2005
Aminoglycosides block the Kv3.1 potassium channel and reduce the ability of inferior colliculus neurons to fire at high frequencies
Liu S, Kaczmarek LK. Aminoglycosides block the Kv3.1 potassium channel and reduce the ability of inferior colliculus neurons to fire at high frequencies. Developmental Neurobiology 2005, 62: 439-452. PMID: 15547932, DOI: 10.1002/neu.20112.Peer-Reviewed Original ResearchConceptsInferior colliculus neuronsKv3.1 potassium channelColliculus neuronsKv3.1 currentsHearing lossAuditory neuronsPotassium channelsInhibition of Kv3.1Progressive hearing lossRate of repolarizationAuditory nucleiPotassium currentFiring propertiesPipette solutionAction potentialsNeuronsHigh frequencyEffect of streptomycinExtracellular TEAKv3.1 geneKv3.1 channelsAminoglycoside antibioticsStreptomycinKv3.1Presence of streptomycin
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
2003
Modulation of the Kv3.1b Potassium Channel Isoform Adjusts the Fidelity of the Firing Pattern of Auditory Neurons
Macica CM, von Hehn CA, Wang LY, Ho CS, Yokoyama S, Joho RH, Kaczmarek LK. Modulation of the Kv3.1b Potassium Channel Isoform Adjusts the Fidelity of the Firing Pattern of Auditory Neurons. Journal Of Neuroscience 2003, 23: 1133-1141. PMID: 12598601, PMCID: PMC6742259, DOI: 10.1523/jneurosci.23-04-01133.2003.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsBrain StemCells, CulturedCHO CellsCricetinaeElectric ConductivityEvoked Potentials, AuditoryKineticsMiceMice, KnockoutNeuronsNeuropeptidesPatch-Clamp TechniquesPhosphorylationPotassium ChannelsPotassium Channels, Voltage-GatedProtein IsoformsProtein Kinase CSerineShaw Potassium ChannelsTetradecanoylphorbol AcetateConceptsTrapezoid bodyMedial nucleusAuditory neuronsHigh-frequency stimulationWild-type neuronsKv3.1 potassium channelHigh-threshold componentPotassium channel isoformsGreat temporal precisionPartial decreaseProtein kinase C activationAction potentialsLocation of soundsMice resultsFiring patternsNeuronsSensory stimulationPotassium channelsChannel isoformsKinase C activationKv3.1Kv3.1 geneStimulationHigh frequencyProtein kinase C
2001
Presynaptic target of Ca2+ action on neuropeptide and acetylcholine release in Aplysia californica
Ohnuma K, Whim M, Fetter R, Kaczmarek L, Zucker R. Presynaptic target of Ca2+ action on neuropeptide and acetylcholine release in Aplysia californica. The Journal Of Physiology 2001, 535: 647-662. PMID: 11559764, PMCID: PMC2278817, DOI: 10.1111/j.1469-7793.2001.00647.x.Peer-Reviewed Original ResearchConceptsSensory neuronsCholinergic synapsesPeptidergic synapsesAcetylcholine releasePostsynaptic responsesAction potentialsMost synaptic contactsIntracellular calcium concentrationPeptidergic vesiclesSingle action potentialAplysia californicaDose-response curveDense-core vesiclesNeuron B2Neuron B3Cholinergic transmissionSynaptic contactsLinear dose-response curvePostsynaptic neuronsPresynaptic neuronsCholinergic releasePresynaptic targetCholinergic vesiclesReleasable poolPatch pipetteLocalization of two high‐threshold potassium channel subunits in the rat central auditory system
