Efflux of glutamate produced by short ischemia of varied severity in rat striatum.

Ueda, Yukihiko; Obrenovitch, Tihomir P.; Lok, S Y; Sarna, G. S.; Symon, Lindsay

doi:10.1161/01.str.23.2.253

Cited by 49 publications

(9 citation statements)

References 43 publications

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“…During the first ischemic insult, 16 anoxic depolarization (as indicated by a rapid negative shift of the DC potential) occurred in approximately half of the rats exposed to 5 minutes of ischemia (no neck ligature). In the 3-minute ischemia group, anoxic depolarization occurred only when four-vessel occlusion was supplemented by neck ligature.…”

Section: Resultsmentioning

confidence: 99%

Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.

Ueda

Obrenovitch

Lok

et al. 1992

Stroke

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Background and Purpose: Evidence suggesting that ischemia-induced neuronal damage may be linked to an extracellular overflow of glutamate has accumulated, and previous studies have shown that repetitive ischemic insults may have a cumulative effect. The purpose of this study was to investigate changes in the extracellular glutamate concentration produced by repeated brief ischemic episodes of varied severity.Methods: Four consecutive 3-or 5-minute periods of bilateral hemispheric ischemia were produced in rats, each ischemic period followed by 27 minutes of reperfusion. Extracellular glutamate in the striatum was monitored using microdialysis, and the electroencephalogram and extracellular direct current potential were recorded in the same tissue site to assess the severity of ischemia.Results: The results suggest that the kinetics of the increase in the extracellular glutamate concentration produced by a brief ischemic episode are similar, irrespective of whether it is a single insult or part of a repeated sequence. In all cases, the extracellular glutamate concentration increased throughout ischemia and returned to its preischemic level early during reperfusion. The pattern of changes in the ischemiainduced glutamate overflow during repetitive insults varied with the severity of ischemia, in common with the pattern of changes in the direct current potential, supporting the concept that ionic changes associated with anoxic depolarization are a major determinant of ischemia-induced glutamate overflow.Conclusions: There may be no cumulative effect of brief repeated episodes of ischemia on the extracellular glutamate concentration, even though repeated 5-minute ischemic episodes apparently caused progressive deterioration of ionic homeostasis in some cases. (Stroke 1992;23:1125-1131 KEY WORDS • cerebral ischemia • electroencephalography • glutamate • rats

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Section: Resultsmentioning

confidence: 99%

Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.

Ueda

Obrenovitch

Lok

et al. 1992

Stroke

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“…Both CCA were isolated and prepared for occlusion with a vascular clip (Aesculap temporary clip). Ischemia was started by clipping of both CCA and sustained for 10 min SSEP (ESAOYA, Florence, Italy) was monitoried during the ischemic period [39,41]. Reperfusion was started by removal of the vascular clips.…”

Section: Methodsmentioning

confidence: 99%

Alterations in superoxide dismutase, glutathione peroxidase and catalase activities in experimental cerebral ischemia-reperfusion

İşlekel

Güner

et al. 1999

Res. Exp. Med.

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Free radicals are thought to be the most important cause of the reperfusion injury subsequent to ischemia. The antioxidant status of the tissue affected by ischemia-reperfusion is of great importance for the primary endogenous defense against the free radical induced injury. This investigation was performed to evaluate the antioxidant enzyme capacity of the brain tissue in the ischemia-reperfusion period using an experimental global moderate (penumbral) ischemia model on rat brains. Experiments were performed on 45 male Sprague Dawley rats. Ischemia was induced by bilateral vertebral arteries cauterization and temporary bilateral carotid arteries occlusion and sustained for 10 minutes. At the end of ischemia (0 min reperfusion) and various reperfusion periods (20 min, 60 min, 240 min), rats were decapitated and brains were frozen in liquid nitrogen. Changes in the intracellular antioxidant enzyme (superoxide dismutase, glutathione peroxidase and catalase) activities were assessed in the rat brain tissues, by spectrophotometric methods. In all moderate ischemia-reperfusion groups, superoxide dismutase activities were found to have decreased significantly compared to the sham operated controls (P < 0.05). During ischemia superoxide dismutase activity was lowered to 31% of that of the control group. The decreases were more significant in reperfusion groups, particularly in 60 min reperfusion (40%). Relatively smaller but still significant diminution was observed in glutathione peroxidase activities (P < 0.05). The ratio of diminution was striking in 20 min and 60 min reperfusion groups with 26% of the sham operated rats. Conversely, moderate ischemia-reperfusion caused significant increase in catalase activities (P < 0.05). The increment was 63% of the preischemic level with 10 min of moderate ischemia. In conclusion, activities of the major antioxidant enzymes were changed significantly in moderate brain ischemia-reperfusion. These results suggest that the disturbance in oxidant-antioxidant balance might play a part in rendering the tissue more vulnerable to free radical induced injuries.

