2025
Relative roles of HCN4 and synaptic excitation in pyramidal neuron firing rates in a hyperactive Rheb‐mTOR condition
Chatzikalymniou A, Getz S, Xu Y, Patel D, Soltesz I, Bordey A. Relative roles of HCN4 and synaptic excitation in pyramidal neuron firing rates in a hyperactive Rheb‐mTOR condition. Epilepsia 2025, 66: 3555-3570. PMID: 40512428, DOI: 10.1111/epi.18456.Peer-Reviewed Original ResearchFocal malformations of cortical developmentExcitatory postsynaptic currentsPyramidal neuronsExcitatory postsynaptic current amplitudeFiring rateMalformations of cortical developmentPyramidal cell excitabilityExcitatory synaptic inputsNeuronal firing rateAcute brain slicesSingle-cell computational modelingIncreased dendritic complexityCortical pyramidal neuronsConstitutively active RhebPostsynaptic currentsFocal malformationsSynaptic excitationNeuronal excitabilityMTOR pathway genesDe Novo somatic mutationsPostnatal dayCell excitabilityFetal developmentIncreased mTOR activitySynaptic inputsChronic Rapamycin Prevents Electrophysiological and Morphological Alterations Produced by Conditional Pten Deletion in Mouse Cortex
Hauptman J, Antonios J, Mathern G, Levine M, Cepeda C. Chronic Rapamycin Prevents Electrophysiological and Morphological Alterations Produced by Conditional Pten Deletion in Mouse Cortex. Cells 2025, 14: 79. PMID: 39851507, PMCID: PMC11764219, DOI: 10.3390/cells14020079.Peer-Reviewed Original ResearchConceptsCortical pyramidal neuronsMice treated with rapamycinGABA releasePTEN deletionWhole-cell patch-clamp recordingsMiniature inhibitory postsynaptic currentsEx vivo slicesNeuronal somatic sizeReduced neuronal firingInhibitory postsynaptic currentsChronic rapamycin treatmentPatch-clamp recordingsIncreased input resistanceInhibitory synaptic inputsDevelopmental brain disordersRapamycin treatmentIncreased membrane capacitanceConditional mouse modelChronic treatmentPostsynaptic currentsClamp recordingsNaive miceSynaptic excitationBrain disordersControl mice
2021
Effects of Altered Excitation-Inhibition Balance on Decision Making in a Cortical Circuit Model
Lam NH, Borduqui T, Hallak J, Roque A, Anticevic A, Krystal JH, Wang XJ, Murray JD. Effects of Altered Excitation-Inhibition Balance on Decision Making in a Cortical Circuit Model. Journal Of Neuroscience 2021, 42: 1035-1053. PMID: 34887320, PMCID: PMC8824494, DOI: 10.1523/jneurosci.1371-20.2021.Peer-Reviewed Original ResearchConceptsCortical circuitsCognitive deficitsCortical circuit modelAltered excitation-inhibition balanceExcitatory pyramidal neuronsNMDA receptor hypofunctionCerebral cortical circuitsExcitation-inhibition balancePyramidal neuronsReceptor hypofunctionDistinct time coursesSynaptic excitationInhibitory interneuronsMultiple neuropsychiatric disordersBehavioral deficitsSynaptic balanceSynaptic levelLatest evidenceNeuropsychiatric disordersCognitive functionCircuit mechanismsBehavioral effectsPsychometric performanceBehavioral levelTask paradigmDopaminergic mechanism underlying reward-encoding of punishment omission during reversal learning in Drosophila
McCurdy LY, Sareen P, Davoudian PA, Nitabach MN. Dopaminergic mechanism underlying reward-encoding of punishment omission during reversal learning in Drosophila. Nature Communications 2021, 12: 1115. PMID: 33602917, PMCID: PMC7893153, DOI: 10.1038/s41467-021-21388-w.Peer-Reviewed Original ResearchConceptsDopaminergic neuronsCholinergic neuronsNeural circuit mechanismsCholinergic relayDopaminergic mechanismsSynaptic excitationSynaptic reconstructionSynaptic inputsVivo functional imagingCircuit mechanismsNeuronsAversive memoryFunctional imagingOdor responsesAversive outcomesReduced activationSuch activationCircuit motifsActivationOutcomesElectric shock punishmentSensory cuesUnexpected omissionShock punishmentBehavioral analysis
2019
Preserving the balance: diverse forms of long-term GABAergic synaptic plasticity
Chiu CQ, Barberis A, Higley MJ. Preserving the balance: diverse forms of long-term GABAergic synaptic plasticity. Nature Reviews Neuroscience 2019, 20: 272-281. PMID: 30837689, DOI: 10.1038/s41583-019-0141-5.Peer-Reviewed Original ResearchConceptsGABAergic synaptic plasticityInhibitory GABAergic synapsesPostsynaptic action potentialsInhibitory synaptic strengthGABAergic synapsesSynaptic excitationLong-term plasticityGlutamatergic signalingNeuronal activitySynaptic plasticityNeuronal circuitsAction potentialsSynaptic strengthIndividual neuronsCellular mechanismsLines of evidenceBody of literaturePlasticityNeuronsFunctional stabilitySynapses
