2022
The Role of Alpha-Tocotrienol during Development of Primary Hippocampal Neurons
Park H, Crowe-White K, Ciesla L, Bannerman S, Scott M, Davis A, Adhikari B, Burnett G, Broman K, Ferdous K, Lackey K, Lickznerski P, Jonas E. The Role of Alpha-Tocotrienol during Development of Primary Hippocampal Neurons. Current Developments In Nutrition 2022, 6: 800. PMCID: PMC9194400, DOI: 10.1093/cdn/nzac064.019.Peer-Reviewed Original ResearchPrimary hippocampal neuronsHippocampal neuronsPrimary rat hippocampal neuronsRat hippocampal neuronsAlpha-tocotrienolProtein levelsBcl-xLMitochondrial functionMitochondrial superoxide levelsNeuroprotective propertiesNeuronal ATPSholl analysisNeurobasal mediumNeurite complexityB cellsVitamin ENeuron developmentNeuronsBeneficial effectsSuperoxide levelsNeuronal growthConditioned mediaNeurite morphologyIntracellular ATPMitochondrial superoxideAlpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL
Park HA, Crowe-White KM, Ciesla L, Scott M, Bannerman S, Davis AU, Adhikari B, Burnett G, Broman K, Ferdous KA, Lackey KH, Licznerski P, Jonas EA. Alpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL. Nutrition Research 2022, 101: 31-42. PMID: 35366596, PMCID: PMC9081260, DOI: 10.1016/j.nutres.2022.02.007.Peer-Reviewed Original ResearchConceptsPrimary hippocampal neuronsControl neuronsHippocampal neuronsAlpha-tocotrienolBcl-xLVitamin E familyCerebral ischemiaNeuronal viabilityMature neuronsB cellsNeurite complexityNeuronal functionMitochondrial energy productionBrain developmentCentral mechanismsNeuronsBeneficial effectsOxidative stressBcl-xL upregulationProtein levelsNeurite branchingTreatmentE familyATP levelsNeurite outgrowth
2020
Roles of Vitamin E in Energy Metabolism During Neurite Outgrowth
Stratton Z, Davis A, Jonas E, Crowe-White K, Park H. Roles of Vitamin E in Energy Metabolism During Neurite Outgrowth. Current Developments In Nutrition 2020, 4: nzaa057_051. PMCID: PMC7259054, DOI: 10.1093/cdn/nzaa057_051.Peer-Reviewed Original ResearchPrimary hippocampal neuronsBrain injuryHippocampal neuronsControl groupNeurite outgrowthNeuronal energy metabolismMaintenance of synapsesVitamin E familyEnergy metabolismNeurite lossNeurobasal mediumVitamin EAlpha-tocotrienolBrain developmentNeuronsOxidative stressNeurite growthBranched neuritesCentral targetMitochondrial inner membrane potentialE familyATP levelsTreatmentNeuritesInjury
2019
Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal Neurons
Park HA, Mnatsakanyan N, Broman K, Davis AU, May J, Licznerski P, Crowe-White KM, Lackey KH, Jonas EA. Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal Neurons. International Journal Of Molecular Sciences 2019, 21: 220. PMID: 31905614, PMCID: PMC6982044, DOI: 10.3390/ijms21010220.Peer-Reviewed Original ResearchConceptsPrimary hippocampal neuronsHippocampal neuronsReactive oxygen speciesMitochondrial dysfunctionBcl-xLMitochondrial membrane potentialMitochondrial functionProduction of ROSExcitotoxic conditionsGlutamate challengeNeuroprotective propertiesMembrane potentialNeuronal deathExcitotoxic stimulationBcl-xL levelsNeuronal survivalIntracellular ATP depletionMitochondrial reactive oxygen speciesB cellsImportant causeDysfunctionNeuronsROS productionATP depletionNeurite outgrowth
2018
Nutritional Regulators of Bcl-xL in the Brain
Park HA, Broman K, Stumpf A, Kazyak S, Jonas EA. Nutritional Regulators of Bcl-xL in the Brain. Molecules 2018, 23: 3019. PMID: 30463183, PMCID: PMC6278276, DOI: 10.3390/molecules23113019.Peer-Reviewed Original ResearchConceptsBcl-xLNormal brain developmentNeuroprotective propertiesBcl-xL expressionB cellsBrain developmentBcl-2 proteinAnti-apoptotic Bcl-2 proteinPathological processesSafe strategyToxic stimulationHuman subjectsMitochondrial functionRegulatory effectsBrainNutritional regulatorsDiseaseNeuronsPathology
2017
ΔN-Bcl-xL, a therapeutic target for neuroprotection
Park HA, Jonas EA. ΔN-Bcl-xL, a therapeutic target for neuroprotection. Neural Regeneration Research 2017, 12: 1791-1794. PMID: 29239317, PMCID: PMC5745825, DOI: 10.4103/1673-5374.219033.Peer-Reviewed Original ResearchΔN-BclNeuronal deathNeuronal viabilityMitochondrial dysfunctionPrimary hippocampal neuronsABT-737Excitotoxic injuryGlutamate toxicityHippocampal neuronsAnti-apoptotic proteinsTherapeutic targetB cellsPrimary neuronsNeuronal functionAcute productionNeuroprotectionAltered metabolismMitochondrial damageNeuronsCentral targetMitochondrial functionDysfunctionDeathMitochondrial anti-apoptotic proteinDependent effects
2016
Metabolic Control of Cell Death : The Role of Bcl‐xL
Park H, Licznerski P, Niu Y, Mnatsakanyan N, Miranda P, Wu J, Sacchetti S, Polster B, Alavian K, Jonas E. Metabolic Control of Cell Death : The Role of Bcl‐xL. The FASEB Journal 2016, 30 DOI: 10.1096/fasebj.30.1_supplement.1162.2.Peer-Reviewed Original ResearchΔN-BclMitochondrial permeability transition poreABT-737Glutamate-exposed neuronsBcl-xLGlutamate-induced excitotoxicityGlutamate-induced deathNeuronal energy metabolismMitochondrial potentialCell deathGlutamate challengeBrain ischemiaNeuroprotective propertiesNeuronal survivalFold lower concentrationCyclosporine ASpecific small molecule inhibitorsATP productionSmall molecule inhibitorsMetabolic controlMitochondrial channel activityMalignant cellsPro-apoptotic roleNeuronsDeath
2015
Bcl-xL Is Necessary for Neurite Outgrowth in Hippocampal Neurons
Park HA, Licznerski P, Alavian KN, Shanabrough M, Jonas EA. Bcl-xL Is Necessary for Neurite Outgrowth in Hippocampal Neurons. Antioxidants & Redox Signaling 2015, 22: 93-108. PMID: 24787232, PMCID: PMC4281845, DOI: 10.1089/ars.2013.5570.Peer-Reviewed Original ResearchConceptsDeath receptor 6Hippocampal neuronsNeurite outgrowthExacerbation of hypoxiaBcl-xLNeuronal outgrowthNeuronal process outgrowthNeuronal injuryNeurodegenerative stimuliVivo ischemiaHypoxic injuryNeuronal survivalBrain injuryImpairs neurite outgrowthHypoxic controlsSynapse numberAxonal pruningNeurite damageB cellsReceptor 6Synaptic plasticityDR6 expressionSynapse formationEarly increaseNeurons
2014
Fluorescent Measurement of Synaptic Activity Using SynaptopHluorin in Isolated Hippocampal Neurons.
