2021
Spreading depression as an innate antiseizure mechanism
Tamim I, Chung D, de Morais A, Loonen I, Qin T, Misra A, Schlunk F, Endres M, Schiff S, Ayata C. Spreading depression as an innate antiseizure mechanism. Nature Communications 2021, 12: 2206. PMID: 33850125, PMCID: PMC8044138, DOI: 10.1038/s41467-021-22464-x.Peer-Reviewed Original ResearchConceptsFocal neocortical seizuresSystemic kainic acidCentral nervous systemVivo mouse modelAntiseizure mechanismsAntiseizure effectsSeizure generalizationFocal seizuresSD occurrenceNeocortical seizuresKainic acidBrain injuryMouse modelNervous systemSeizuresNeurological disordersProlonged depolarizationSDDepressionBicucullineMigraineInjury
2019
Branched-Chain Amino Acids and Seizures: A Systematic Review of the Literature
Gruenbaum SE, Chen EC, Sandhu MRS, Deshpande K, Dhaher R, Hersey D, Eid T. Branched-Chain Amino Acids and Seizures: A Systematic Review of the Literature. CNS Drugs 2019, 33: 755-770. PMID: 31313139, DOI: 10.1007/s40263-019-00650-2.Peer-Reviewed Original ResearchConceptsGenetic absence epilepsyBCAA supplementationAbsence epilepsyAnimal modelsBranched-chain amino acid supplementationSystematic reviewLong-term BCAA supplementationEpilepsy experience seizuresAnti-seizure effectsEffect of BCAAMost animal modelsPossible underlying mechanismsAmino acid supplementationChain amino acidsBCAA administrationBCAA mixtureRefractory epilepsyNeuron lossSeizure disorderAntiepileptic drugsSeizure modelSeizure propagationCochrane LibrarySeizure activityKainic acid
2018
Development of a Model of Hemispheric Hypodensity (“Big Black Brain”)
Costine-Bartell B, McGuone D, Price G, Crawford E, Keeley K, Munoz-Pareja J, Dodge CP, Staley K, Duhaime AC. Development of a Model of Hemispheric Hypodensity (“Big Black Brain”). Journal Of Neurotrauma 2018, 36: 815-833. PMID: 30039743, PMCID: PMC6387571, DOI: 10.1089/neu.2018.5736.Peer-Reviewed Original ResearchConceptsHemispheric hypodensitySubdural hematomaAbusive head traumaMultiple vascular territoriesMechanism of traumaSevere brain damagePatterns of injuryDeep gray matterSeizure durationHead traumaMultiple injuriesPathological examinationKainic acidSevere seizuresVasogenic edemaBrain damageContralateral sideVascular territoriesCommon findingMetabolic mismatchRelative sparingAnimal modelsRadiological indicatorsCortical ribbonGray matter
2016
Mitochondrial Uncoupling Protein 2 (UCP2) Regulates Retinal Ganglion Cell Number and Survival
Barnstable CJ, Reddy R, Li H, Horvath TL. Mitochondrial Uncoupling Protein 2 (UCP2) Regulates Retinal Ganglion Cell Number and Survival. Journal Of Molecular Neuroscience 2016, 58: 461-469. PMID: 26846222, PMCID: PMC4833669, DOI: 10.1007/s12031-016-0728-5.Peer-Reviewed Original ResearchConceptsRetinal ganglion cellsUncoupling protein 2Mitochondrial uncoupling protein 2Ganglion cellsRetinal ganglion cell numberNeurotrophic factor BDNFSurvival-promoting effectsGanglion cell numberUCP2 levelsRetinal neuron survivalProtein 2Critical developmental periodIntraocular injectionKainic acidNeuron survivalNeuronal survivalMouse retinaRetinal cellsElevated numbersAdult animalsSurvivalCell numberCell survivalImportant regulatorCell death
2002
Endogenous parathyroid hormone-related protein functions as a neuroprotective agent