Li W, Kaczmarek L, Perney T. Localization of two high‐threshold potassium channel subunits in the rat central auditory system. The Journal Of Comparative Neurology 2001, 437: 196-218. PMID: 11494252, DOI: 10.1002/cne.1279.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAuditory PathwaysCochlear NucleusFemaleGene ExpressionGeniculate BodiesImmunohistochemistryIn Situ HybridizationInferior ColliculiNeuronsNeuropeptidesOligonucleotide ProbesOlivary NucleusPotassium ChannelsPotassium Channels, Voltage-GatedRatsRats, Sprague-DawleyRNA, MessengerShaw Potassium ChannelsConceptsAuditory neuronsKv3.1 mRNAPotassium channelsMost auditory neuronsBrainstem auditory neuronsRat central auditory systemAction potential thresholdSubpopulation of neuronsCentral auditory systemLateral superior oliveRat auditory systemAuditory systemVoltage-sensitive potassium channelsRapid deactivation kineticsPotassium channel subunitsTrapezoid bodyRat brainstemMedial nucleusVentral nucleusLateral lemniscusTerminal arborizationsSynaptic inputsAuditory nucleiSuperior oliveChannel expressionCasein Kinase 2 Determines the Voltage Dependence of the Kv3.1 Channel in Auditory Neurons and Transfected Cells
Macica C, Kaczmarek L. Casein Kinase 2 Determines the Voltage Dependence of the Kv3.1 Channel in Auditory Neurons and Transfected Cells. Journal Of Neuroscience 2001, 21: 1160-1168. PMID: 11160386, PMCID: PMC6762230, DOI: 10.1523/jneurosci.21-04-01160.2001.Peer-Reviewed Original ResearchMeSH KeywordsAlkaline PhosphataseAnimalsAuditory PathwaysBinding SitesBrain StemCasein Kinase IICDC2-CDC28 KinasesCHO CellsCricetinaeCyclin-Dependent Kinase 2Cyclin-Dependent KinasesElectric StimulationEnzyme InhibitorsIn Vitro TechniquesMembrane PotentialsNeuronsNeuropeptidesPatch-Clamp TechniquesPhosphorylationPotassium ChannelsPotassium Channels, Voltage-GatedPrecipitin TestsProtein Kinase CProtein Serine-Threonine KinasesRatsShaw Potassium ChannelsTetradecanoylphorbol AcetateTransfectionConceptsCasein kinase 2Kinase 2Casein kinase IIProtein kinase CKv3.1 channelsChinese hamster ovary cellsHamster ovary cellsConstitutive phosphorylationPhosphatase treatmentKinase IIKinase CTransfected CellsVoltage-dependent activationOvary cellsWhole-cell conductancePhosphorylationPotassium channelsRectifier channelsBiophysical characteristicsInactivationKv3.1 potassium channelVoltage dependenceActivationKv3.1Patch-clamp recordings
1999
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
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
Heterologous Expression of the Kv3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons
Whim M, Kaczmarek L. Heterologous Expression of the Kv3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons. Journal Of Neuroscience 1998, 18: 9171-9180. PMID: 9801357, PMCID: PMC6792887, DOI: 10.1523/jneurosci.18-22-09171.1998.Peer-Reviewed Original ResearchConceptsBag cell neuronsCell neuronsAction potentialsCalcium entryUse-dependent inactivationExpression of Kv3.1Kv3.1 potassium channelPeptidergic bag cell neuronsControl neuronsSpontaneous firingBrief synaptic stimulationCalcium currentNeuronal excitabilityIntracellular calciumCalcium influxSynaptic stimulationDepolarizing afterpotentialsBAPTA-AMAfterpotentialsNeuronsPotassium channelsClusters of cellsKv3.1InductionPhysiological roleDepolarization Selectively Increases the Expression of the Kv3.1 Potassium Channel in Developing Inferior Colliculus Neurons
Liu S, Kaczmarek L. Depolarization Selectively Increases the Expression of the Kv3.1 Potassium Channel in Developing Inferior Colliculus Neurons. Journal Of Neuroscience 1998, 18: 8758-8769. PMID: 9786983, PMCID: PMC6793528, DOI: 10.1523/jneurosci.18-21-08758.1998.Peer-Reviewed Original ResearchMeSH KeywordsAgingAnimalsAnimals, NewbornCalciumGene Expression Regulation, DevelopmentalIn Vitro TechniquesInferior ColliculiMembrane PotentialsNeuropeptidesPatch-Clamp TechniquesPotassiumPotassium ChannelsPotassium Channels, Voltage-GatedRatsRats, Sprague-DawleyRNA, MessengerShaw Potassium ChannelsConceptsInferior colliculus neuronsOnset of hearingColliculus