0000000000719112

AUTHOR

Momoko Nagata

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The neuroprotective effect of lactate is not due to improved glutamate uptake after controlled cortical impact in rats.

2012

For many years lactate was considered to be a waste product of glycolysis. Data are accumulating that suggest that lactate is an important energy substrate for neurons during activation. In severe traumatic brain injury (TBI) glutamate release and ischemic cerebral blood flow (CBF) are major factors for a mismatch between energy demand and supply and for neuronal cell death. Although ATP and behavior could be improved by lactate treatment after TBI, no histological correlate nor any linkage to better astrocytic glutamate uptake or CBF as possible mechanisms have been described. We subjected male rats to a controlled cortical impact (CCI; 5 m/sec, 2.5 mm). To study the effects of lactate tre…

Malemedicine.medical_specialtyMicrodialysisCoumaric AcidsMicrodialysisGlutamic AcidNeuroprotectionRats Sprague-DawleyStereotaxic TechniquesOxygen ConsumptionInternal medicinemedicineAnimalsGlycolysisLactic AcidChromatography High Pressure LiquidBrain ChemistryCerebral CortexSkull FracturesChemistryGlutamate receptorGlutamic acidRatsmedicine.anatomical_structureEndocrinologyNeuroprotective AgentsCerebral blood flowCerebral cortexAnesthesiaBrain InjuriesCerebrovascular CirculationStereotaxic techniqueNeurology (clinical)Extracellular SpaceJournal of neurotrauma
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