2021
Presynaptic Kv3 channels are required for fast and slow endocytosis of synaptic vesicles
Wu XS, Subramanian S, Zhang Y, Shi B, Xia J, Li T, Guo X, El-Hassar L, Szigeti-Buck K, Henao-Mejia J, Flavell RA, Horvath TL, Jonas EA, Kaczmarek LK, Wu LG. Presynaptic Kv3 channels are required for fast and slow endocytosis of synaptic vesicles. Neuron 2021, 109: 938-946.e5. PMID: 33508244, PMCID: PMC7979485, DOI: 10.1016/j.neuron.2021.01.006.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsCHO CellsCricetulusEndocytosisMiceMutationPresynaptic TerminalsShaw Potassium ChannelsSynaptic TransmissionSynaptic VesiclesConceptsSlow endocytosisVesicle mobilizationF-actin cytoskeletonChannel mutationsPotassium channelsKv3.3 proteinsInhibits endocytosisRapid endocytosisNovel functionF-actinEndocytosisCrucial functionSynaptic vesiclesFamily channelsSynaptic transmissionDiscovery decadesMembrane potentialNeurotransmitter releaseDiverse neurological disordersIon conductanceMutationsReleasable poolMouse nerve terminalsPotassium channel mutationsPathological effects
2016
Molecular interrogation of hypothalamic organization reveals distinct dopamine neuronal subtypes
Romanov RA, Zeisel A, Bakker J, Girach F, Hellysaz A, Tomer R, Alpár A, Mulder J, Clotman F, Keimpema E, Hsueh B, Crow AK, Martens H, Schwindling C, Calvigioni D, Bains JS, Máté Z, Szabó G, Yanagawa Y, Zhang MD, Rendeiro A, Farlik M, Uhlén M, Wulff P, Bock C, Broberger C, Deisseroth K, Hökfelt T, Linnarsson S, Horvath TL, Harkany T. Molecular interrogation of hypothalamic organization reveals distinct dopamine neuronal subtypes. Nature Neuroscience 2016, 20: 176-188. PMID: 27991900, PMCID: PMC7615022, DOI: 10.1038/nn.4462.Peer-Reviewed Original ResearchMetabolism and Mental Illness
Sestan-Pesa M, Horvath TL. Metabolism and Mental Illness. Trends In Molecular Medicine 2016, 22: 174-183. PMID: 26776095, DOI: 10.1016/j.molmed.2015.12.003.Peer-Reviewed Original ResearchConceptsCentral nervous systemMental illnessBasic metabolic principlesHigher brain functionsCerebral cortexNovel therapiesNervous systemBrain functionSystemic controlPathological conditionsIllnessAppetiteCrucial regulatorFuture research strategiesOverwhelming evidenceMetabolic principlesFeeding behaviorMetabolismHypothalamusTherapyCortexBrain
2015
Synaptic lipids in cortical function and psychiatric disorders
Stutz B, Horvath TL. Synaptic lipids in cortical function and psychiatric disorders. EMBO Molecular Medicine 2015, 8: 3-5. PMID: 26671988, PMCID: PMC4718156, DOI: 10.15252/emmm.201505749.Peer-Reviewed Original ResearchConceptsPsychiatric disordersClinical therapeutic strategiesPathophysiologic mechanismsCortical circuitryCortical functionExcitatory neuronsTherapeutic strategiesAnimal modelsReliable biomarkersPsychiatric diseasesPsychiatric consequencesEMBO Molecular MedicinePsychiatric conditionsMillions of peopleHuman subjectsCircuit functionDisordersLipidsMolecular medicinePatientsPathophysiologyEtiologyDiseaseMiceNeurons
2014
Role of Synaptic Plasticity and EphA5-EphrinA5 Interaction Within the Ventromedial Hypothalamus in Response to Recurrent Hypoglycemia
Szepietowska B, Horvath TL, Sherwin RS. Role of Synaptic Plasticity and EphA5-EphrinA5 Interaction Within the Ventromedial Hypothalamus in Response to Recurrent Hypoglycemia. Diabetes 2014, 63: 1140-1147. PMID: 24222347, PMCID: PMC3931406, DOI: 10.2337/db13-1259.Peer-Reviewed Original ResearchConceptsRecurrent hypoglycemiaVentromedial hypothalamusEphA5 receptorNondiabetic ratsCounterregulatory responsesSynaptic plasticityAntecedent recurrent hypoglycemiaCounterregulatory hormone releaseDefective glucose counterregulationExpression of ephrinA5Counterregulatory hormone responsesIntensive insulin treatmentInsulin-induced hypoglycemiaHyperinsulinemic-hypoglycemic clamp studyGlucose infusion rateHypoglycemic clamp studiesGlucose counterregulationSynaptic coverageHypoglycemic stimulusGlucagon secretionGlucagon releaseAcute hypoglycemiaInsulin treatmentHormone releaseInfusion rate
