Glutamate dehydrogenase in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex

Kügler, P.; Weeger, T.; Horváth, Ervin

doi:10.1016/0306-4522(94)00358-c

Cited by 9 publications

(9 citation statements)

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“…Fourteen and 60 days postlesion ipsilateral to the lesion side, a decrease of the height of the molecular layer was observed amounting ≈ 30% and ≈ 34%, respectively. Similar values have been reported previously (Kugler et al ., 1995). No changes were observed contralateral to the lesion side compared with controls (sham‐operated animals).…”

Section: Resultsmentioning

confidence: 99%

“…In the lesion model used in the present study, proliferation and replacement processes take place in the deafferented entorhinal terminal field (for reference, see Kugler et al ., 1995), but even after long survival times (up to 7 months following entorhinal cortex lesion), the bouton density of the denervated terminal field reaches only ≈ 40% of control values (Steward & Vinsant, 1983). In the survival times used in the present study (up to 60 days), there was no measurable restitution of glutamate transporter expression in astrocytes.…”

Section: Discussionmentioning

confidence: 99%

“…As we have shown in a previous study (Kugler et al ., 1995), the activity of glutamate dehydrogenase also decreases significantly in the deafferented entorhinal terminal field, and there is no reestablishment of enzyme activities up to 90 days postlesion. Glutamate dehydrogenase is detected at the protein and activity level preferentially in astrocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Several previous studies show that there is a shrinkage of the dentate gyrus molecular layer following lesioning of the entorhinal cortex (Kugler et al ., 1995; for review, see Scheff, 1989). Therefore, this shrinkage was also determined in the present study and was considered in the evaluation of the microphotometric data (discussed earlier).…”

Section: Methodsmentioning

confidence: 99%

“…It is shown that ISH using alkaline‐phosphatase(aP) ‐labelled oligonucleotide probes is an appropriate procedure for microphotometric determination of relative mRNA amounts in nervous tissue (Asan & Kugler, 1995). The postlesional shrinkage of the outer molecular layer ipsilateral to the lesion side (Scheff et al ., 1980; Wagner et al ., 1983; Scheff, 1989; Kugler et al ., 1995) was determined and considered in the evaluation of ISH data. To test the validity of ISH using the oligonucleotide probes, we also performed ISH with cRNA probes.…”

Section: Introductionmentioning

confidence: 99%

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Glutamate transporter expression in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex

Hein

Horváth

Kügler

2001

Eur J of Neuroscience

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The glutamate transporters GLT-1 and GLAST localized in astrocytes are essential in limiting transmitter signalling and restricting harmful receptor overstimulation. To show changes in the expression of both transporters following lesion of the entorhinal cortex (and degeneration of the glutamatergic tractus perforans), quantitative microscopic in situ hybridization (ISH) using alkaline-phosphatase-labelled oligonucleotide probes was applied to the outer molecular layer of the hippocampal dentate gyrus of rats (termination field of the tractus perforans). Four groups of rats were studied: sham-operated controls, and animals 3, 14 and 60 days following unilateral electrolytic lesion of the entorhinal cortex. The postlesional shrinkage of the terminal field of the perforant path, ipsilateral to the lesion side, was determined and considered in the evaluation of quantitative ISH data. Statistical analysis revealed that ipsilateral to the lesion side there was a significant decrease of the GLT-1 mRNA at every postlesional time-point and of the GLAST mRNA at 14 and 60 days postlesion. The maximal decrease was approximately 45% for GLT-1 and approximately 35% for GLAST. In the terminal field of the perforant path contralateral to the lesion side, no significant changes of ISH labelling were measured. The results were complemented by immunocytochemical data achieved using antibodies against synthetic GLT-1 and GLAST peptides. In accordance with ISH results, there was an obvious decrease of GLT-1 and GLAST immunostaining in the terminal field of the perforant path ipsilateral to the lesion side. From these data we conclude that, following a lesioning of the entorhinal cortex, the loss of glutamatergic synapses in the terminal field of the perforant path resulted in a strong downregulation of glutamate transporters in astrocytes. The decrease of synaptically released glutamate or of other neuronal factors could be involved in this downregulation.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Glutamate transporter expression in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex

Hein

Horváth

Kügler

2001

Eur J of Neuroscience

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Topical correlation of increased hippocampal glutamine synthetase immunoreactivity and glutamatergic terminal fields after entorhinal cortex lesion

Derouiche

2000

Glia

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Many astrocyte functions are related to glutamatergic transmission and to other synaptic functions, such as glutamate uptake and glutamate metabolism. While many of these functions can be executed by perisynaptic astrocyte processes, it is not clear how these processes are formed. One of the factors guiding them to the synapse may be synaptically released glutamate. This would explain the topical correlation between laminated glutamatergic terminal fields and laminae most intensely labeled by a cytoplasmic astrocyte marker, anti‐glutamine synthetase (GS). This hypothesis was tested by selectively increasing the glutamate content in one terminal field. The rat entorhinal cortex, the origin of the glutamatergic projection to the outer molecular layer (OML) of the hippocampal fascia dentata, was lesioned electrolytically. In line with the hypothesis, GS immunoreactivity was strongly increased in the OML at 6 and 8 days postlesion. Lesion of only the medial entorhinal cortex resulted in heavily increased GS immunoreactivity only in the central portion of the molecular layer (i.e., the corresponding terminal field). The laminae affected were always separated from neighboring fields by a straight and clear‐cut line. Although many other factors are released in the terminal field after lesion, the results are consistent with a guiding role for glutamate. The lamina‐specific effect suggests that the factor(s) involved have a very limited diffusion distance. The straight border line between affected and unaffected laminae, which cuts across astrocyte territories, can best be explained by ramification of only those processes of a given astrocyte that are contained within the lamina affected. GLIA 29:386–391, 2000. © 2000 Wiley‐Liss, Inc.

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Developmental expression of glutamate transporters and glutamate dehydrogenase in astrocytes of the postnatal rat hippocampus

Kügler

Schleyer

2004

Hippocampus

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Glutamate is the major excitatory transmitter in the CNS and plays distinct roles in a number of developmental events. Its extracellular concentration, which mediates these activities, is regulated by glutamate transporters in glial cells and neurons. In the present study, we have used nonradioactive in situ hybridization, immunocytochemistry, and immunoblotting to show the cellular and regional expression of the high-affinity glutamate transporters GLAST (EAAT1) and generic GLT1 (EAAT2; glial form of GLT1) in the rat hippocampus during postnatal development (P1-60). The results of transporter expression were compared with the localization and activity pattern of glutamate dehydrogenase (GDH), an important glutamate-metabolizing enzyme. The study showed that both transporters and GDH were demonstrable at P1 (day of birth). The expression of GLAST (detected by in situ hybridization and immunocytochemistry) in the early postnatal development was higher than GLT1. Thereafter, the expression of both transporters increased, showing adult levels at between P20 and P30 (detected by in situ hybridization and immunoblotting). At these time points, the expression of GLT1 appeared to be significantly higher than the GLAST expression. GLT1 and GLAST proteins were demonstrable only in astrocytes. The increase of GDH activities (steepest increase from P5-P8), which were localized preferentially in astrocytes, was in agreement with the increase of transporter expression, preferentially with that of GLT1. These observations suggest that the extent of glutamate transporter expression and of glutamate-metabolizing GDH activity in astrocytes is intimately correlated with the formation of glutamatergic synapses in the developing hippocampus.

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Glutamate dehydrogenase in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex

Cited by 9 publications

References 46 publications

Glutamate transporter expression in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex

Glutamate transporter expression in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex

Topical correlation of increased hippocampal glutamine synthetase immunoreactivity and glutamatergic terminal fields after entorhinal cortex lesion

Developmental expression of glutamate transporters and glutamate dehydrogenase in astrocytes of the postnatal rat hippocampus

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