2007
Evolution of a Focal Brain Lesion Produced by Interlaced Microplanar X-Rays
Anschel D, Romanelli P, Benveniste H, Foerster B, Kalef-Ezra J, Zhong Z, Dilmanian F. Evolution of a Focal Brain Lesion Produced by Interlaced Microplanar X-Rays. Min - Minimally Invasive Neurosurgery 2007, 50: 43-46. PMID: 17546543, DOI: 10.1055/s-2007-976514.Peer-Reviewed Original ResearchConceptsT2 signalCentral nervous system diseaseHigh T2 signalNervous system diseasesTesla magnetic resonance imagingFocal brain lesionsMagnetic resonance imagingBrain lesionsRadiosurgical approachRat brainSystem diseasesStereotactic radiosurgeryHigh-dose irradiationFuture treatmentLow dosesLesionsResonance imagingLow T1Dose irradiationBrainTreatmentPrecise targetsX-ray
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
1999
Anxiety, vocalization, and agitation following peripheral nerve block with ropivacaine
Klein S, Benveniste H. Anxiety, vocalization, and agitation following peripheral nerve block with ropivacaine. Regional Anesthesia & Pain Medicine 1999, 24: 175-178. PMID: 10204906, DOI: 10.1016/s1098-7339(99)90081-0.Peer-Reviewed Case Reports and Technical NotesConceptsCentral nervous systemLocal anesthetics-induced toxicityAnesthetic-induced toxicityPeripheral nerve blockadePeripheral nerve blocksAdministration of ropivacainePotential side effectsMediation of anxietyCNS toxicityNerve blockNerve blockadeCardiovascular toxicityCase reportClassical signsLocal anestheticsRopivacaineSide effectsUnusual symptomsNervous systemNeural pathwaysUnexpected behavioral changesCardiovascular systemHuman volunteersVerbal commandsPatientsAnxiety, Vocalization, and Agitation Following Peripheral Nerve Block With Ropivacaine
Klein S, Benveniste H. Anxiety, Vocalization, and Agitation Following Peripheral Nerve Block With Ropivacaine. Regional Anesthesia & Pain Medicine 1999, 24: 175-178. DOI: 10.1097/00115550-199924020-00014.Peer-Reviewed Case Reports and Technical NotesConceptsCentral nervous systemLocal anesthetics-induced toxicityAnesthetic-induced toxicityPeripheral nerve blockadePeripheral nerve blocksAdministration of ropivacainePotential side effectsMediation of anxietyCNS toxicityNerve blockNerve blockadeCase reportCardiovascular toxicityClassical signsLocal anestheticsRopivacaineSide effectsUnusual symptomsNervous systemNeural pathwaysUnexpected behavioral changesCardiovascular systemHuman volunteersVerbal commandsPatients
1998
Nervous System Defects of AnkyrinB (−/−) Mice Suggest Functional Overlap between the Cell Adhesion Molecule L1 and 440-kD AnkyrinB in Premyelinated Axons
Scotland P, Zhou D, Benveniste H, Bennett V. Nervous System Defects of AnkyrinB (−/−) Mice Suggest Functional Overlap between the Cell Adhesion Molecule L1 and 440-kD AnkyrinB in Premyelinated Axons. Journal Of Cell Biology 1998, 143: 1305-1315. PMID: 9832558, PMCID: PMC2133070, DOI: 10.1083/jcb.143.5.1305.Peer-Reviewed Original ResearchConceptsNervous systemOptic nervePyramidal tractCorpus callosumOptic nerve axonsPostnatal day 21Long fiber tractsPostnatal day 1Postnatal day 7Mouse nervous systemNervous system defectsL1 miceCell adhesion molecule L1Internal capsuleSpinal cordAdhesion molecule L1Extensive degenerationCell adhesion moleculeLateral columnDay 1Day 21Day 7Human patientsL1 mutationsDay 20
1995
Nitric oxide synthase inhibition and extracellular glutamate concentration after cerebral ischemia/reperfusion.
