2012
De novo gain-of-function KCNT1 channel mutations cause malignant migrating partial seizures of infancy
Barcia G, Fleming MR, Deligniere A, Gazula VR, Brown MR, Langouet M, Chen H, Kronengold J, Abhyankar A, Cilio R, Nitschke P, Kaminska A, Boddaert N, Casanova JL, Desguerre I, Munnich A, Dulac O, Kaczmarek LK, Colleaux L, Nabbout R. De novo gain-of-function KCNT1 channel mutations cause malignant migrating partial seizures of infancy. Nature Genetics 2012, 44: 1255-1259. PMID: 23086397, PMCID: PMC3687547, DOI: 10.1038/ng.2441.Peer-Reviewed Original Research
2010
Localization of Kv1.3 channels in presynaptic terminals of brainstem auditory neurons
Gazula V, Strumbos JG, Mei X, Chen H, Rahner C, Kaczmarek LK. Localization of Kv1.3 channels in presynaptic terminals of brainstem auditory neurons. The Journal Of Comparative Neurology 2010, 518: 3205-3220. PMID: 20575068, PMCID: PMC2894291, DOI: 10.1002/cne.22393.Peer-Reviewed Original ResearchConceptsPresynaptic terminalsBrainstem auditory neuronsPattern of stainingMNTB neuronsPrincipal neuronsSynaptic markersTrapezoid bodyCochlear nucleusAfferent inputAxonal stainingMedial nucleusAuditory brainstemPresynaptic endingsOlfactory bulbAuditory neuronsPotassium channel genesTonotopic axisTonotopic gradientNeuronsKv1.3 channelsProminent labelingPrincipal cellsAuditory stimuliKv1 familyKv1.3The Slack Sodium-Activated Potassium Channel Provides a Major Outward Current in Olfactory Neurons of Kv1.3−/− Super-Smeller Mice
Lu S, Das P, Fadool DA, Kaczmarek LK. The Slack Sodium-Activated Potassium Channel Provides a Major Outward Current in Olfactory Neurons of Kv1.3−/− Super-Smeller Mice. Journal Of Neurophysiology 2010, 103: 3311-3319. PMID: 20393063, PMCID: PMC2888249, DOI: 10.1152/jn.00607.2009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBiophysicsCardiovascular AgentsCells, CulturedElectric StimulationGene Expression RegulationIn Vitro TechniquesKv1.3 Potassium ChannelMembrane PotentialsMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeuronsOlfactory BulbPatch-Clamp TechniquesPotassium ChannelsPotassium Channels, Sodium-ActivatedPyrimidinesRNA InterferenceSodium Channel BlockersTetrodotoxinTransfectionConceptsMitral cellsOlfactory bulbOutward currentsOlfactory neuronsWildtype animalsPotassium channelsMajor outward currentVoltage-clamp recordingsVoltage-dependent potassium channelsNet outward currentIntracellular sodiumOB slicesPotassium channel genesCompensatory increaseFiring patternsWestern blottingRNA interference approachPrimary culturesEnhanced expressionDetection of odorsSame treatmentChannel genesMiceNeuronsOlfactory phenotypes
2004
Loss of Kv3.1 Tonotopicity and Alterations in cAMP Response Element-Binding Protein Signaling in Central Auditory Neurons of Hearing Impaired Mice
von Hehn CA, Bhattacharjee A, Kaczmarek LK. Loss of Kv3.1 Tonotopicity and Alterations in cAMP Response Element-Binding Protein Signaling in Central Auditory Neurons of Hearing Impaired Mice. Journal Of Neuroscience 2004, 24: 1936-1940. PMID: 14985434, PMCID: PMC6730406, DOI: 10.1523/jneurosci.4554-03.2004.Peer-Reviewed Original ResearchMeSH KeywordsAcoustic StimulationAge FactorsAnimalsAuditory PathwaysBrain StemCerebellumCyclic AMP Response Element-Binding ProteinDisease ProgressionMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, Inbred DBANeuronsNeuropeptidesPhosphorylationPotassium ChannelsPotassium Channels, Voltage-GatedPresbycusisReflex, StartleShaw Potassium ChannelsConceptsCAMP response element-binding proteinResponse element-binding proteinTonotopic axisBL/6 miceElement-binding proteinCochlear hair cell lossPCREB-positive cellsAuditory brainstem neuronsCentral auditory neuronsHair cell lossCBA/JTranscription factor cAMP response element-binding proteinBrainstem neuronsKv3.1 potassium channel geneTrapezoid bodyImpaired miceMedial nucleusAuditory brainstemImmunopositive cellsAuditory neuronsMedial endPotassium channel genesGood hearingCell lossCREB expression
1999
Shaw‐like potassium currents in the auditory rhombencephalon throughout embryogenesis
Hendriks R, Morest D, Kaczmarek L. Shaw‐like potassium currents in the auditory rhombencephalon throughout embryogenesis. Journal Of Neuroscience Research 1999, 58: 791-804. PMID: 10583910, DOI: 10.1002/(sici)1097-4547(19991215)58:6<791::aid-jnr6>3.0.co;2-3.Peer-Reviewed Original ResearchConceptsPotassium currentNucleus magnocellularisOutward currentsWhole-cell patch recordingsInitial transient componentTransient outward currentsEarly neuronal developmentEarly neuronal differentiationHigh activation thresholdFirst synapsesAuditory nucleiPatch recordingsPotassium channel genesSynaptic functionCharacteristic response propertiesSynapses formNeuronal developmentNeuronal differentiationActivation thresholdDevelopmental appearanceTetraethylammoniumMagnocellularisEarly ageChannel genesNeuroblastsCell Type‐Specific Expression of the Kv3.1 Gene Is Mediated by a Negative Element in the 5′ Untranslated Region of the Kv3.1 Promoter
