLAST. No neuronal or microglial staining was observed. This is in line with uptake of exogenous [3H]glutamate previously localized specifically in Müller cells and pigment epithelium (Ehinger and Falck: Brain Res 33:157-172, 1971). Since endogenous glutamate can only be demonstrated in Müller cells if glutamine synthetase (GS) is inhibited (Pow and Robinson: Neuroscience 60:355-366, 1994), the immunocytochemical localization of GS was determined. GS immunoreactivity was found in all but only those cell types immunoreactive for GLAST. The light and electron microscopic patterns of immunoreactivity were very similar, particularly in the outer plexiform layer. The three cell types containing both GS and GLAST (Müller cells, astrocytes, and retinal pigment epithelium) are related developmentally. In the light of the two references quoted the present data indicate that the proteins mediating retinal uptake and degradation of synaptically released glutamate may be GLAST and GS, respectively, and that they may operate in concert to terminate the neurotransmitter action of glutamate.

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Section: Astrocytescontrasting

confidence: 95%

Coincidence of L‐glutamate/L‐aspartate transporter (GLAST) and glutamine synthetase (GS) immunoreactions in retinal glia: Evidence for coupling of GLAST and GS in transmitter clearance

Derouiche

Rauen

1995

J of Neuroscience Research

239

155

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“…9c). Glutamine immunoreactivity within Mü ller's cells occurred along their entire cellular extent and coincided with the development of glutamine synthetase (GS) activity in the rat retina (Riepe and Norenberg, 1978), which localises within this cell population (Moscona, 1983;Lewis et al, 1988). The numbers of amacrine cells that displayed glutamine immunoreactivity appeared more sparse those seen in younger retinae (e.g., PND 6), suggesting an alteration in the precursor turnover by this age.…”

Section: Localisation Of Neurotransmitter Precursorsmentioning

confidence: 85%

Localisation of amino acid neurotransmitters during postnatal development of the rat retina

1997

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We used postembedding immunocytochemistry to determine the localisation of the amino acid neurotransmitters glutamate, gamma-aminobutyrate (GABA), and glycine, potential neurotransmitter precursors (aspartate and glutamine), and taurine in the rat retina during postnatal development. All amino acids investigated were present at birth; however, only the inhibitory neurotransmitters GABA and glycine displayed neuronal localisation. GABA was localised in a sparse population of amacrine cells, and glycine immunoreactivity was found in cells within the ventricular zone that appeared to migrate through the neuroblastic layer. Glutamate labelling was diffuse across the retina until postnatal day (PND) 8. Localisation of glutamine was evident within Müller's cells by PND 6, in agreement with the known age of onset of glutamine synthetase activity. Based on the findings of uptake of radiolabelled glutamate and GABA by PND 8 and changes in immunoreactivity, we propose that Müller's cells evolve at PND 6-8 from their precursor cells, the radial glial cells. Evidence for differences in glutamate turnover in the infant retina was seen on examination of aspartate and glutamine immunoreactivity. Aspartate labelling was weak until PND 11, when ganglion cells and some amacrine cells were labelled. Unlike the mature retina, a large number of amacrine cells were glutamine immunoreactive in the PND 6 retina. One reason for the observed differences in precursor pooling may be a lack of neuronal neurotransmitter release and overall low metabolic activity. We also investigated the response of the developing retina to ischaemic insult to test the physiological hypoxia model of vascular development. Our findings are consistent with the hypothesis that the developing retina has increased tolerance to ischaemic insult. Our findings suggest that, although the retina is morphologically adult like by PND 8, there are differences in neurotransmitter turnover in the immature rat retina.

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“…GFAP reliably labels astrocytes and gliotic Müller cells in the retina, as well as a small percentage of normal functioning Müller cells in the feline. [42][43][44] In order to examine retinal ganglion cell survival, retinae were labeled with anti-RNA-binding protein with multiple splicing (RBPMS). RBPMS consistently labels retinal ganglion cell somas across multiple species and has previously been tested in mouse, rat, guinea pig, rabbit, and monkey retina.…”

Section: 18mentioning

confidence: 99%

Stimulation of a Suprachoroidal Retinal Prosthesis Drives Cortical Responses in a Feline Model of Retinal Degeneration

Aplin

Fletcher

Luu

et al. 2016

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Retinal prostheses have emerged as a promising technology to restore vision in patients with severe photoreceptor degeneration. To better understand how neural degeneration affects the efficacy of electronic implants, we investigated the function of a suprachoroidal retinal implant in a feline model. METHODS.Unilateral retinal degeneration was induced in four adult felines by intravitreal injection of adenosine triphosphate (ATP). Twelve weeks post injection, animals received suprachoroidal electrode array implants in each eye, and responses to electrical stimulation were obtained using multiunit recordings from the visual cortex. Histologic measurements of neural and glial changes in the retina at the implant site were correlated with cortical thresholds from individual stimulating electrodes.RESULTS. Adenosine triphosphate-injected eyes displayed changes consistent with mid-to-late stage retinal degeneration and remodeling. A significant increase in electrical charge was required to induce a cortical response from stimulation of the degenerated retina compared to that in the fellow control eye. Spatial and temporal characteristics of the electrically evoked cortical responses were no different between eyes. Individual electrode thresholds varied in both the control and the ATP-injected eyes and were correlated with ganglion cell density. In ATP-injected eyes, cortical threshold was also independently correlated with an increase in the extent of retinal gliosis.CONCLUSIONS. These data suggest that even when ganglion cell density remains unaffected, glial changes in the retina following degeneration can influence the efficacy of suprachoroidal electrical stimulation. A better understanding of how glial change impacts retinal prosthesis function may help to further the optimization of retinal implants.

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An immunocytochemical comparison of Müller cells and astrocytes in the cat retina

Cited by 92 publications

References 49 publications

Coincidence of L‐glutamate/L‐aspartate transporter (GLAST) and glutamine synthetase (GS) immunoreactions in retinal glia: Evidence for coupling of GLAST and GS in transmitter clearance

Coincidence of L‐glutamate/L‐aspartate transporter (GLAST) and glutamine synthetase (GS) immunoreactions in retinal glia: Evidence for coupling of GLAST and GS in transmitter clearance

Localisation of amino acid neurotransmitters during postnatal development of the rat retina

Stimulation of a Suprachoroidal Retinal Prosthesis Drives Cortical Responses in a Feline Model of Retinal Degeneration

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