Cytochemical demonstration of aspartate aminotransferase activity in the rat retina

Gebhard, R.

doi:10.1016/0006-8993(91)91641-d

Cited by 25 publications

(16 citation statements)

References 20 publications

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“…Aspartate immunoreactivity was observed in the outer nuclear layer, amacrine cells and ganglion cells of the normal rat retina (Fig. 2a), which is consistent with immunocytochemical localization of AAT in the rat retina (Brandon and Lam, 1983;Lin et al, 1983;Gebhard, 1991). Aspartate labelled photoreceptor inner segments and nuclei, whilst the terminal region within the outer plexiform layer displayed weaker immunoreactivity (Fig.…”

Section: Results Immunocytochemistrysupporting

confidence: 86%

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 Immunocytochemistrysupporting

confidence: 86%

Neurochemical architecture of the normal and degenerating rat retina

Fletcher

Kalloniatis

1996

J. Comp. Neurol.

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“…Previous studies reported that photoreceptor ISs have glutamate and GABA uptake systems, and enzymes such as glutamate dehydrogenase and phosphate-activated glutaminase in mitochondria [19,30,31]. We believe that under the physiological conditions, glutamate and GABA are rapidly enzymatically converted to other amino acids in the ISs.…”

Section: Discussionmentioning

confidence: 99%

“…However, no labeling was found at the outer segment of the photoreceptor cell. Aspartate aminotransferase is the enzyme by which aspartate is converted to glutamate [19,31]. The enzymatic activity was in the mitochondria-rich IS of the photoreceptor cell layer, but not the outer segment [32].…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Localization of Amino Acids in the Diabetic Retina of Goto-Kakizaki Rats

Takeo-Goto

Doi

et al. 2002

Ophthalmic Res

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The Goto-Kakizaki (GK) rat is a spontaneous model of non-insulin-dependent diabetes mellitus without obesity and diabetic retinopathy. We examined the retinal distribution of L-glutamate, gamma aminobutyric acid (GABA), glycine, and L-aspartate as neurotransmitters in the GK rat retina, using an immunohistochemical method with high-affinity antibodies. The retinal structures in the GK rats were the same as the controls. However, in the GK rats, immunoreactivity of L-glutamate and GABA was observed in the Müller and photoreceptor cells in addition to the immunoreactivity in normal rats. There was no change in glycine distribution between GK rats and controls. In the GK rats, L-aspartate accumulated in the inner segment of the photoreceptor cells in addition to the normal distribution. We consider that these immunoreactivity patterns in the GK rat retina might be induced by ischemia associated with diabetes mellitus.

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“…It is possible that a part of the excess ammonia and F-ketoglutarate may be converted to glutamate by GDH, and this may lead to an intracellular increase in glutamate. The parallel changes in the level of aspartate and glutamate in photoreceptor cells suggest that aspartate levels are maintained at an equilibrium with glutamate by the activity of aspartate aminotransferase [26] , although reportedly 90 min of ischemia causes a 20% decrease in mitochondrial aspartate aminotransferase activity [25] . Additionally, the impairment of the cell membrane due to metabolic disruption may be related to the increase in the amino acids.…”

Section: Discussionmentioning

confidence: 99%

“…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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Cytochemical demonstration of aspartate aminotransferase activity in the rat retina

Cited by 25 publications

References 20 publications

Neurochemical architecture of the normal and degenerating rat retina

Neurochemical architecture of the normal and degenerating rat retina

Immunohistochemical Localization of Amino Acids in the Diabetic Retina of Goto-Kakizaki Rats

Changes in Localization of Amino Acids in the Detached Cat Retina

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