2010
Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity
Horvath TL, Sarman B, García-Cáceres C, Enriori PJ, Sotonyi P, Shanabrough M, Borok E, Argente J, Chowen JA, Perez-Tilve D, Pfluger PT, Brönneke HS, Levin BE, Diano S, Cowley MA, Tschöp MH. Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 14875-14880. PMID: 20679202, PMCID: PMC2930476, DOI: 10.1073/pnas.1004282107.Peer-Reviewed Original ResearchConceptsHigh-fat dietSynaptic input organizationReactive gliosisPOMC neuronsDIO ratsDR ratsArcuate nucleusMelanocortin systemPOMC cellsNeuropeptide Y cellsInput organizationLoss of synapsesDiet-induced obesityBlood-brain barrierHFD-fed animalsDIO animalsAnorexigenic proopiomelanocortinGlial ensheathmentSynaptic organizationInhibitory inputsLean ratsDR animalsNeuronal circuitsCell bodiesGliosis
2007
Anticonvulsant effects of leptin in epilepsy
Diano S, Horvath TL. Anticonvulsant effects of leptin in epilepsy. Journal Of Clinical Investigation 2007, 118: 26-28. PMID: 18097479, PMCID: PMC2147676, DOI: 10.1172/jci34511.Peer-Reviewed Original ResearchMeSH Keywords4-AminopyridineAdministration, IntranasalAlpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsConvulsantsHypothalamusJanus Kinase 2LeptinMaleMiceMice, KnockoutNeuronsPentylenetetrazolePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPotassium Channel BlockersPotassium Channels, Voltage-GatedRatsRats, Sprague-DawleyReceptors, AMPAReceptors, LeptinSeizuresSynaptic TransmissionConceptsPeripheral metabolic hormonesTreatment of epilepsyRodent seizure modelsHigher brain functionsAnticonvulsant effectsSeizure modelGlutamate neurotransmissionHormone leptinMetabolic hormonesTherapeutic approachesMetabolic disordersNasal epitheliumLeptinAdipose tissueEpileptic seizuresTherapeutic potentialEnergy homeostasisBrain functionNeuronal processesFat storesEpilepsySeizuresEnergy metabolismCritical regulatorDirect effect
2006
Ghrelin controls hippocampal spine synapse density and memory performance
Diano S, Farr SA, Benoit SC, McNay EC, da Silva I, Horvath B, Gaskin FS, Nonaka N, Jaeger LB, Banks WA, Morley JE, Pinto S, Sherwin RS, Xu L, Yamada KA, Sleeman MW, Tschöp MH, Horvath TL. Ghrelin controls hippocampal spine synapse density and memory performance. Nature Neuroscience 2006, 9: 381-388. PMID: 16491079, DOI: 10.1038/nn1656.Peer-Reviewed Original ResearchConceptsHippocampal spine synapse densitySpine synapse densitySpine synapse formationGrowth hormone releaseNovel therapeutic strategiesLong-term potentiationHigher brain functionsEnhanced spatial learningGut hormonesGhrelin administrationHypothalamic actionSynapse densitySpine synapsesCA1 regionHormone releaseNeuropeptide ghrelinGhrelin bindingHippocampal formationTherapeutic strategiesMelanocortin systemGhrelinBrain areasMetabolic controlSynaptic changesSynaptic plasticityUncoupling protein 2/3 immunoreactivity and the ascending dopaminergic and noradrenergic neuronal systems: Relevance for volume transmission
