2020
Nesfatin-1 decreases the motivational and rewarding value of food
Dore R, Krotenko R, Reising JP, Murru L, Sundaram SM, Di Spiezio A, Müller-Fielitz H, Schwaninger M, Jöhren O, Mittag J, Passafaro M, Shanabrough M, Horvath TL, Schulz C, Lehnert H. Nesfatin-1 decreases the motivational and rewarding value of food. Neuropsychopharmacology 2020, 45: 1645-1655. PMID: 32353862, PMCID: PMC7419560, DOI: 10.1038/s41386-020-0682-3.Peer-Reviewed Original ResearchMeSH KeywordsCalcium-Binding ProteinsDNA-Binding ProteinsMotivationNerve Tissue ProteinsNucleobindinsRewardConceptsNUCB2/nesfatinNesfatin-1Nucleobindin-2Food intakeNesfatin-1 actionDopaminergic neuron activityFasting-induced increaseReward-related brain areasOutward potassium currentHedonic pathwaysHedonic feedingGABA neuronsLeptin resistanceBrain areasPotassium currentNeuron activityFood rewardEnergy intakeReward circuitryElectrophysiological recordingsNesfatinCentral administrationEnhanced sensitizationIntakeHomeostatic mechanisms
2009
Nesfatin-1-Regulated Oxytocinergic Signaling in the Paraventricular Nucleus Causes Anorexia through a Leptin-Independent Melanocortin Pathway
Maejima Y, Sedbazar U, Suyama S, Kohno D, Onaka T, Takano E, Yoshida N, Koike M, Uchiyama Y, Fujiwara K, Yashiro T, Horvath TL, Dietrich MO, Tanaka S, Dezaki K, Oh-I S, Hashimoto K, Shimizu H, Nakata M, Mori M, Yada T. Nesfatin-1-Regulated Oxytocinergic Signaling in the Paraventricular Nucleus Causes Anorexia through a Leptin-Independent Melanocortin Pathway. Cell Metabolism 2009, 10: 355-365. PMID: 19883614, DOI: 10.1016/j.cmet.2009.09.002.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnorexiaAutocrine CommunicationCalcium-Binding ProteinsDNA-Binding ProteinsLeptinMelanocortinsMiceNerve Tissue ProteinsNeuroendocrine CellsNucleobindinsOxytocinParacrine CommunicationParaventricular Hypothalamic NucleusPro-OpiomelanocortinRatsRats, ZuckerSignal TransductionSolitary NucleusConceptsNucleus tractus solitariusNesfatin-1Oxytocin releaseParacrine/autocrine actionsNesfatin-1 neuronsParaventricular nucleus functionPro-opiomelanocortin (POMC) neuronsZucker fatty ratsOxytocin receptor antagonistOxytocin terminalsPVN neuronsTractus solitariusReceptor antagonistCentral injectionParaventricular nucleusAutocrine actionMelanocortin pathwayNeuronal activityNeural pathwaysPVNAnorexiaNeuronsNucleus functionOxytocinImmunoelectron micrographs
2004
Estradiol enhances light-induced expression of transcription factors in the SCN
Abizaid A, Mezei G, Horvath TL. Estradiol enhances light-induced expression of transcription factors in the SCN. Brain Research 2004, 1010: 35-44. PMID: 15126115, DOI: 10.1016/j.brainres.2004.01.089.Peer-Reviewed Original ResearchAnimalsCalbindinsCholesterolCircadian RhythmCREB-Binding ProteinCyclic AMP Response Element-Binding ProteinDNA-Binding ProteinsEarly Growth Response Protein 1EstradiolEstrous CycleFemaleImmediate-Early ProteinsLightNuclear ProteinsOvariectomyPhotic StimulationProto-Oncogene Proteins c-fosRatsRats, Sprague-DawleyS100 Calcium Binding Protein GSuprachiasmatic NucleusTrans-ActivatorsTranscription FactorsUp-RegulationDisruption of neural signal transducer and activator of transcription 3 causes obesity, diabetes, infertility, and thermal dysregulation
Gao Q, Wolfgang MJ, Neschen S, Morino K, Horvath TL, Shulman GI, Fu XY. Disruption of neural signal transducer and activator of transcription 3 causes obesity, diabetes, infertility, and thermal dysregulation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 4661-4666. PMID: 15070774, PMCID: PMC384803, DOI: 10.1073/pnas.0303992101.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsAdipose Tissue, BrownAnimalsBody Temperature RegulationCorticosteroneDiabetes MellitusDNA-Binding ProteinsFemaleInfertility, FemaleInfertility, MaleIntermediate Filament ProteinsKineticsLeptinMaleMiceMice, KnockoutMice, TransgenicNerve Tissue ProteinsNestinObesityRatsSTAT3 Transcription FactorTime FactorsTrans-ActivatorsConceptsSignal transducerActivator of transcriptionApparent developmental abnormalitiesEnergy homeostasisGenetic modelsTranscription 3Mendelian ratioHomozygous mutantsCold stressNeonatal lethalityPhysiological roleMutantsGlial differentiationUnique phenotypeSTAT3Essential roleDevelopmental abnormalitiesHomeostasisActivatorNeuroendocrine defectsTranscriptionDisruptionProteinKnockoutReproduction