Metabolic and transmitter changes in core and penumbra after middle cerebral artery occlusion in mice

Kiewert, Cornelia; Mdzinarishvili, Alexander; Hartmann, J.; Bickel, Ulrich; Klein, Jochen

doi:10.1016/j.brainres.2009.11.068

Cited by 64 publications

(64 citation statements)

References 27 publications

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“…4A) and remained low at 20-30% of basal levels throughout the experiment (Fig. 4A); this is likely due to consumption of local glucose and lack of supply of fresh glucose due to limited blood flow [23]. Pretreatment with EGb761 did not strongly affect the changes due to ischemia indicating that neither blood supply nor consumption of glucose was affected by the extract to a relevant extent (Fig.…”

Section: Effectsmentioning

confidence: 96%

Ginkgo Extract EGb761 Confers Neuroprotection by Reduction of Glutamate Release in Ischemic Brain

et al. 2012

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-Purpose -Ginkgo extract EGb761 has shown anti-edema and anti-ischemic effects in various experimental models. In the present study, we demonstrate neuroprotective effects of EGb761 in experimental stroke while monitoring brain metabolism by microdialysis. Methods -We have used oxygenglucose deprivation in brain slices in vitro and middle cerebral artery occlusion (MCAO) in vivo to induce ischemia in mouse brain. We used microdialysis in mouse striatum to monitor extracellular concentrations of glucose and glutamate. Results -In vitro, EGb761 reduced ischemia-induced cell swelling in hippocampal slices by 60%. In vivo, administration of EGb761 (300 mg/kg) reduced cell degeneration and edema formation after MCAO by 35-50%. Immediately following MCAO, striatal glucose levels dropped to 25% of controls, and this reduction was not significantly affected by EGb761. Striatal glutamate levels, in contrast, increased 15-fold after MCAO; after pretreatment with EGb761, glutamate levels only increased by 4-5fold. Conclusions -We show that pretreatment with EGb761 strongly reduces cellular edema formation and neurodegeneration under conditions of ischemia. The mechanism of action seems to be related to a reduction of excitotoxicity, because ischemia-induced release of glutamate was strongly suppressed. Ginkgo extracts such as EGb761 may be valuable to prevent ischemia-induced damage in stroke-prone patients.

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Section: Effectsmentioning

confidence: 96%

Ginkgo Extract EGb761 Confers Neuroprotection by Reduction of Glutamate Release in Ischemic Brain

et al. 2012

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“…In adult mice the release of taurine was severalfold greater that that of glutamate, GABA, glycine or aspartate. This finding is in keeping with the more than tenfold greater extracellular concentration of taurine than for instance that of glutamate in vivo in the adult rodent brain [38][39][40][41]. Brain cells are able to maintain very steep concentration gradients across their cell membranes of neurotransmitter amino acids.…”

Section: Discussionmentioning

confidence: 73%

Release of Endogenous Amino Acids from the Striatum from Developing and Adult Mice in Ischemia

Oja

Saransaari

2011

Neurochem Res

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In most other studies the release of amino acid neurotransmitters and modulators in vitro has been studied mostly using labeled preloaded compounds. For several reasons the estimated release may not reliably reflect the release of endogenous compounds. The magnitudes of the release cannot thus be quite correctly estimated using radioactive labels. The basal and K(+)-evoked release of the neuroactive endogenous amino acids γ-aminobutyrate (GABA), glycine, taurine, glutamate and aspartate was now studied in slices from the striatum from 7-day-old to 3-month-old mice under control (normoxic) and ischemic conditions. The release of alanine, threonine and serine was assessed as control. GABA and glutamate release was much greater in 3-month-old than in 7-day-old mice, whereas with taurine the situation was the opposite. Ischemia markedly enhanced the release of all these three amino acids. The release of aspartate and glycine was markedly enhanced as well whereas no effects were discernible in the release of glutamine, alanine, serine and threonine. K(+) stimulation (50 mM) enhanced the release of GABA, glutamate, taurine, aspartate and glycine in most cases, except with taurine in 3-month-old mice under the ischemic conditions and with aspartate in 7-day-old mice under the control conditions. K(+) stimulation did not affect the release of glutamine, alanine, serine or threonine. The results on endogenous amino acids are qualitatively similar to those obtained in our earlier experiments with labeled preloaded amino acids. In conclusion, in developing mice only inhibitory taurine is released in such amounts that may counteract the harmful effects of excitatory amino acids in ischemia.

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“…A small hole (1 mm) was then drilled according to the following coordinates for the striatum from the bregma: ?0.5 mm anterior and ?2.2 mm lateral. Y-shaped self-built dialysis probes were constructed as previously described [14,15] with minor modifications. The dialysis membrane (o.d.…”

Section: Intracerebral Microdialysismentioning

confidence: 99%

“…To our knowledge, alterations in glucose levels with concomitant changes in lactate levels have not been investigated after acute and prolonged (24 h) probe implantation. Since disruption of cerebral metabolism is a key element of ischemic stroke, a possible cause of brain damage after probe implantation may be ischemia which leads to accumulation of excitatory neurotransmitters such as glutamate, and cell membrane breakdown which is reflected in increases of glycerol [14] and eventually cell death. Though the effect of probe implantation on altered neurotransmitter release has been studied [5][6][7], the extent of cell membrane degradation following probe implantation is ill defined.…”

Section: Introductionmentioning

confidence: 99%

Acute Depression of Energy Metabolism after Microdialysis Probe Implantation is Distinct from Ischemia-Induced Changes in Mouse Brain

2010

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The current study used measurements of metabolites and markers of membrane integrity to determine the most suitable time point for microdialysis experiments following probe implantation. Leakage of Evans blue and sodium fluorescein indicated increased BBB permeability only immediately (15 min), but not 1.5 and 24 h following probe implantation. Acute implantation decreased glucose and lactate levels relative to the levels after 24 h (to 13-37% and 25-60%, respectively). No change in extracellular levels of glutamate or glycerol was seen. In comparison to acute probe implantation, the pattern of damage under brain ischemia (middle cerebral artery occlusion) differed: While glucose levels dropped, lactate levels rose after ischemia, and glutamate (tenfold) and glycerol (eightfold) increased sharply. In conclusion, acute implantation of a microdialysis probe causes transient depression of the energy metabolites, glucose and lactate, likely due to injury-induced hypermetabolism. However, no massive tissue damage or severe ischemic conditions around the probe occur.

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Metabolic and transmitter changes in core and penumbra after middle cerebral artery occlusion in mice

Cited by 64 publications

References 27 publications

Ginkgo Extract EGb761 Confers Neuroprotection by Reduction of Glutamate Release in Ischemic Brain

Ginkgo Extract EGb761 Confers Neuroprotection by Reduction of Glutamate Release in Ischemic Brain

Release of Endogenous Amino Acids from the Striatum from Developing and Adult Mice in Ischemia

Acute Depression of Energy Metabolism after Microdialysis Probe Implantation is Distinct from Ischemia-Induced Changes in Mouse Brain

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