2019
Phactr1 regulates Slack (KCNT1) channels via protein phosphatase 1 (PP1)
Ali SR, Malone TJ, Zhang Y, Prechova M, Kaczmarek LK. Phactr1 regulates Slack (KCNT1) channels via protein phosphatase 1 (PP1). The FASEB Journal 2019, 34: 1591-1601. PMID: 31914597, PMCID: PMC6956700, DOI: 10.1096/fj.201902366r.Peer-Reviewed Original ResearchConceptsProtein phosphatase 1Phosphatase 1Binding of PP1C-terminusCytoplasmic signaling proteinsCytoplasmic C-terminusActin-binding proteinsSlack channelsPKC phosphorylation sitesPhosphoprotein substratesDisease-causing mutationsPhosphorylation sitesSignaling proteinsSlack currentsHuman mutationsSodium-activated potassium channelsPHACTR1Slack genePotassium channelsProteinActinMutationsPatch-clamp recordingsCentral nervous systemMutantsRole of KCNQ potassium channels in stress-induced deficit of working memory
Arnsten AFT, Jin LE, Gamo NJ, Ramos B, Paspalas CD, Morozov YM, Kata A, Bamford NS, Yeckel MF, Kaczmarek LK, El-Hassar L. Role of KCNQ potassium channels in stress-induced deficit of working memory. Neurobiology Of Stress 2019, 11: 100187. PMID: 31832507, PMCID: PMC6889760, DOI: 10.1016/j.ynstr.2019.100187.Peer-Reviewed Original ResearchStress-induced deficitsKCNQ potassium channelsKCNQ blockersPrefrontal cortexNeuronal firingLayers II/IIIRat medial prefrontal cortexStress exposurePotassium channelsRat medial PFCMedial PFCChronic stress exposurePatch-clamp recordingsPyramidal cell firingMedial prefrontal cortexSystemic administrationPyramidal cellsAged ratsLow dosePFC dysfunctionHigh dosesKCNQ channelsLow dosesCell firingCognitive function
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
2014
Disrupted in Schizophrenia 1 Modulates Medial Prefrontal Cortex Pyramidal Neuron Activity Through cAMP Regulation of Transient Receptor Potential C and Small-Conductance K+ Channels
El-Hassar L, Simen AA, Duque A, Patel KD, Kaczmarek LK, Arnsten AF, Yeckel MF. Disrupted in Schizophrenia 1 Modulates Medial Prefrontal Cortex Pyramidal Neuron Activity Through cAMP Regulation of Transient Receptor Potential C and Small-Conductance K+ Channels. Biological Psychiatry 2014, 76: 476-485. PMID: 24560582, PMCID: PMC4104266, DOI: 10.1016/j.biopsych.2013.12.019.Peer-Reviewed Original ResearchConceptsCyclic adenosine monophosphateIntracellular Ca2Prefrontal cortical pyramidal neuronsReceptor-mediated intracellular Ca2Regulation of cAMPPrefrontal cortical slicesCortical pyramidal neuronsDISC1 functionMajor depressive disorderPyramidal neuron activityPatch-clamp recordingsTRPC channel activityDISC1 disruptionPrefrontal cortex activityPyramidal neuronsCortical slicesDepressive disorderAdult ratsIntracellular calcium wavesSustained depolarizationViral knockdownNeuron activityBipolar disorderMental disordersCAMP generation
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 generation
2001
Casein 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
Role in neuronal cell migration for high‐threshold potassium currents in the chicken hindbrain
Hendriks R, Morest D, Kaczmarek L. Role in neuronal cell migration for high‐threshold potassium currents in the chicken hindbrain. Journal Of Neuroscience Research 1999, 58: 805-814. PMID: 10583911, DOI: 10.1002/(sici)1097-4547(19991215)58:6<805::aid-jnr7>3.0.co;2-v.Peer-Reviewed Original ResearchConceptsChannel blockersPotassium currentWhole-cell patch-clamp recordingsPotassium conductanceN-type calcium channelsPotassium channelsHigh-threshold potassium currentsCalcium channel blockersSensitive potassium channelsPotassium channel blockerPatch-clamp recordingsTetraethylammonium chlorideChronic blockadeNovel potassium channelNeuronal cell migrationTEA exposureCalcium channelsClamp recordingsEmbryonic neuronsSynaptic functionOutward currentsNeuronal migrationElectrical excitabilityMigratory activityIndividual neuroblasts
1998
High-frequency firing helps replenish the readily releasable pool of synaptic vesicles
Wang L, Kaczmarek L. High-frequency firing helps replenish the readily releasable pool of synaptic vesicles. Nature 1998, 394: 384-388. PMID: 9690475, DOI: 10.1038/28645.Peer-Reviewed Original ResearchConceptsReleasable poolPotassium channel blocker tetraethylammoniumChannel blocker Cd2Synaptic vesiclesPresynaptic action potentialHigh-frequency stimulationVoltage-gated Ca2Short-term synaptic depressionCentral nervous systemPatch-clamp recordingsHigh-frequency firingGiant synapsesPostsynaptic mechanismsBuffer EGTAMouse auditoryBlocker tetraethylammoniumSynaptic activitySynaptic depressionPresynaptic terminalsNervous systemAction potentialsRate of replenishmentSynapsesCa2Key signal