Histochemical demonstration of glutamate dehydrogenase and phosphate-activated glutaminase activities in semithin sections of the rat retina

Gebhard, R.

doi:10.1007/bf00271288

Cited by 22 publications

(8 citation statements)

References 13 publications

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“…Previous studies have shown that PAG activity in the rat retina is highest in the photoreceptor inner segments, and of similar activity across the inner nuclear, inner plexiform, and ganglion cell layers (Ross et al, 1987;Gebhard, 1992). In this study, glutamine immunoreactivity was localized in photoreceptor inner segments, bipolar cells, horizontal cells, Muller's cells, and some…”

Section: Results Immunocytochemistrymentioning

confidence: 53%

Neurochemical architecture of the normal and degenerating rat retina

Fletcher

Kalloniatis

1996

J. Comp. Neurol.

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We used post-embedding immunocytochemistry to determine the cellular localization of glutamate, gamma-amino butyric acid (GABA), glycine, aspartate, glutamine, arginine, and taurine in the normal and degenerating rat retina. Müller's cell function was also evaluated by determining the uptake and degradation characteristics for glutamate. Immunocytochemical localization of amino acids in adult Royal College of Surgeons (RCS) and control rat retinas were similar with respect to cell classes. Differences in the intensity of labelling for glutamate, aspartate, glutamine, and glycine were observed in several classes of neurons, but the most prominent differences were shown by bipolar cells of the adult RCS rat retina. In addition, glutamine labelling within Müller's cells was higher in the RCS rat than the control. These changes may have occurred because of alterations in the glutamate production or degradation pathways. We tested this hypothesis by determining Müller's cells glutamate uptake and degradation characteristics in adult and postnatal day 16 RCS retinas. High affinity uptake of 3[H]-glutamate revealed an accumulation of grains over Müller's cell bodies in the adult RCS retina implying glutamate degradation anomalies. We confirmed anomalies in glutamate metabolism in RCS Müller's cells by showing that exogenously applied glutamate was degraded over a longer time course in postnatal day 16 RCS retinas, compared to control retinas. Differences in arginine immunoreactivity in adult and immature RCS retinas conform to the presumed dysfunction of Müller's cells in these degenerating retinas. The anomalies of amino acid localization, uptake and degradation lead us to conclude that Müller's cells in the RCS retina show abnormal function by postnatal day 16; an earlier time to previously reported anatomical and functional changes in this animal model of retinal degeneration.

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Section: Results Immunocytochemistrymentioning

confidence: 53%

Neurochemical architecture of the normal and degenerating rat retina

Fletcher

Kalloniatis

1996

J. Comp. Neurol.

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“…Müller cells possess enzymes that are involved in the de novo synthesis of glutamate from pyruvate, e.g., pyruvate carboxylase, that catalyzes the carboxylation of pyruvate to oxaloacetate as substrate of the Krebs cycle, and glutamate dehydrogenase, that converts α-ketoglutarate to glutamate (Gebhard, 1992; Ola et al, 2011a). Glutamate dehydrogenase is able to metabolize glutamate at relatively low pH (Zaganas et al, 2012) that prevails in glial cells following glutamate uptake (Bouvier et al, 1992).…”

Section: Glutamate Uptake and Metabolismmentioning

confidence: 99%

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Bringmann¹,

Grosche²,

Pannicke³

et al. 2013

Front. Endocrinol.

144

123

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Müller cells, the principal glial cells of the retina, support the synaptic activity by the uptake and metabolization of extracellular neurotransmitters. Müller cells express uptake and exchange systems for various neurotransmitters including glutamate and γ-aminobutyric acid (GABA). Müller cells remove the bulk of extracellular glutamate in the inner retina and contribute to the glutamate clearance around photoreceptor terminals. By the uptake of glutamate, Müller cells are involved in the shaping and termination of the synaptic activity, particularly in the inner retina. Reactive Müller cells are neuroprotective, e.g., by the clearance of excess extracellular glutamate, but may also contribute to neuronal degeneration by a malfunctioning or even reversal of glial glutamate transporters, or by a downregulation of the key enzyme, glutamine synthetase. This review summarizes the present knowledge about the role of Müller cells in the clearance and metabolization of extracellular glutamate and GABA. Some major pathways of GABA and glutamate metabolism in Müller cells are described; these pathways are involved in the glutamate-glutamine cycle of the retina, in the defense against oxidative stress via the production of glutathione, and in the production of substrates for the neuronal energy metabolism.

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“…Secondly, this trend might be attributable to disruption of energy metabolism including glutamate due to ischemia. Except for glutamine synthetase, enzymes for glutamate metabolism including glutamate dehydrogenase (GDH), phosphateactivated glutaminase, aspartate aminotransferase and ornithine aminotransferase show the highest level of activity in the photoreceptor inner segments [26][27][28] . Ischemia increases intracellular ammonia concentration in rat retinas [25] .…”

Section: Discussionmentioning

confidence: 99%

Changes in Localization of Amino Acids in the Detached Cat Retina

Sasoh

Ma²,

Esaki³

et al. 2006

Ophthalmic Res

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Purpose: To investigate the distribution of amino acids (glutamate, aspartate, glutamine, GABA, glycine) in detached retinas with minimum postmortem artifact and to clarify the relation between amino acid distribution and histopathological change in the outer portion of detached retinas. Methods: Unilateral retinal detachment was produced in cats by injecting 0.25% sodium hyaluronate into the subretinal space using a glass micropipet. The eyes were fixed by perfusion for 10 min, 1, 3, 6 and 24 h, 2, 3 and 7 days after detachment and then examined under conventional light- and electron-microscopic immunocytochemistry. Results: For glutamate, aspartate and glutamine, the inner segments and perikarya of the photoreceptor cells, which were not immunopositive in the normal retinas, showed various degrees of immunoreactivity immediately after retinal detachment. Photoreceptor cells with the strong immunoreactivity developed necrosis. The staining pattern of GABA and glycine scarcely changed during the course of retinal detachment. Conclusions: Excess intracellular glutamate, aspartate and glutamine in photoreceptor cells may cause a part of neuronal death after retinal detachment.

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Histochemical demonstration of glutamate dehydrogenase and phosphate-activated glutaminase activities in semithin sections of the rat retina

Cited by 22 publications

References 13 publications

Neurochemical architecture of the normal and degenerating rat retina

Neurochemical architecture of the normal and degenerating rat retina

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Changes in Localization of Amino Acids in the Detached Cat Retina

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