2018
Homeostatic Control of Spontaneous Activity in the Developing Auditory System
Babola TA, Li S, Gribizis A, Lee BJ, Issa JB, Wang HC, Crair MC, Bergles DE. Homeostatic Control of Spontaneous Activity in the Developing Auditory System. Neuron 2018, 99: 511-524.e5. PMID: 30077356, PMCID: PMC6100752, DOI: 10.1016/j.neuron.2018.07.004.Peer-Reviewed Original ResearchConceptsSpiral ganglion neuronsSpontaneous activityAuditory systemDirect neuronal excitationGlutamate releaseEnhanced excitabilityGanglion neuronsUnanesthetized miceSynaptic excitationHearing onsetNeuronal excitationTherapeutic approachesMouse modelSpontaneous burstsCongenital formSynchronized activityHair cellsHomeostatic mechanismsNeuronsHomeostatic controlSimilar frequencyCircuit developmentMiceInfluence developmentDeafnessInput-Specific NMDAR-Dependent Potentiation of Dendritic GABAergic Inhibition
Chiu CQ, Martenson JS, Yamazaki M, Natsume R, Sakimura K, Tomita S, Tavalin SJ, Higley MJ. Input-Specific NMDAR-Dependent Potentiation of Dendritic GABAergic Inhibition. Neuron 2018, 97: 368-377.e3. PMID: 29346754, PMCID: PMC5777295, DOI: 10.1016/j.neuron.2017.12.032.Peer-Reviewed Original ResearchConceptsDendritic inhibitionInput-specific long-term potentiationNMDA-type glutamate receptorsGABAergic inhibitory synapsesSomatostatin-expressing interneuronsGABA-A receptorsNormal brain functionLong-term potentiationForms of plasticityHomeostatic cellular mechanismsGABAergic inhibitionSynaptic excitationPerisomatic inhibitionPostsynaptic spikingInhibitory synapsesLong-term plasticityGlutamate receptorsInhibitory inputsSynaptic transmissionDependent potentiationCortical circuitsGenetic deletionBrain functionNeuronal dendritesCellular mechanisms
2016
Potentiation of Synaptic GluN2B NMDAR Currents by Fyn Kinase Is Gated through BDNF-Mediated Disinhibition in Spinal Pain Processing
Hildebrand ME, Xu J, Dedek A, Li Y, Sengar AS, Beggs S, Lombroso PJ, Salter MW. Potentiation of Synaptic GluN2B NMDAR Currents by Fyn Kinase Is Gated through BDNF-Mediated Disinhibition in Spinal Pain Processing. Cell Reports 2016, 17: 2753-2765. PMID: 27926876, DOI: 10.1016/j.celrep.2016.11.024.Peer-Reviewed Original ResearchConceptsBrain-derived neurotrophic factorN-methyl-D-aspartate receptorsLaminae INeurotrophin brain-derived neurotrophic factorPeripheral nerve injury modelSynaptic N-methyl-D-aspartate receptorsBDNF-TrkB signalingSpinal pain processingNerve injury modelChronic pain statesActivation of TrkBNMDAR dysregulationNMDAR potentiationPain amplificationPain hypersensitivityNeuropathic painPain statesPain processingNeurotrophic factorSpinal neuronsSynaptic excitationSynaptic inhibitionNMDAR currentsInjury modelPotentiation
2015
Functional Circuitry of the Retina
Demb JB, Singer JH. Functional Circuitry of the Retina. Annual Review Of Vision Science 2015, 1: 263-289. PMID: 28532365, PMCID: PMC5749398, DOI: 10.1146/annurev-vision-082114-035334.Peer-Reviewed Original ResearchGanglion cellsImportant model systemCell typesSynaptic excitationMammalian retinaParallel pathwaysMouse retinaModel systemNeural circuitryFunctional circuitryRetinaRetinal computationCellular compositionOutput neuronsBasic mechanismsApparent complexityDynamic balanceCellsStraightforward mechanismSpeciesPathwayInterneuronsMechanismNeuronsBrain
2011
Impaired α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) Receptor Trafficking and Function by Mutant Huntingtin*
Mandal M, Wei J, Zhong P, Cheng J, Duffney L, Liu W, Yuen E, Twelvetrees A, Li S, Li X, Kittler J, Yan Z. Impaired α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) Receptor Trafficking and Function by Mutant Huntingtin*. Journal Of Biological Chemistry 2011, 286: 33719-33728. PMID: 21832090, PMCID: PMC3190808, DOI: 10.1074/jbc.m111.236521.Peer-Reviewed Original ResearchConceptsMiniature excitatory postsynaptic currentsMouse modelMutant huntingtinAMPAR-mediated synaptic transmissionHuntington Disease PathophysiologyAMPAR-mediated miniature excitatory postsynaptic currentsExcitatory postsynaptic currentsTransgenic mouse modelHD mouse modelsIsoxazolepropionic acid receptor (AMPAR) traffickingReceptor traffickingAMPA receptor traffickingPolyQ-httGlutamatergic transmissionPostsynaptic currentsSynaptic excitationSynaptic transmissionAMPA receptorsWild-type huntingtinNeuronal culturesDisease pathophysiologySynaptic functionAMPAR traffickingΑ-aminoDiminished strength
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