Zhang J, Benveniste H, Klitzman B, Piantadosi C. Nitric oxide synthase inhibition and extracellular glutamate concentration after cerebral ischemia/reperfusion. Stroke 1995, 26: 298-304. PMID: 7530389, DOI: 10.1161/01.str.26.2.298.Peer-Reviewed Original ResearchConceptsIschemia/reperfusionBlood-brain barrierCerebral blood flowBrain ischemia/reperfusionExcitatory amino acidsExtracellular glutamate concentrationL-NAMEBlood flowGlutamate concentrationSynthase inhibitionL-arginineExcitatory amino acid toxicityL-NAME-treated ratsPostischemic cerebral blood flowNitric oxide synthase inhibitionCerebral ischemia/reperfusionBlood-brain barrier functionL-arginine methyl esterCerebral blood flow responseBlood-brain barrier permeabilityGlobal brain ischemia/reperfusionElevated glutamate concentrationsImmediate postischemic periodInterstitial glutamate concentrationL-NAME administration
1993
Inhibition of nitric oxide synthase increases extracellular cerebral glutamate concentration after global ischemia
Zhang J, Benveniste H, Piantadosi C. Inhibition of nitric oxide synthase increases extracellular cerebral glutamate concentration after global ischemia. Neuroscience Letters 1993, 157: 179-182. PMID: 7694195, DOI: 10.1016/0304-3940(93)90731-y.Peer-Reviewed Original ResearchConceptsGlutamate releaseGlutamate concentrationNitric oxide synthase inhibitionCerebral glutamate concentrationsOxide synthase inhibitionGlobal brain ischemiaInhibition of NOSNitric oxide synthaseExtracellular glutamate releaseCerebral microdialysisBrain ischemiaForebrain ischemiaControl ratsGlobal ischemiaNOS inhibitorOxide synthaseSynthase inhibitionCarotid arteryBrain flowDialysis probeIschemiaDialysate concentrationsControl valuesRatsReperfusionMicrodialysis measurements of PGD2, TXB2 and 6-keto-PGF1α in rat CA1 hippocampus during transient cerebral ischemia
Huttemeier P, Kamiyama Y, Su M, Watkins W, Benveniste H. Microdialysis measurements of PGD2, TXB2 and 6-keto-PGF1α in rat CA1 hippocampus during transient cerebral ischemia. Prostaglandins 1993, 45: 177-187. PMID: 8430228, DOI: 10.1016/0090-6980(93)90033-4.Peer-Reviewed Original ResearchConceptsCerebral ischemiaPGF1 alphaMicrodialysis probeRat CA1 hippocampusGlobal cerebral ischemiaTransient cerebral ischemiaRole of PGD2Arachidonic acid metabolismAverage peak concentrationDistinct brain regionsIschemic brainEicosanoid concentrationsCA1 hippocampusEicosanoid releaseAA metabolitesPG metabolitesMicrodialysis measurementsBaseline levelsBrain regionsIschemiaPGD2TXB2Implanted microdialysis probesPeak concentrationAcid metabolismHydrogen 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 production
1989
Ischemic Damage in Hippocampal CA1 is Dependent on Glutamate Release and Intact Innervation from CA3
Benveniste H, Jørgensen M, Sandberg M, Christensen T, Hagberg H, Diemer N. Ischemic Damage in Hippocampal CA1 is Dependent on Glutamate Release and Intact Innervation from CA3. Cerebrovascular And Brain Metabolism Reviews 1989, 9: 629-639. PMID: 2570785, DOI: 10.1038/jcbfm.1989.90.Peer-Reviewed Original ResearchConceptsCA1 regionPyramidal cellsGlutamate releaseIntact innervationHippocampal tissueCA1 tissueInjection siteIschemia-induced releaseIschemia-induced damageTransient global ischemiaCA1 pyramidal cellsRelease of glutamateGlutamatergic afferentsIschemic damageHippocampal CA1CA1 pyramidsGlobal ischemiaCA3 regionPathogenetic significanceIschemiaNeurotoxic potentialCA3CA1GlutamateInnervationDetermination of Brain Interstitial Concentrations by Microdialysis
Benveniste H, Hansen A, Ottosen N. Determination of Brain Interstitial Concentrations by Microdialysis. Journal Of Neurochemistry 1989, 52: 1741-1750. PMID: 2723633, DOI: 10.1111/j.1471-4159.1989.tb07252.x.Peer-Reviewed Original Research
