2020
Mechanisms underlying auditory processing deficits in Fragile X syndrome
McCullagh EA, Rotschafer SE, Auerbach BD, Klug A, Kaczmarek LK, Cramer KS, Kulesza RJ, Razak KA, Lovelace JW, Lu Y, Koch U, Wang Y. Mechanisms underlying auditory processing deficits in Fragile X syndrome. The FASEB Journal 2020, 34: 3501-3518. PMID: 32039504, PMCID: PMC7347277, DOI: 10.1096/fj.201902435r.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAuditory PerceptionAutism Spectrum DisorderFragile X SyndromeHumansModels, BiologicalConceptsAuditory dysfunctionAutism spectrum disorderAuditory brainstem circuitsFragile X syndromeAuditory processing deficitsCommon monogenetic causeNetwork hyperexcitabilityBrainstem circuitsAuditory pathwayAuditory cortexNeuronal plasticityAnimal modelsAuditory hypersensitivitySynaptic developmentHyperacusisMonogenetic causeDysfunctionX syndromeAberrant synaptic developmentBody of dataUnderlying mechanismMultiple mechanismsHuman therapySyndromeProcessing deficits
2017
Pharmacological modulation of Kv3.1 mitigates auditory midbrain temporal processing deficits following auditory nerve damage
Chambers AR, Pilati N, Balaram P, Large CH, Kaczmarek LK, Polley DB. Pharmacological modulation of Kv3.1 mitigates auditory midbrain temporal processing deficits following auditory nerve damage. Scientific Reports 2017, 7: 17496. PMID: 29235497, PMCID: PMC5727503, DOI: 10.1038/s41598-017-17406-x.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsAuditory PathwaysAuditory PerceptionCochlear NerveCompulsive BehaviorDisease Models, AnimalImidazolesMembrane Transport ModulatorsMesencephalonMiceModels, BiologicalNeuronsOuabainPyrimidinesRecovery of FunctionShaw Potassium ChannelsTissue Culture TechniquesVestibulocochlear Nerve DiseasesConceptsTemporal processing deficitsAuditory nerve damageCochlear nerve synapsesTemporal sound featuresCentral auditory pathwayAuditory brainstem neuronsPromising therapeutic approachPatch-clamp recordingsOtotoxic drug exposurePrecise temporal codingTemporal firing patternsHigh-threshold channelsVoltage-gated potassium channelsProcessing deficitsNerve damageBrainstem neuronsAfferent inputCentral neuronsDrug exposureAfferent synapsesContralateral earSystemic injectionCompensatory plasticityTherapeutic approachesAuditory cortex
2008
Repetitive Firing Triggers Clustering of Kv2.1 Potassium Channels in Aplysia Neurons*
Zhang Y, McKay SE, Bewley B, Kaczmarek LK. Repetitive Firing Triggers Clustering of Kv2.1 Potassium Channels in Aplysia Neurons*. Journal Of Biological Chemistry 2008, 283: 10632-10641. PMID: 18276591, DOI: 10.1074/jbc.m800253200.Peer-Reviewed Original ResearchConceptsBag cell neuronsKv2.1 channelsPotassium channelsPlasma membraneC-terminusKv2.1 clustersKv2.1 potassium channelCell neuronsMammalian neuronsReproductive behaviorRectifier potassium channelFrequency-dependent broadeningRapid redistributionAplysia neuronsClamp recordingsAcid peptidePartial inactivationRing-like clustersPhysiological changesKv2.1Neuronal excitabilityCentral nervous systemAction potentialsGenesNervous system
2006
Non-conducting functions of voltage-gated ion channels
Kaczmarek LK. Non-conducting functions of voltage-gated ion channels. Nature Reviews Neuroscience 2006, 7: 761-771. PMID: 16988652, DOI: 10.1038/nrn1988.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Adhesion MoleculesCell Physiological PhenomenaCytoskeletonHumansIon ChannelsModels, BiologicalSignal TransductionConceptsMitogen-activated protein kinaseΒ-subunitProtein kinaseIntrinsic protein kinase activityTRP familyΑ-subunitNon-conducting functionCell-cell adhesionTranscription factor activityDependent protein kinase IIProtein kinase activityLarge extracellular domainCell proliferationSynaptic release machineryTranscription factor CREBProtein kinase IIVoltage-gated ion channelsKey PointsIn additionMAPK/ERKIntrinsic enzyme activityNon-selective cation channelsCell adhesion moleculeReductase functionC-terminusKinase activityPolicing the Ball: A New Potassium Channel Subunit Determines Inactivation Rate
Kaczmarek LK. Policing the Ball: A New Potassium Channel Subunit Determines Inactivation Rate. Neuron 2006, 49: 642-644. PMID: 16504937, DOI: 10.1016/j.neuron.2006.02.011.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsHumansKv1.2 Potassium ChannelMembrane PotentialsModels, BiologicalNeural InhibitionProtein Subunits
2004
The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity
Xu J, Wang P, Li Y, Li G, Kaczmarek LK, Wu Y, Koni PA, Flavell RA, Desir GV. The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 3112-3117. PMID: 14981264, PMCID: PMC365752, DOI: 10.1073/pnas.0308450100.Peer-Reviewed Original ResearchMeSH KeywordsAdipose TissueAnimalsBiological TransportFastingGlucoseInsulinInterleukin-6JNK Mitogen-Activated Protein KinasesKineticsKv1.3 Potassium ChannelMaleMiceMice, Inbred C57BLMice, KnockoutMice, ObeseMitogen-Activated Protein KinasesModels, BiologicalMuscle, SkeletalPotassium ChannelsPotassium Channels, Voltage-GatedTumor Necrosis Factor-alphaConceptsKv1.3-/- micePeripheral glucose homeostasisPeripheral insulin sensitivityPlasma membraneGene inactivationInsulin sensitivityAmount of GLUT4Skeletal muscleTerminal kinase (JNK) activityGlucose homeostasisAdipose tissueLower blood insulin levelsVoltage-gated potassium channelsInsulin-stimulated glucose uptakeVoltage-gated potassium channel Kv1.3Tumor necrosis factor productionExperimental autoimmune encephalitisBlood insulin levelsHigh-fat dietPotassium channel Kv1.3Tumor necrosis factor secretionPeripheral T lymphocytesKinase activityNecrosis factor productionNumber of tissues
1998
Activation 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
1991
The molecular biology of K+ channels
Perney T, Kaczmarek L. The molecular biology of K+ channels. Current Opinion In Cell Biology 1991, 3: 663-670. PMID: 1772658, DOI: 10.1016/0955-0674(91)90039-2.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements