Alpha-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 outgrowthAlpha-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 outgrowthA Bcl-xL–Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosis
Li H, Alavian KN, Lazrove E, Mehta N, Jones A, Zhang P, Licznerski P, Graham M, Uo T, Guo J, Rahner C, Duman RS, Morrison RS, Jonas EA. A Bcl-xL–Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosis. Nature Cell Biology 2013, 15: 773-785. PMID: 23792689, PMCID: PMC3725990, DOI: 10.1038/ncb2791.Peer-Reviewed Original ResearchConceptsBcl-xLVesicle retrievalProtein-protein interactionsClathrin-coated pitsProtein Bcl-xLCalmodulin-dependent mannerRecruitment of vesiclesNeurotransmitter releaseDepletion of Drp1GTPase Drp1Vesicle endocytosisEndocytic vesiclesMembrane dynamicsPlasma membraneClathrin complexMutagenesis studiesPresynaptic plasticityMitochondrial ATPATP availabilityReserve poolDrp1EndocytosisVesiclesHippocampal neuronsComplexesAn uncoupling channel within the c-subunit ring of the F1FO ATP synthase is the mitochondrial permeability transition pore
Alavian KN, Beutner G, Lazrove E, Sacchetti S, Park HA, Licznerski P, Li H, Nabili P, Hockensmith K, Graham M, Porter GA, Jonas EA. An uncoupling channel within the c-subunit ring of the F1FO ATP synthase is the mitochondrial permeability transition pore. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 10580-10585. PMID: 24979777, PMCID: PMC4115574, DOI: 10.1073/pnas.1401591111.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCell DeathHEK293 CellsHumansIon Channel GatingIon ChannelsLiposomesMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial MembranesMitochondrial Permeability Transition PoreMutationProtein ConformationProtein SubunitsProton-Translocating ATPasesRatsReactive Oxygen SpeciesConceptsMitochondrial PT poreF1Fo-ATP synthaseATP synthasePermeability transitionCell deathCellular metabolic efficiencyInner mitochondrial membrane permeabilityOxygen species-induced cell deathC subunit ringATP synthase F1Mitochondrial membrane permeabilityMitochondrial permeability transitionC subunitPT poreTight regulationATP productionMolecular identitySingle-channel conductanceChannel closureLeak channelsMPTP openingMetabolic efficiencyMembrane permeabilityHealthy cellsOsmotic shiftsBcl-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 increaseNeuronsDecreased expression of synapse-related genes and loss of synapses in major depressive disorder
Kang HJ, Voleti B, Hajszan T, Rajkowska G, Stockmeier CA, Licznerski P, Lepack A, Majik MS, Jeong LS, Banasr M, Son H, Duman RS. Decreased expression of synapse-related genes and loss of synapses in major depressive disorder. Nature Medicine 2012, 18: 1413-1417. PMID: 22885997, PMCID: PMC3491115, DOI: 10.1038/nm.2886.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsCalmodulinCell LineDepressive Disorder, MajorGATA1 Transcription FactorGene Expression ProfilingGene Expression RegulationHumansMicroarray AnalysisMicroscopy, ElectronPrefrontal CortexRab3A GTP-Binding ProteinRab4 GTP-Binding ProteinsRatsReverse Transcriptase Polymerase Chain ReactionSynapsesSynapsinsTubulinNeuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress
Son H, Banasr M, Choi M, Chae SY, Licznerski P, Lee B, Voleti B, Li N, Lepack A, Fournier NM, Lee KR, Lee IY, Kim J, Kim JH, Kim YH, Jung SJ, Duman RS. Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 11378-11383. PMID: 22733766, PMCID: PMC3396528, DOI: 10.1073/pnas.1201191109.Peer-Reviewed Original ResearchConceptsChronic unpredictable stressAntidepressant actionAtrophy of dendritesDepressive-like behaviorAntidepressant treatment responseSymptoms of depressionExpression of neuritinActivity-dependent genesAntidepressant treatmentLimbic structuresHippocampal expressionUnpredictable stressTreatment responseMood disordersBehavioral deficitsNeuronal plasticityTreatment reversesAnxiety behaviorChronic stressNeuritinDendrite branchingUnique actionHippocampusNeuroplasticityModel of stressActin/α-Actinin-Dependent Transport of AMPA Receptors in Dendritic Spines: Role of the PDZ-LIM Protein RIL
Schulz TW, Nakagawa T, Licznerski P, Pawlak V, Kolleker A, Rozov A, Kim J, Dittgen T, Köhr G, Sheng M, Seeburg PH, Osten P. Actin/α-Actinin-Dependent Transport of AMPA Receptors in Dendritic Spines: Role of the PDZ-LIM Protein RIL. Journal Of Neuroscience 2004, 24: 8584-8594. PMID: 15456832, PMCID: PMC6729893, DOI: 10.1523/jneurosci.2100-04.2004.Peer-Reviewed Original ResearchConceptsAMPA receptorsDendritic spinesLIM domain-containing proteinsDomain-containing proteinsActin-dependent mannerCultured neuronsPostsynaptic density fractionSynaptic AMPA receptorsLIM domainsPDZ domainProtein complexesActin cytoskeletonC-terminal peptideNovel regulationHeterologous cellsReceptor transportRILsExcitatory transmissionForebrain synaptosomesMiniature EPSCsSynaptic accumulationRat forebrainSynaptic sitesSynaptic surfaceReceptorsPostsynaptic excitability is necessary for strengthening of cortical sensory responses during experience-dependent development
Komai S, Licznerski P, Cetin A, Waters J, Denk W, Brecht M, Osten P. Postsynaptic excitability is necessary for strengthening of cortical sensory responses during experience-dependent development. Nature Neuroscience 2006, 9: 1125-1133. PMID: 16921372, DOI: 10.1038/nn1752.Peer-Reviewed Original ResearchConceptsSomatodendritic excitabilityExperience-dependent developmentLayer 2/3 pyramidal neuronsCortical networksSensory responsesRat somatosensory cortexNormal cortical developmentCortical sensory responsesDevelopmental strengtheningPostsynaptic excitabilityPyramidal neuronsSomatosensory cortexCortical neuronsBarrel cortexPostsynaptic neuronsCortical developmentSensory cortexSensory pathwaysSensory responsivenessSynaptic strengthExcitabilitySensory deprivationCortexNeuronsVivo recordingsA negative regulator of MAP kinase causes depressive behavior
Duric V, Banasr M, Licznerski P, Schmidt HD, Stockmeier CA, Simen AA, Newton SS, Duman RS. A negative regulator of MAP kinase causes depressive behavior. Nature Medicine 2010, 16: 1328-1332. PMID: 20953200, PMCID: PMC3066515, DOI: 10.1038/nm.2219.Peer-Reviewed Original Research