Chatterjee O, Nakchbandi IA, Philbrick WM, Dreyer BE, Zhang J, Kaczmarek LK, Brines ML, Broadus AE. Endogenous parathyroid hormone-related protein functions as a neuroprotective agent. Brain Research 2002, 930: 58-66. PMID: 11879796, DOI: 10.1016/s0006-8993(01)03407-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrain NeoplasmsCalcium ChannelsCells, CulturedCerebral CortexDose-Response Relationship, DrugExcitatory Amino Acid AgonistsFemaleInjections, IntraperitonealKainic AcidL-Lactate DehydrogenaseMiceMice, KnockoutNeuroblastomaNeuronsNeuroprotective AgentsParathyroid Hormone-Related ProteinPatch-Clamp TechniquesPregnancyProteinsConceptsL-type voltage-sensitive calcium channelsCalcium channelsHippocampal c-Fos expressionVoltage-sensitive calcium channelsKainic acid-induced excitotoxicityCerebral cortical culturesFunction of PTHrPKainic acid excitotoxicityL-type calcium channelsCultured cerebellar granule cellsSensitive calcium channelsHormone-related proteinCentral nervous systemWhole-cell techniqueC-fos expressionCultured mouse neuroblastoma cellsCerebellar granule cellsMouse neuroblastoma cellsKainate toxicityCerebral cortexNeuroprotective agentsKainic acidLittermate miceCortical culturesPTHrP functions
1997
Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene
Yang D, Kuan C, Whitmarsh A, Rinócn M, Zheng T, Davis R, Rakic P, Flavell R. Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene. Nature 1997, 389: 865-870. PMID: 9349820, DOI: 10.1038/39899.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisDrug ResistanceExcitatory Amino Acid AgonistsGene ExpressionGene TargetingGlutamic AcidHippocampusKainic AcidMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 10Mitogen-Activated Protein KinasesNeuronsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junSeizuresSignal TransductionTranscription Factor AP-1ConceptsKainic acidGlutamate receptor agonist kainic acidAgonist kainic acidExcitotoxicity-induced apoptosisExcitatory amino acidsHippocampal neuron apoptosisHippocampus of miceStress-induced neuronal apoptosisObserved neuroprotectionGlutamate neurotoxicitySeizure activityNeuron apoptosisGlutamate toxicityNeuronal apoptosisAP-1 transcription factor complexJNK3 geneMutant miceMiceMembrane depolarizationNoxious stressTranscription factor complexApoptosisC-JunRecent studiesTranscriptional activity
1995
Preferential neuronal loss in layer III of the medial entorhinal cortex in rat models of temporal lobe epilepsy
Du F, Eid T, Lothman E, Kohler C, Schwarcz R. Preferential neuronal loss in layer III of the medial entorhinal cortex in rat models of temporal lobe epilepsy. Journal Of Neuroscience 1995, 15: 6301-6313. PMID: 7472396, PMCID: PMC6577998, DOI: 10.1523/jneurosci.15-10-06301.1995.Peer-Reviewed Original ResearchConceptsPreferential neuronal lossTemporal lobe epilepsyNeuronal lossMedial entorhinal cortexEntorhinal cortexLayer IIILobe epilepsyRat modelIntractable temporal lobe epilepsyAcute status epilepticusLithium/pilocarpineParvalbumin-positive neuronsIntracellular calcium ion concentrationKainic acid administrationNerve cell lossAdult male ratsInjection of diazepamSurviving neuronsProlonged seizuresStatus epilepticusAcid administrationNissl stainingVentral hippocampusKainic acidPathological elevation
1988
DARPP‐32 and Phosphatase Inhibitor‐1, Two Structurally Related Inhibitors of Protein Phosphatase‐1, Are Both Present in Striatonigral Neurons