Li H, Park HA, Jonas EA. Fluorescent Measurement of Synaptic Activity Using SynaptopHluorin in Isolated Hippocampal Neurons. Bio-protocol 2014, 4 PMID: 27446978, PMCID: PMC4950945, DOI: 10.21769/bioprotoc.1304.Peer-Reviewed Original Research
2012
Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency
Alavian KN, Dworetzky SI, Bonanni L, Zhang P, Sacchetti S, Mariggio MA, Onofrj M, Thomas A, Li H, Mangold JE, Signore AP, DeMarco U, Demady DR, Nabili P, Lazrove E, Smith PJ, Gribkoff VK, Jonas EA. Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency. Brain Research 2012, 1446: 1-11. PMID: 22364637, PMCID: PMC3746080, DOI: 10.1016/j.brainres.2012.01.046.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAdrenergic beta-AntagonistsAnalysis of VarianceAnimalsBiophysical PhenomenaBrainCell SurvivalCells, CulturedCyclosporineDose-Response Relationship, DrugEnergy MetabolismEnzyme InhibitorsHumansMaleMembrane Potential, MitochondrialMiceMitochondriaMitochondrial MembranesNeuroblastomaNeuronsOligopeptidesOxygen ConsumptionPatch-Clamp TechniquesPropranololRatsRats, Sprague-DawleyConceptsAmyotrophic lateral sclerosisParkinson's diseaseRisk of deathChronic neurological disorderLateral sclerosisInefficient energy productionNeurological disordersMitochondrial dysfunctionMembrane currentsDiseaseCellular energy productionDysfunctional mitochondriaCellular stressSclerosisDysfunctionDexpramipexoleInjuryNeurons
2003
Modulation of mitochondrial function by endogenous Zn2+ pools
Sensi SL, Ton-That D, Sullivan PG, Jonas EA, Gee KR, Kaczmarek LK, Weiss JH. Modulation of mitochondrial function by endogenous Zn2+ pools. Proceedings Of The National Academy Of Sciences Of The United States Of America 2003, 100: 6157-6162. PMID: 12724524, PMCID: PMC156342, DOI: 10.1073/pnas.1031598100.Peer-Reviewed Original ResearchConceptsDirect patch-clamp recordingsCultured cortical neuronsPatch-clamp recordingsCertain brain regionsNeuronal injuryPool of intracellularCortical neuronsIntact neuronsReactive oxygen species generationPostsynaptic neuronsClamp recordingsSynaptic spacePotent effectsBrain regionsOxygen species generationBrain mitochondriaMitochondrial poolMembrane depolarizationNeuronsRecent evidenceFurther studiesMitochondrial functionROS generationNovel evidenceSpecies generationBAK Alters Neuronal Excitability and Can Switch from Anti- to Pro-Death Function during Postnatal Development
Fannjiang Y, Kim CH, Huganir RL, Zou S, Lindsten T, Thompson CB, Mito T, Traystman RJ, Larsen T, Griffin DE, Mandir AS, Dawson TM, Dike S, Sappington AL, Kerr DA, Jonas EA, Kaczmarek LK, Hardwick JM. BAK Alters Neuronal Excitability and Can Switch from Anti- to Pro-Death Function during Postnatal Development. Developmental Cell 2003, 4: 575-585. PMID: 12689595, DOI: 10.1016/s1534-5807(03)00091-1.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAnimals, NewbornApoptosisBcl-2 Homologous Antagonist-Killer ProteinCentral Nervous SystemCentral Nervous System DiseasesCentral Nervous System Viral DiseasesDisease Models, AnimalEpilepsyExcitatory Postsynaptic PotentialsGenetic VectorsHippocampusKainic AcidMaleMembrane ProteinsMiceMice, KnockoutNeurodegenerative DiseasesNeuronsNeurotoxinsProtein Structure, TertiarySindbis VirusStrokeSynaptic TransmissionConceptsNeuronal excitabilityVirus infectionPostnatal developmentAlters neuronal excitabilityKainate-induced seizuresSpinal cord neuronsIschemia/strokeSindbis virus infectionNeuronal injuryCord neuronsNeuronal deathProtective effectSynaptic activityMouse modelParkinson's diseaseNeuron subtypesNeurotransmitter releasePro-death functionMiceNeuronsSpecific death stimuliDeathSeizuresPossible roleExcitability