neuronsCalcium influxChannel subunitsPotassium currentAction potentialsElevated external potassium concentrationCalcium channel blockersDepolarization-induced increaseSpontaneous neuronal activityNoninactivating potassium currentKv3.1 potassium channelVoltage-clamp experimentsChannel blockersNeuronal excitabilityElevated potassiumAuditory neuronsNeuronal activityExternal potassium concentrationExternal potassium ionsNeuronsPotassium channelsMRNA levelsMarked increaseWhen, 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 activityGenesActivation of Kv3.1 channels in neuronal spine-like structures may induce local potassium ion depletion
Wang L, Gan L, Perney T, Schwartz I, Kaczmarek L. Activation of Kv3.1 channels in neuronal spine-like structures may induce local potassium ion depletion. Proceedings Of The National Academy Of Sciences Of The United States Of America 1998, 95: 1882-1887. PMID: 9465111, PMCID: PMC19207, DOI: 10.1073/pnas.95.4.1882.Peer-Reviewed Original ResearchConceptsSpine-like structuresIon channelsMembrane structureMembrane compartmentsVesicle compartmentKv3.1 channelsBulk cytoplasmElectron immunomicroscopyCHO cellsPostsynaptic membraneVesiclesMembrane patchesSpine-like protrusionsNeuronal membrane structurePotassium channel Kv3.1Channel Kv3.1CellsComplete inactivationInactivationCompartmentsRapid depletionCentral nervous systemSlow refillingSynaptic stimulationNeuronal structures
1997
The Secretion of Classical and Peptide Cotransmitters from a Single Presynaptic Neuron Involves a Synaptobrevin-Like Molecule
Whim M, Niemann H, Kaczmarek L. The Secretion of Classical and Peptide Cotransmitters from a Single Presynaptic Neuron Involves a Synaptobrevin-Like Molecule. Journal Of Neuroscience 1997, 17: 2338-2347. PMID: 9065494, PMCID: PMC6573516, DOI: 10.1523/jneurosci.17-07-02338.1997.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAnimalsAplysiaCalciumCells, CulturedCoculture TechniquesElectric ConductivityGanglia, InvertebrateKineticsMagnesiumMembrane PotentialsMembrane ProteinsNerve Tissue ProteinsNeuronsNeurons, AfferentNeuropeptidesPatch-Clamp TechniquesPresynaptic TerminalsRecombinant ProteinsR-SNARE ProteinsSynapsesTetanus ToxinConceptsClassical transmittersSingle presynaptic neuronRelease of neuropeptidesSingle action potentialPresynaptic release sitesSecretion of peptidesNeuron B2Peptidergic synapsesSynaptic typesSensory neuronsPresynaptic neuronsTetanus toxinPeptide cotransmittersAction potentialsPresynaptic injectionSecretionNeuronsMolecular mechanismsSynapseTypes of transmittersB2CotransmitterNeuropeptidesPeptidesReleaseRegulation 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
Cloning and Characterization of the Promoter for a Potassium Channel Expressed in High Frequency Firing Neurons (∗)
Gan L, Perney T, Kaczmarek L. Cloning and Characterization of the Promoter for a Potassium Channel Expressed in High Frequency Firing Neurons (∗). Journal Of Biological Chemistry 1996, 271: 5859-5865. PMID: 8621457, DOI: 10.1074/jbc.271.10.5859.Peer-Reviewed Original Research3T3 Cells8-Bromo Cyclic Adenosine MonophosphateAnimalsBase SequenceBinding SitesBucladesineCell DifferentiationChloramphenicol O-AcetyltransferaseCloning, MolecularCyclic AMPDNA PrimersDNA, ComplementaryFibroblastsGene ExpressionGenomic LibraryIonomycinKineticsMiceMolecular Sequence DataNeuronsNeuropeptidesPC12 CellsPlasmidsPodophyllinPodophyllotoxinPotassium ChannelsPotassium Channels, Voltage-GatedPromoter Regions, GeneticRatsRecombinant ProteinsRegulatory Sequences, Nucleic AcidRestriction MappingSequence DeletionShaw Potassium ChannelsTransfection