Nairn A, Hemmings H, Walaas S, Greengard P. DARPP‐32 and Phosphatase Inhibitor‐1, Two Structurally Related Inhibitors of Protein Phosphatase‐1, Are Both Present in Striatonigral Neurons. Journal Of Neurochemistry 1988, 50: 257-262. PMID: 3335843, DOI: 10.1111/j.1471-4159.1988.tb13258.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBasal GangliaCarrier ProteinsCorpus StriatumDopamine and cAMP-Regulated Phosphoprotein 32Electrophoresis, Polyacrylamide GelIntracellular Signaling Peptides and ProteinsKainic AcidMaleMusclesNerve Tissue ProteinsNeuronsPhosphoproteinsPhosphorylationProteinsRatsRats, Inbred StrainsSubstantia NigraConceptsPhosphatase inhibitor-1Protein phosphatase 1Phosphatase 1DARPP-32Inhibitor-1Striatonigral neuronsSubstantia nigraKainic acidStriatonigral fibersBiochemical propertiesRelated inhibitorsSpecific neuronal subpopulationsIpsilateral substantia nigraBovine caudate nucleusSpecific activityStriatal neuronsNeuronal localizationRat neostriatumNeuronal subpopulationsRat brainCaudate nucleusLesioned neostriatumNeostriatumNeuronsInhibitors
1986
Enkephalin convertase: localization to specific neuronal pathways
Lynch DR, Strittmatter SM, Venable JC, Snyder SH. Enkephalin convertase: localization to specific neuronal pathways. Journal Of Neuroscience 1986, 6: 1662-1675. PMID: 3086516, PMCID: PMC6568706, DOI: 10.1523/jneurosci.06-06-01662.1986.Peer-Reviewed Original ResearchConceptsSpecific neuronal pathwaysPyramidal cellsDentate gyrusStria terminalisNeuronal pathwaysAcid lesionsBed nucleusCaudate nucleusGranule cellsSubstantia nigra pars reticulataDentate gyrus granule cellsKnife-cut lesionsGyrus granule cellsQuinolinic acid lesionsHypothalamic magnocellular nucleiIbotenic acid lesionsWhite matter tractsBrain tissue sectionsPars reticulataTrigeminal ganglionKainic acidEnkephalinergic pathwaysLateral septumSensory neuronsMedian eminence
1982
Intracortical kainic acid induces an assymmetrical behavioral response in the rat
Kubos K, Pearlson G, Robinson R. Intracortical kainic acid induces an assymmetrical behavioral response in the rat. Brain Research 1982, 239: 303-309. PMID: 7093686, DOI: 10.1016/0006-8993(82)90857-5.Peer-Reviewed Original ResearchConceptsKainic acidCortical noradrenergic terminalsDay postoperative periodRight frontal cortexNoradrenergic terminalsPostoperative periodRight hemisphere lesionsSpontaneous hyperactivityFrontal cortexIdentical injectionsHemisphere lesionsNanomolar dosesLeft hemisphereHyperactivityRatsNeural asymmetriesInjectionBehavioral responsesPrevious studiesLesionsCortexDosesWeeks
1978
Acute and chronic haloperidol treatment: Comparison of effects on nigral dopaminergic cell activity
Bunney B, Grace A. Acute and chronic haloperidol treatment: Comparison of effects on nigral dopaminergic cell activity. Life Sciences 1978, 23: 1715-1727. PMID: 31529, DOI: 10.1016/0024-3205(78)90471-x.Peer-Reviewed Original ResearchConceptsChronic haloperidol treatmentDA cellsHaloperidol treatmentControl animalsCell activityExtracellular single-unit recordingsDopaminergic cell activityDopaminergic neuronal activityNigral DA cellsNeurological side effectsDopamine cell activitySingle-unit recordingsFeedback pathwaysComparison of effectsDA neuronsTime-dependent mannerMicroiontophoretic techniquesClinical effectsKainic acidAntipsychotic drugsDepolarization blockCaudate nucleusNeuronal activitySide effectsUnit recordings
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