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 accumulationEarly Postischemic 45Ca Accumulation in Rat Dentate Hilus
Benveniste H, Diemer N. Early Postischemic 45Ca Accumulation in Rat Dentate Hilus. Cerebrovascular And Brain Metabolism Reviews 1988, 8: 713-719. PMID: 3417798, DOI: 10.1038/jcbfm.1988.118.Peer-Reviewed Original Research
1987
Cellular reactions to implantation of a microdialysis tube in the rat hippocampus
Benveniste H, Diemer N. Cellular reactions to implantation of a microdialysis tube in the rat hippocampus. Acta Neuropathologica 1987, 74: 234-238. PMID: 3673515, DOI: 10.1007/bf00688186.Peer-Reviewed Original ResearchConceptsMicrodialysis tubeNumber of astrocytesAdjacent tissue reactionExtracellular neurotransmitter concentrationsNormal neuropilGranuloma formationOccasional hemorrhageRat hippocampusRat dorsalCollagen depositsAstrocyte processesTissue changesNeurotransmitter concentrationsFiber implantationTissue reactionAstrocytesImplantationNeuropilCellular reactionsDaysOptimal timeRegional Cerebral Glucose Phosphorylation and Blood Flow After Insertion of a Microdialysis Fiber Through the Dorsal Hippocampus in the Rat
Benveniste H, Drejer J, Schousboe A, Diemer N. Regional Cerebral Glucose Phosphorylation and Blood Flow After Insertion of a Microdialysis Fiber Through the Dorsal Hippocampus in the Rat. Journal Of Neurochemistry 1987, 49: 729-734. PMID: 3612121, DOI: 10.1111/j.1471-4159.1987.tb00954.x.Peer-Reviewed Original ResearchConceptsLocal cerebral blood flowBlood flowDorsal hippocampusGlucose metabolismMicrodialysis fibersLocal cerebral glucose metabolismCerebral glucose metabolismCerebral blood flowRat dorsal hippocampusGlucose phosphorylationNear normalizationFocal disturbanceRecovery periodPronounced disturbancesHippocampusRatsImplantationMetabolismPhosphorylationRecovery timeGliosisSlight reductionLCMRglcLCMRglu
1985
Cellular Origin of Ischemia‐Induced Glutamate Release from Brain Tissue In Vivo and In Vitro
Drejer J, Benveniste H, Diemer N, Schousboe A. Cellular Origin of Ischemia‐Induced Glutamate Release from Brain Tissue In Vivo and In Vitro. Journal Of Neurochemistry 1985, 45: 145-151. PMID: 2860206, DOI: 10.1111/j.1471-4159.1985.tb05486.x.Peer-Reviewed Original ResearchConceptsPotassium-induced releaseGlutamatergic neuronsAspartate uptakeConditions of hypoglycemiaCultured glutamatergic neuronsTransient cerebral ischemiaHigh potassiumExtracellular glutamate contentCerebral ischemiaGlutamate releaseTransmitter poolExtracellular glutamateMicrodialysis techniqueIschemiaBrain tissuePotassium stimulationPerfusion mediumHypoglycemiaGlutamate contentNeuronsInduced increasesCellular originVivo experimentsAstrocytesPrevious reports
1984
Elevation of the Extracellular Concentrations of Glutamate and Aspartate in Rat Hippocampus During Transient Cerebral Ischemia Monitored by Intracerebral Microdialysis
Benveniste H, Drejer J, Schousboe A, Diemer N. Elevation of the Extracellular Concentrations of Glutamate and Aspartate in Rat Hippocampus During Transient Cerebral Ischemia Monitored by Intracerebral Microdialysis. Journal Of Neurochemistry 1984, 43: 1369-1374. PMID: 6149259, DOI: 10.1111/j.1471-4159.1984.tb05396.x.Peer-Reviewed Original ResearchConceptsGamma-aminobutyric acidCerebral ischemiaIschemic periodTransient complete cerebral ischemiaTransient cerebral ischemiaComplete cerebral ischemiaExtracellular contentAmino acid glutamateDiameter dialysisIntracerebral microdialysisConcentrations of alanineExtracellular glutamateRat hippocampusCertain neuronsTaurine concentrationsIschemiaExtracellular concentrationHippocampusExtracellular fluidRinger's solutionGlutamateSame periodAspartateCausal factorsPeriod