Glial fibrillary acidic protein in the retina of the developing albino rat: An immunoperoxidase study of paraffin‐embedded tissue

Dixon, Richard F.; Eng, Lawrence F.

doi:10.1002/cne.901950210

Cited by 107 publications

(25 citation statements)

References 56 publications

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“…Immunostaining of retinal wholemounts using antibodies directed against GFAP confirmed previous findings regarding the location and general morphology of rat retinal astrocytes (Dixon and Eng, 1981;Stone and Dreher, 1987;Chan-Ling and Stone, 1991). GFAP-IR astrocytes were found throughout the nerve fiber layer of the rat retina.…”

Section: Distribution and Morphology Of Rat Retinal Astrocytessupporting

confidence: 77%

“…This observation is consistent with our impression that GFAP-IR processes do not extend completely underneath veins. GFAP-IR processes were observed to follow capillaries as far as the inner plexiform layer, as observed previously in the retinas of albino rats (Dixon and Eng, 1981) and humans (Triviñ o et al, 1997).…”

Section: Distribution and Morphology Of Rat Retinal Astrocytessupporting

confidence: 58%

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Confocal microscopic study of glial-vascular relationships in the retinas of pigmented rats

Zahs

Wang

2000

J. Comp. Neurol.

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Astroglia are interposed between the cerebral vasculature and neurons, where they may mediate the transfer of substances from the circulation to neurons and couple changes in neuronal activity to changes in cerebral blood flow. The retina is a particularly advantageous model system for studying glial-vascular interactions in situ. Confocal microscopy and three-dimensional image reconstruction were used to study the anatomical relationships between glia and the surface vasculature in retinas acutely isolated from adult pigmented rats. Retinas were immunostained using antibodies directed against the basal lamina surrounding the vasculature as well as antibodies directed against glial fibrillary acidic protein. Surface vessels of all calibers were contacted by the processes of astrocytes. The vitreal surfaces of the large retinal vessels were covered by a meshwork of immunoreactive astrocyte processes of a variety of shapes, whereas the scleral surfaces of the vessels were supported by thick bundles of astrocyte processes. In addition, glial cells were filled intracellularly with the gap junction-permeable tracers Lucifer yellow and Neurobiotin. Intracellular fills clearly demonstrated the presence of astrocytes with somata that were closely apposed to the large retinal vessels. Tracer-filled astrocytes displayed a variety and complexity of shapes that was not apparent in immunostained material. Gap junctional coupling was stronger between astrocytes adjacent to the same artery than between periarterial astrocytes and astrocytes located away from arteries. Significantly fewer Müller cells were labeled when Neurobiotin was injected into astrocytes associated with arteries than when Neurobiotin was injected into astrocytes that were distant from arteries.

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Section: Distribution and Morphology Of Rat Retinal Astrocytessupporting

confidence: 77%

Section: Distribution and Morphology Of Rat Retinal Astrocytessupporting

confidence: 58%

Confocal microscopic study of glial-vascular relationships in the retinas of pigmented rats

Zahs

Wang

2000

J. Comp. Neurol.

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“…Identical hybridization patterns are observed with both partially digested and full-length RNA probes. Labeling is not associated with endothelial cells lining blood vessels nor with astrocytes, which are mainly located in the ganglion cell axon layer (Dixon and Eng, 1981;Schnitzer, 1988). Only background labeling is observed over the distal INL, outer plexiform layer and outer nuclear layer, and in sections incubated with the sense RNA probe (Fig.…”

Section: Distribution Of Gaba Transporter Mrna In Retinal Sectionsmentioning

confidence: 93%

Expression of GAT‐1, a high‐affinity gamma‐aminobutyric acid plasma membrane transporter in the rat retina