1997
Regulation by insulin of a unique neuronal Ca2+ pool and of neuropeptide secretion
Jonas E, Knox R, Smith T, Wayne N, Connor J, Kaczmarek L. Regulation by insulin of a unique neuronal Ca2+ pool and of neuropeptide secretion. Nature 1997, 385: 343-346. PMID: 9002519, DOI: 10.1038/385343a0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBenzoquinonesCalciumCalcium ChannelsCells, CulturedCyclic AMPEndoplasmic ReticulumHeparinInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsInsulinInvertebrate HormonesLactams, MacrocyclicNeuronsNeuropeptidesProtein-Tyrosine KinasesQuinonesReceptors, Cytoplasmic and NuclearRifabutinThapsigarginConceptsIntracellular Ca2Neuropeptide secretionSpontaneous action potentialsEffect of insulinSecretion of neuropeptidesTyrosine kinase receptorsAcute riseBag cell neuronsDistal tipNeuronal dischargeNeuronal Ca2Distinct intracellular poolsCell neuronsAction potentialsCyclic AMP analogueInsulinNeuropeptidesInsulin receptorKinase receptorsSecretionPresumed siteNeuronsIntracellular poolMitochondrial Ca2Receptors
1996
Ca2+ influx and activation of a cation current are coupled to intracellular Ca2+ release in peptidergic neurons of Aplysia californica.
Knox RJ, Jonas EA, Kao LS, Smith PJ, Connor JA, Kaczmarek LK. Ca2+ influx and activation of a cation current are coupled to intracellular Ca2+ release in peptidergic neurons of Aplysia californica. The Journal Of Physiology 1996, 494: 627-639. PMID: 8865062, PMCID: PMC1160665, DOI: 10.1113/jphysiol.1996.sp021520.Peer-Reviewed Original ResearchConceptsBag cell neuronsCell neuronsThapsigargin-sensitive Ca2Cation currentReversal potentialVoltage-activated Ba2Non-selective cation currentAplysia californicaApparent reversal potentialSteady-state Ca2Thapsigargin-induced elevationMin. 3Endoplasmic reticulum Ca2Voltage-clamp experimentsMicroM tetrodotoxinPeptidergic neuronsIntact gangliaAbdominal ganglionExtracellular Ca2Intracellular Ca2Intracellular storesBAPTA-AMSmall depolarizationBasal levelsNeuronsInsulin receptor in Aplysia neurons: characterization, molecular cloning, and modulation of ion currents
Jonas E, Knox R, Kaczmarek L, Schwartz J, Solomon D. Insulin receptor in Aplysia neurons: characterization, molecular cloning, and modulation of ion currents. Journal Of Neuroscience 1996, 16: 1645-1658. PMID: 8774433, PMCID: PMC6578688, DOI: 10.1523/jneurosci.16-05-01645.1996.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAmino Acid SequenceAnimalsAplysiaBase SequenceCalcium ChannelsCloning, MolecularDNA, ComplementaryElectrophysiologyImmunohistochemistryInsulinIon ChannelsMolecular ProbesMolecular Sequence DataNeuronsPotassium ChannelsProtein-Tyrosine KinasesReceptor, InsulinTissue DistributionConceptsBag cell neuronsInsulin receptorInsulin-like peptidesImmunocytochemical staining showCell neuronsTyrosine kinase receptorsVertebrate insulinsMolecular cloningHerbimycin ATyrosine residuesTyrosine kinaseKinase receptorsInsulin-like growth factor-1Factor 1Staining showsVoltage-clamped neuronsVoltage-dependent Ca2Growth factor-1Aplysia californicaAplysia neuronsNervous systemReceptorsAction potentialsNeuronsInsulin