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“…[1][2][3][4] Abnormal release of excitatory amino acids is proposed to be a critical factor for neuronal death during ischemia, 5,6 and, according to this hypothesis, in the ischemic striatum glutamate and aspartate concentrations increase significantly. [7][8][9] Moreover, glutamate receptor antagonists prevent ischemic damage in this brain area. 10 -12 Ischemia also causes a large increase in dopamine levels in the striatum, 13 and considerable evidence supports the idea that monoamines or their metabolic by-products may become neurotoxic during metabolic impairment, either directly or from interplay with the glutamatergic system.…”

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Endogenous Dopamine Amplifies Ischemic Long-Term Potentiation via D1 Receptors

Saulle

Centonze

Martín

et al. 2002

Stroke

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Background and Purpose-Several observations indicate that, during energy deprivation, endogenous dopamine may become neurotoxic. Accordingly, the nucleus striatum is a preferential site of silent infarcts in humans, and experimental ischemia caused by homolateral carotid occlusion selectively damages this dopamine-enriched brain area. In an attempt to clarify how dopamine takes part in ischemia-induced neuronal damage, we performed in vitro electrophysiological recordings from neurons of the nucleus striatum. Methods-Intracellular recordings with sharp microelectrodes were performed from corticostriatal slices. Slices were obtained from both rats and wild-type and dopamine D1 receptor-lacking mice. In some experiments, the striatum was unilaterally denervated by injecting the dopamine-specific neurotoxin 6-hydroxydopamine in the homolateral substantia nigra. Dopamine agonists and antagonists, as well as drugs targeting the intracellular cascade coupled to dopamine receptor stimulation, were applied at known concentrations. Results-Manipulation of the dopamine system failed to affect the membrane depolarization of striatal neurons exposed to combined oxygen and glucose deprivation of short duration, but it reduced the amplitude of postischemic long-term potentiation (LTP) expressed at corticostriatal synapses. In particular, pharmacological blockade or genetic inactivation of D1/cAMP/protein kinase A pathway prevented the long-term increase of the excitatory postsynaptic potential (EPSP) amplitude caused by a transient ischemic episode, while it failed to prevent the increase of the EPSP half-decay coupled to ischemic LTP. Conclusions-The present data suggest that endogenous dopamine, via D1 receptors, selectively facilitates the expression of ischemic LTP on the AMPA-mediated component of the EPSPs, while it does not alter the expression of this form of synaptic plasticity on the N-methyl-D-aspartate-mediated component of corticostriatal synaptic potentials. Understanding the cellular and molecular mechanisms of ischemia-triggered excitotoxicity offers hope for the development of specific treatments able to interfere with this pathological process.

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Efflux of glutamate produced by short ischemia of varied severity in rat striatum.

Cited by 49 publications

References 43 publications

Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.

Changes in extracellular glutamate concentration produced in the rat striatum by repeated ischemia.

Alterations in superoxide dismutase, glutathione peroxidase and catalase activities in experimental cerebral ischemia-reperfusion

Endogenous Dopamine Amplifies Ischemic Long-Term Potentiation via D1 Receptors

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