1994
Autoactive peptides act at three distinct receptors to depolarize the bag cell neurons of Aplysia
Loechner K, Kaczmarek L. Autoactive peptides act at three distinct receptors to depolarize the bag cell neurons of Aplysia. Journal Of Neurophysiology 1994, 71: 195-203. PMID: 8158229, DOI: 10.1152/jn.1994.71.1.195.Peer-Reviewed Original Research
1993
The peptide FMRFa terminates a discharge in Aplysia bag cell neurons by modulating calcium, potassium, and chloride conductances
Fisher T, Lin C, Kaczmarek L. The peptide FMRFa terminates a discharge in Aplysia bag cell neurons by modulating calcium, potassium, and chloride conductances. Journal Of Neurophysiology 1993, 69: 2164-2173. PMID: 7688803, DOI: 10.1152/jn.1993.69.6.2164.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAplysiaCalcium ChannelsCells, CulturedChloride ChannelsElectric StimulationElectrophysiologyFMRFamideGangliaImmunohistochemistryIon ChannelsMembrane PotentialsMembrane ProteinsNeuritesNeuronsNeuropeptidesNeurotransmitter AgentsPotassium ChannelsStereotyped BehaviorTetradecanoylphorbol AcetateConceptsBag cell neuronsCell neuronsAction potentialsElectrical stimulationVoltage-activated calcium currentsOnset of afterdischargePowerful inhibitory influenceIntact abdominal gangliaIon substitution experimentsVoltage-clamp experimentsAfferent nervesProtein kinase C. 5Channel blockersCalcium currentPrimary cell culturesAbdominal ganglionInhibitory influenceAfterdischargesCyclic AMP analogueFMRFaOutward currentsNeuronal processesNeuronsAplysia bag cell neuronsReversal potential
1992
Recruitment of Ca2+ channels by protein kinase C during rapid formation of putative neuropeptide release sites in isolated Aplysia neurons
Knox R, Quattrocki E, Connor J, Kaczmarek L. Recruitment of Ca2+ channels by protein kinase C during rapid formation of putative neuropeptide release sites in isolated Aplysia neurons. Neuron 1992, 8: 883-889. PMID: 1316764, DOI: 10.1016/0896-6273(92)90202-o.Peer-Reviewed Original Research
1991
Neuropeptide inhibition of voltage-gated calcium channels mediated by mobilization of intracellular calcium
Kramer R, Kaczmarek L, Levitan E. Neuropeptide inhibition of voltage-gated calcium channels mediated by mobilization of intracellular calcium. Neuron 1991, 6: 557-563. PMID: 1849723, DOI: 10.1016/0896-6273(91)90058-8.Peer-Reviewed Original ResearchConceptsThyrotropin-releasing hormoneVoltage-gated calcium channelsVoltage-gated Ca2Protein kinase CInactivation of Ca2Pituitary tumor cellsVariety of agentsHormone secretionNeurotransmitter inhibitionIntracellular calciumResult of Ca2Calcium channelsIntracellular Ca2Inhibits Ca2Kinase CEndocrine cellsRoutine useTumor cellsPatch-clamp electrodesPlasma membrane channelsDependent inactivationInhibitionHormoneSecretionCa2
1990
Control of potassium currents and cyclic AMP levels by autoactive neuropeptides in Aplysia neurons
Loechner K, Kaczmarek L. Control of potassium currents and cyclic AMP levels by autoactive neuropeptides in Aplysia neurons. Brain Research 1990, 532: 1-6. PMID: 2178030, DOI: 10.1016/0006-8993(90)91733-w.Peer-Reviewed Original ResearchConceptsVoltage-dependent potassium currentsCyclic AMP levelsBag cell neuronsPotassium currentCell neuronsAMP levelsAlpha-BCPWhole-cell patch-clamp techniqueCell patch-clamp techniqueBag cell afterdischargeTransient voltage-dependent potassium currentPatch-clamp techniqueDelayed potassium currentPharmacologic elevationClamp techniqueOutward currentsAfterdischargesNeuronsCell peptidesAplysia neuronsNeuropeptidesBeta-BCPConsistent effectSecond messengerAlpha