Gan L, Hahn S, Kaczmarek L. Cell Type‐Specific Expression of the Kv3.1 Gene Is Mediated by a Negative Element in the 5′ Untranslated Region of the Kv3.1 Promoter. Journal Of Neurochemistry 1999, 73: 1350-1362. PMID: 10501178, DOI: 10.1046/j.1471-4159.1999.0731350.x.Peer-Reviewed Original ResearchMeSH Keywords3T3 Cells5' Untranslated RegionsAnimalsBase SequenceBeta-GalactosidaseBrainCell LineCHO CellsCloning, MolecularCricetinaeGene Expression RegulationGliomaHumansMiceMice, TransgenicMolecular Sequence DataNeuropeptidesOrgan SpecificityPC12 CellsPotassium ChannelsPotassium Channels, Voltage-GatedPromoter Regions, GeneticRatsRecombinant Fusion ProteinsRegulatory Sequences, Nucleic AcidRNA, MessengerShaw Potassium ChannelsTranscription, GeneticTransfectionConceptsType-specific expressionUntranslated regionCell type-specific enhancersCell type-specific expressionCell linesTissue-specific expressionThymidine kinase promoterCell-type specificityTransient transfection assaysKv3.1 potassium channel genePotassium channel genesKv3.1 geneDifferent tissue originsRegulatory fragmentDeletion analysisRegulatory regionsTranscriptional mechanismsTransgenic miceTransfection assaysKinase promoterFunctional analysisChannel genesType specificityPromoterGenes
1998
Formation of intermediate-conductance calcium-activated potassium channels by interaction of Slack and Slo subunits
Joiner W, Tang M, Wang L, Dworetzky S, Boissard C, Gan L, Gribkoff V, Kaczmarek L. Formation of intermediate-conductance calcium-activated potassium channels by interaction of Slack and Slo subunits. Nature Neuroscience 1998, 1: 462-469. PMID: 10196543, DOI: 10.1038/2176.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsElectric ConductivityIntermediate-Conductance Calcium-Activated Potassium ChannelsIsomerismLarge-Conductance Calcium-Activated Potassium ChannelsMolecular Sequence DataNerve Tissue ProteinsPotassium ChannelsPotassium Channels, Calcium-ActivatedPotassium Channels, Sodium-ActivatedConceptsCalcium-activated potassium channelsIntracellular calciumNervous systemIntermediate-conductance calcium-activated potassium channelsPotassium channelsLarge-conductance calcium-activated potassium channelsControl of excitabilitySlo subunitIntermediate conductance channelPotassium channel genesPharmacological propertiesIntermediate conductanceCytoplasmic calciumChannel subunitsSlo channelsSlack channelsChannel genesSingle-channel conductanceUnitary conductanceCalciumExcitabilitySLOSecretionWhen, where, and how much? Expression of the Kv3.1 potassium channel in high‐frequency firing neurons
Gan L, Kaczmarek L. When, where, and how much? Expression of the Kv3.1 potassium channel in high‐frequency firing neurons. Developmental Neurobiology 1998, 37: 69-79. PMID: 9777733, DOI: 10.1002/(sici)1097-4695(199810)37:1<69::aid-neu6>3.0.co;2-6.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsAuditory brain stem neuronsVoltage-dependent potassium currentsBrain stem neuronsHigh-frequency firing neuronsKv3.1 potassium channelStem neuronsKv3.1 potassium channel geneLong-term regulationSynaptic inputsPotassium currentPotassium channel genesNeuronsPotassium channelsKv3.1 geneKv3.1 subunitsFiring neuronsHigh frequencyChannel genesCurrent knowledgeChannels altersTranscriptional mechanismsCell-type specificityExpressionGene transcriptionExtrinsic factorsThe Expression of Two Splice Variants of the Kv3.1 Potassium Channel Gene Is Regulated by Different Signaling Pathways
Liu S, Kaczmarek L. The Expression of Two Splice Variants of the Kv3.1 Potassium Channel Gene Is Regulated by Different Signaling Pathways. Journal Of Neuroscience 1998, 18: 2881-2890. PMID: 9526005, PMCID: PMC6792597, DOI: 10.1523/jneurosci.18-08-02881.1998.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsCerebellumFibroblast Growth FactorsGene Expression Regulation, DevelopmentalMembrane PotentialsNerve Growth FactorsNeuropeptidesPotassium ChannelsPotassium Channels, Voltage-GatedProtein Kinase CRatsRats, Sprague-DawleyRNA, MessengerSecond Messenger SystemsShaw Potassium ChannelsSignal TransductionTranscription, GeneticConceptsDifferent signaling pathwaysKv3.1 potassium channel genePotassium channel genesBasic fibroblast growth factorChannel genesSignaling pathwaysNuclear protein kinase C activityMRNA levelsDifferent channel proteinsProtein kinase C inhibitorProtein kinase C activityKinase C inhibitorKinase C activityAlternative splicingNuclear RNAChannel proteinsMolecular mechanismsFibroblast growth factorDifferential regulationDevelopmental stagesSplice variantsC inhibitorPKC activityC activityGenes