2001
Tracking Brain Volume Changes in C57BL/6J and ApoE-Deficient Mice in a Model of Neurodegeneration: A 5-Week Longitudinal Micro-MRI Study
McDaniel B, Sheng H, Warner D, Hedlund L, Benveniste H. Tracking Brain Volume Changes in C57BL/6J and ApoE-Deficient Mice in a Model of Neurodegeneration: A 5-Week Longitudinal Micro-MRI Study. NeuroImage 2001, 14: 1244-1255. PMID: 11707081, DOI: 10.1006/nimg.2001.0934.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApolipoproteins EAtrophyBrainBrain IschemiaBrain MappingCerebral VentriclesDisease Models, AnimalHippocampusImage EnhancementImage Processing, Computer-AssistedImaging, Three-DimensionalMagnetic Resonance ImagingMaleMiceMice, Inbred C57BLMice, Neurologic MutantsMicroscopyNeurodegenerative DiseasesProsencephalonConceptsApoE-deficient miceModels of neurodegenerationPostischemic dayBrain atrophyMouse modelNeurodegenerative diseasesDorsal hippocampal volumeBrain volume changesMin of ischemiaHigh signal intensity areaTransgenic mouse modelProgression of pathologyCorresponding time pointsSignal intensity areaMagnetic resonance imagingHigh-resolution MRIT1-weighted MR imagingC57 miceDorsal hippocampusHippocampal volumeClinical conditionsIschemiaMRI studiesPredetermined protocolCognitive decline
1993
Hydrogen Peroxide Production by Monoamine Oxidase during Ischemia-Reperfusion in the Rat Brain
Simonson S, Zhang J, Canada A, Su Y, Benveniste H, Piantadosi C. Hydrogen Peroxide Production by Monoamine Oxidase during Ischemia-Reperfusion in the Rat Brain. Cerebrovascular And Brain Metabolism Reviews 1993, 13: 125-134. PMID: 8417001, DOI: 10.1038/jcbfm.1993.15.Peer-Reviewed Original ResearchConceptsInhibition of MAOMonoamine oxidaseRat brainMAO inhibitorsForebrain blood flowMin of ischemiaBrain reperfusionIschemia reperfusionCatecholamine concentrationsBlood flowForebrain homogenatesReperfusionIschemiaGlutathione peroxidaseGlutathione concentrationBiochemical indicationsThreefold increaseBrainInhibitorsInhibitionH2O2 productionSurvivalHydrogen peroxide productionCatalasePeroxide productionIschemia as an Excitotoxic Lesion: Protection Against Hippocampal Nerve Cell Loss by Denervation
Diemer N, Johansen F, Benveniste H, Bruhn T, Berg M, Valente E, Jørgensen M. Ischemia as an Excitotoxic Lesion: Protection Against Hippocampal Nerve Cell Loss by Denervation. Acta Neurochirurgica Supplement 1993, 57: 94-101. PMID: 8380675, DOI: 10.1007/978-3-7091-9266-5_14.Peer-Reviewed Original ResearchConceptsPyramidal neuronsIschemic neuron damageVulnerable nerve cellsTransient cerebral ischemiaGABA-ergic interneuronsNerve cell lossMin of ischemiaHippocampal pyramidal neuronsRelease of glutamateExtracellular glutamate releaseKainate/Neuroexcitatory mechanismsNeuron damagePostischemic periodCerebral ischemiaHilus cellsPostischemic hypoperfusionCalcium blockersGlutamate releaseIntact innervationIschemic animalsDenervated ratsDentate hilusReceptor autoradiographyCA1 neurons
1988
Calcium accumulation by glutamate receptor activation is involved in hippocampal cell damage after ischemia
Benveniste H, Jørgensen M, Diemer N, Hansen A. Calcium accumulation by glutamate receptor activation is involved in hippocampal cell damage after ischemia. Acta Neurologica Scandinavica 1988, 78: 529-536. PMID: 2906199, DOI: 10.1111/j.1600-0404.1988.tb03697.x.Peer-Reviewed Original ResearchConceptsGlutamate N-methyl-D-aspartate receptorN-methyl-D-aspartate receptorsCell damageNerve cell destructionComplete cerebral ischemiaBrain cell damageMin of ischemiaOnset of ischemiaHippocampal cell damageGlutamate receptor activationCA 1 regionRole of intracellularCerebral ischemiaIschemic periodBilateral destructionDenervated hippocampusAfferent inputSynaptic transmissionCalcium influxIschemiaCompetitive antagonistReceptor activationHistological studyCell destructionCalcium accumulation