Brain glutaminase activity in relation to transmitter glutamate biosynthesis

Ward, H. K.; Thanki, C. M.; Peterson, D.W.; Bradford, H. F.

doi:10.1042/bst0100369

Cited by 10 publications

(5 citation statements)

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“…Thus chemical stimulation, which evoked an increase in glutamate, evoked a decrease in glutamine, whereas the decrease in glutamate following application of Lproline or 2CA or after cortical ablation was accompanied by an increase in glutamine. Previous investigators have reported similar inverse relationships between responses of glutamate and glutamine in vitro (Reubi et al, 1978;Ward et al, 1982) and in vivo (Thanki et al, 1983;Korf and Venema, 1985), supporting the theory that glutamine may be the predominant precursor for neurotransmitter glutamate (Bradford et al, 1978;Hamberger et al, 1979).…”

Section: Amino Acidsupporting

confidence: 63%

Excitatory Amino Acid Neurotransmitters in the Corticostriate Pathway: Studies Using Intracerebral Microdialysis In Vivo

Young

Bradford

1986

Journal of Neurochemistry

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108

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The concentration of extracellular excitatory amino acids in the striatum of conscious, unrestrained rats was measured using intracerebral microdialysis, during chemical stimulation of the striatum in intact and hemidecorticate animals. Chemical stimulation of the striatum with tityustoxin (0.1 microM) evoked a rise in dialysate concentration of glutamate (to 383% of basal) and aspartate (to 156% of basal), accompanied by a drop in glutamine (to 55% of basal). These changes showed significant attenuation after treatment with L-proline (1 mM) or 2-chloroadenosine (15 microM). Unilateral degeneration of the corticostriate pathway, produced by frontal hemidecortication, caused a reduction in both basal and stimulated levels of glutamate in the lesioned side, whereas no effect was observed in the intact side. Similarly, basal and stimulated levels of glutamine were unchanged in the intact side, but were increased in the lesioned side. These results provide in vivo evidence for glutamate and possibly aspartate being neurotransmitters in the corticostriate pathway. In addition they lend support to previous studies in vitro, which implicated glutamine as the principal precursor for neurotransmitter glutamate.

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Section: Amino Acidsupporting

confidence: 63%

Excitatory Amino Acid Neurotransmitters in the Corticostriate Pathway: Studies Using Intracerebral Microdialysis In Vivo

Young

Bradford

1986

Journal of Neurochemistry

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108

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“…Previous reports on glutaminase in striatal homogenates give rates that vary from 4 to 245 nmol/ min/mg protein (Ward et al, 1982;Butterworth and Yates, 1983), which clearly illustrates the varying kinetic characteristics that are seen at different substrate and phosphate concentrations (Butterworth and Yates, 1983).…”

Section: Effects Of Cortico-striate Lesions On Enzyme Levelsmentioning

confidence: 54%

“…One previous study found no significant change in striatal glutaminase activity after sectioning of the cortico-striatal pathway (McGeer and McGeer, 1979), whereas another study detected a 20% reduction after employing a lesion technique similar to that used by McGeer and McGeer (1979), but with a different assay for glutaminase (Ward et al, 1982). The reason for these discrepancies is not known, but different assays, survival times, and lesion techniques may explain some of the contrasting findings.…”

Section: Vulmentioning

confidence: 94%

Effect of Cortico‐Striate Pathway Lesion on the Activities of Enzymes Involved in Synthesis and Metabolism of Amino Acid Neurotransmitters in the Striatum

Sandberg

Ward

Bradford

1985

Journal of Neurochemistry

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The activities of several enzymes involved in the metabolism of aspartate and glutamate were measured in striatal (nucleus caudatus and putamen) homogenates 2-3, 6-7, and 35-40 days following frontoparietal and frontal cortical ablation. The activity of glutamine synthetase (GS) was substantially increased (46-48%) on the operated side 6-7 days following the lesion whereas smaller changes were observed at 2-3 and 35-40 days after lesion. In contrast, decreased levels of glutaminase and malate dehydrogenase (MDH) were observed by 6-7 days while no significant change was found at either 2-3 or 35-40 after the lesion. The activities of glutamate dehydrogenase (GDH) and glutamate decarboxylase (GAD) were elevated after 35-40 days whereas no changes in the levels of either GDH or aspartate aminotransferase (ASAT) were found at 2-3 or 6-7 days after the fronto-parietal decortication. When only the frontal cortex was removed quantitatively similar changes were observed in striatal GS and glutaminase activity. The content of glutamate and glutamine in the denervated striatum followed qualitatively the changes in glutaminase and GS. The results indicate that the degeneration of cortico-striatal terminals causes a profound glial reaction in the striatum, and both glutaminase and MDH are present in relatively high concentrations in the corticostriatal terminals.

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“…Phosphate-activated glutaminase belongs to the large group of mitochondria1 enzymes that are preferentially but not exclusively localized to nerve terminals Bradford and Ward, 1976). Degeneration of the glutamergic terminals in neostriatum or cochlear nucleus was accompanied by a small but significant fall (approximately 20%) of glutaminase (Walker and Fonnum, unpublished;Ward et al, 1982;Wenthold, 1980). Immunohistochemical localization has shown that the enzyme is at least preferentially localized to glutamergic terminals in cochlear nucleus (Wenthold, personal communication).…”

Section: Synthesis Of Glutamate In Brainmentioning

confidence: 99%