Rivera A, Agnati LF, Horvath TL, Valderrama JJ, de La Calle A, Fuxe K. Uncoupling protein 2/3 immunoreactivity and the ascending dopaminergic and noradrenergic neuronal systems: Relevance for volume transmission. Neuroscience 2006, 137: 1447-1461. PMID: 16387447, DOI: 10.1016/j.neuroscience.2005.05.051.Peer-Reviewed Original ResearchConceptsConfocal laser microscopy analysisReactive oxygen species productionLaser microscopy analysisProtein 2/3Oxygen species productionUncouple oxidative phosphorylationOxidative phosphorylationATP synthesisProteinSpecies productionDouble immunolabelingImportant roleMicroscopy analysisPhosphorylationMitochondriaRegulationCell groupsPlastic changesLocalizationIslandsAnimal modelsMagnaTyrosine hydroxylaseNeuronal systems
2005
Mitochondrial uncoupling proteins in the cns: in support of function and survival
Andrews ZB, Diano S, Horvath TL. Mitochondrial uncoupling proteins in the cns: in support of function and survival. Nature Reviews Neuroscience 2005, 6: 829-840. PMID: 16224498, DOI: 10.1038/nrn1767.Peer-Reviewed Original ResearchConceptsNeuronal functionNeurological disordersTraumatic brain injuryAmyotrophic lateral sclerosisClinical treatment strategiesMitochondrial calcium influxModels of neurodegenerationMitochondrial uncouplingFree radical productionReactive oxygen species productionNeuronal deteriorationNeuronal deathSubstantia nigraBrain injurySpinal cordVentral tegmentumTreatment strategiesOxygen species productionNeuronal microenvironmentSynaptic transmissionCalcium influxLimbic systemNeurological conditionsLateral sclerosisParkinson's disease
2004
Dynamics of volume transmission in the brain. Focus on catecholamine and opioid peptide communication and the role of uncoupling protein 2
Fuxe K, Rivera A, Jacobsen KX, Höistad M, Leo G, Horvath TL, Staines W, De la Calle A, Agnati LF. Dynamics of volume transmission in the brain. Focus on catecholamine and opioid peptide communication and the role of uncoupling protein 2. Journal Of Neural Transmission 2004, 112: 65-76. PMID: 15599605, DOI: 10.1007/s00702-004-0158-3.Peer-Reviewed Original Research
1998
An Alternate Pathway for Visual Signal Integration into the Hypothalamo-Pituitary Axis: Retinorecipient Intergeniculate Neurons Project to Various Regions of the Hypothalamus and Innervate Neuroendocrine Cells Including Those Producing Dopamine
Horvath TL. An Alternate Pathway for Visual Signal Integration into the Hypothalamo-Pituitary Axis: Retinorecipient Intergeniculate Neurons Project to Various Regions of the Hypothalamus and Innervate Neuroendocrine Cells Including Those Producing Dopamine. Journal Of Neuroscience 1998, 18: 1546-1558. PMID: 9454860, PMCID: PMC6792709, DOI: 10.1523/jneurosci.18-04-01546.1998.Peer-Reviewed Original ResearchConceptsHypothalamo-pituitary axisIntergeniculate leafletNeuroendocrine cellsSuprachiasmatic nucleusHypothalamic dopamine neuronsMedial preoptic areaFenestrated capillariesPopulations of neuronsNeurons projectBilateral enucleationHypothalamic projectionsDistal dendritesRetrograde tracerVentromedial nucleusDopamine neuronsIntraperitoneal injectionProjection sitesPeriventricular nucleusPreoptic areaRetinal fibersTract tracingHypothalamic cellsRetinal axonsSynaptic targetsEfferents
1997
Control of gonadotropin feedback: The possible role of estrogen-induced hypothalamic synaptic plasticity
Horvath TL, Garcia-segura LM, Naftolin F. Control of gonadotropin feedback: The possible role of estrogen-induced hypothalamic synaptic plasticity. Gynecological Endocrinology 1997, 11: 139-143. PMID: 9174856, DOI: 10.3109/09513599709152525.Peer-Reviewed Original ResearchConceptsSynaptic plasticityEstrogen-induced synaptic plasticityHypothalamic arcuate nucleusPreovulatory gonadotropin surgeInhibitory synaptic connectionsGonadotropin feedbackGonadotropin surgeArcuate nucleusPreovulatory surgePituitary gonadotrophsSynaptic connectionsSecretion resultsRecent evidenceMassive releaseEstrogenPossible roleGonadotropinHypothalamusCritical eventsGonadotrophs