Brecha

Weigmann

1994

J of Comparative Neurology

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Gamma-aminobutyric acid (GABA) plasma membrane transporters influence synaptic transmission by high-affinity, Na(+)-dependent transport processes. The cDNA clone, GAT-1, encodes a high-affinity Na(+)- and Cl(-)-dependent GABA plasma membrane transporter, which has kinetic and pharmacological properties similar to those of high-affinity GABA uptake systems associated with neurons. The present study evaluates the distribution and cellular localization of this putative neuronal GABA transporter by RNA blot hybridization and in situ hybridization histochemistry in the rat retina. Northern blot hybridization analysis of total retinal and cerebellar RNA extracts demonstrated a single band of hybridization at 4.2 kilobases. GABA transporter mRNA is expressed by numerous cells that are distributed to the proximal inner nuclear layer and the ganglion cell layer and by a few cells located in the inner plexiform layer. Double label studies combining the retrograde transport of the fluorescent dye Fluorogold from the superior colliculus to identify ganglion cells and in situ hybridization histochemistry demonstrated that most GAT-1 mRNA-containing cells in the ganglion cell layer are displaced amacrine cells, although some ganglion cells containing GAT-1 mRNA were visualized. In freshly dissociated retinal cell preparations, the GAT-1 RNA signal is strong in neurons and weak to moderate in specialized glial cells called Müller cells. Müller cells were identified by both their morphology and the presence of the selective Müller cell marker cellular retinaldehyde-binding protein. Only background labeling is seen with the sense GAT-1 RNA probe in both tissue sections and dissociated retinal cell preparations. These findings demonstrate that GAT-1 mRNA is expressed in both the retina and brain. In the retina, this transporter is predominantly localized to amacrine, displaced amacrine and interplexiform cells, and some ganglion cells. This transporter mRNA is also expressed by Müller cells but at a lower level than by neurons. These observations indicate that GABA transport by GAT-1 plasma membrane transporters in the retina is mediated by both neurons and glia cells.

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“…Ethanol fixation improved the staining intensity of OF AP in gray matter astrocytes compared with that obtained with formalin or aldehyde fixatives (Dixon and Eng, 1981) and allowed astrocyte immunostaining of vimentin (personal observations). Pri mary antibodies, diluted I: 100, included rabbit anti OFAP polyclonal IgO (Dako Corp.), mouse monoclonal anti-OFAP IgO (Oncogene Science, Inc.), and mouse monoclonal anti-vimentin IgO (Dako Corp.).…”

Section: Immunohistochemistrymentioning

confidence: 97%

The Two Patterns of Reactive Astrocytosis in Postischemic Rat Brain

Petito

Morgello

Felix

et al. 1990

J Cereb Blood Flow Metab

320

140

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Summary:The distribution and time course of postisch emic astrocyte hypertrophy and hyperplasia and the re lationship to neuronal viability or necrosis was studied in rats subjected to 30 min of carotid and vertebral artery occlusion followed by reperfusion from 3 h to 5 weeks. Intermediate filaments (IFs) were evaluated by electron microscopy, IF proteins by immunohistochemistry, and astrocyte division by [ 3 H]thymidine uptake. Glial fibril lary acidic protein (GF AP) increased in damaged and nondamaged brain regions by 2 days and was associated with cell enlargement, increases in IF, and transformation of GF AP-negative into GF AP-positive glia. Cell hyper trophy and increased GFAP persisted only in regions of neuronal necrosis whereas the number and size of GF AP positive astrocytes returned to control levels in nondam aged regions by 2 weeks. Astrocyte hyperplasia was notInteractions between astrocytes and neurons have gained increasing importance since in vitro studies have shown that metabolic properties of as trocytes are important in maintaining the normal homeostasis of the interstitial fluid compartment of the brain. These cells have high-affinity uptake sys tems (Faivre-Bauman et aI., 1974; Hertz et aI., 1974;Hertz, 1978; Cooper et aI., 1979;Kimelberg et al., 1982;Kraig et al., 1986) for many of the extra cellular ions and excitatory neurotransmitters that are elevated after ischemia, including hydrogen ions and glutamate, both of which have been implicated in causing ischemic injury. Thus, the initiation of Received January 15, 1990; revised April 23, 1990; accepted April 25, 1990.Address correspondence and reprint requests to Dr. C. K. Petito at Department of Pathology, Cornell University Medical College, 1300 York Avenue, New York, NY 10021, U.S.A.Abbreviations used: ABC, avidin-biotin complex; GFAP, glial fibrillary acidic protein; HRP, horseradish peroxidase; IFs, in termediate filaments; OD, optical density; RER, rough endoplas mic reticulum. 850seen until 3 days and was confined to damaged brain re gions. Vimentin-positive astrocytes were numerous by 2 days in damaged brain and remained only in those regions at 5 weeks. The data demonstrate that reactive astrocy to sis develops in undamaged brain, but is reversible with prolonged survival, whereas reactive astrocytosis that ac companies structural brain damage persists for prolonged periods and is associated with hyperplasia, as well as hy pertrophy. In addition, the results show that astrocyte expression of vimentin is more specific than GFAP in identifying regions of permanent ischemic injury during the early postischemic period.

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Glial fibrillary acidic protein in the retina of the developing albino rat: An immunoperoxidase study of paraffin‐embedded tissue

Cited by 107 publications

References 56 publications

Confocal microscopic study of glial-vascular relationships in the retinas of pigmented rats

Confocal microscopic study of glial-vascular relationships in the retinas of pigmented rats

Expression of GAT‐1, a high‐affinity gamma‐aminobutyric acid plasma membrane transporter in the rat retina

The Two Patterns of Reactive Astrocytosis in Postischemic Rat Brain

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