2019
Dopamine neuronal protection in the mouse Substantia nigra by GHSR is independent of electric activity
Stutz B, Nasrallah C, Nigro M, Curry D, Liu ZW, Gao XB, Elsworth JD, Mintz L, Horvath TL. Dopamine neuronal protection in the mouse Substantia nigra by GHSR is independent of electric activity. Molecular Metabolism 2019, 24: 120-138. PMID: 30833218, PMCID: PMC6531791, DOI: 10.1016/j.molmet.2019.02.005.Peer-Reviewed Original ResearchConceptsSN DA neuronsDA neuronsSubstantia nigraDA cellsDopamine outputNeuronal protectionNeuronal survivalParkinson's diseaseDA neuron survivalDA neuronal survivalDesigner drugs (DREADD) technologyNeuronal pacemaker activityElectrical activityMouse substantia nigraElectric activityNeuron electrical activityAnimal motor behaviorGhrelin activationGHSR activationTetrahydropyridine (MPTP) treatmentNeuroprotective factorsNeuron survivalDopamine neuronsGhrelin receptorExogenous administration
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 diseaseUncoupling protein 2 protects dopaminergic neurons from acute 1,2,3,6‐methyl‐phenyl‐tetrahydropyridine toxicity
Conti B, Sugama S, Lucero J, Winsky‐Sommerer R, Wirz SA, Maher P, Andrews Z, Barr AM, Morale MC, Paneda C, Pemberton J, Gaidarova S, Behrens MM, Beal F, Sanna PP, Horvath T, Bartfai T. Uncoupling protein 2 protects dopaminergic neurons from acute 1,2,3,6‐methyl‐phenyl‐tetrahydropyridine toxicity. Journal Of Neurochemistry 2005, 93: 493-501. PMID: 15816872, DOI: 10.1111/j.1471-4159.2005.03052.x.Peer-Reviewed Original ResearchConceptsDopaminergic neuronsParkinson's diseaseOxidative stressSpecific neuronal expressionTyrosine hydroxylase promoterTetrahydropyridine (MPTP) toxicityCatecholaminergic neuronsSubstantia nigraHydroxylase promoterLocomotor functionMouse modelNeuronal expressionAcute exposureTransgenic miceSporadic formsTwofold elevationUCP2 expressionDiseaseMarked reductionNeuronsMiceNeuroprotectionProtein 2UCP familyDrug targets
2003
Coenzyme Q Induces Nigral Mitochondrial Uncoupling and Prevents Dopamine Cell Loss in a Primate Model of Parkinson’s Disease
Horvath TL, Diano S, Leranth C, Garcia-Segura LM, Cowley MA, Shanabrough M, Elsworth JD, Sotonyi P, Roth RH, Dietrich EH, Matthews RT, Barnstable CJ, Redmond DE. Coenzyme Q Induces Nigral Mitochondrial Uncoupling and Prevents Dopamine Cell Loss in a Primate Model of Parkinson’s Disease. Endocrinology 2003, 144: 2757-2760. PMID: 12810526, DOI: 10.1210/en.2003-0163.Peer-Reviewed Original ResearchConceptsDopamine cell lossParkinson's diseaseCell lossShort-term oral administrationMitochondrial uncouplingSubstantia nigraDopamine neuronsTetrahydropyridine (MPTP) administrationCoenzyme QPrimate modelOral administrationDiseaseOxidative stressState 4 respirationMitochondrial uncoupling proteinAdministrationUncoupling proteinUncouplingNeuronsNigraTetrahydropyridine
2000
Estrogen Is Essential for Maintaining Nigrostriatal Dopamine Neurons in Primates: Implications for Parkinson's Disease and Memory
Leranth C, Roth R, Elsworth J, Naftolin F, Horvath T, Redmond D. Estrogen Is Essential for Maintaining Nigrostriatal Dopamine Neurons in Primates: Implications for Parkinson's Disease and Memory. Journal Of Neuroscience 2000, 20: 8604-8609. PMID: 11102464, PMCID: PMC6773080, DOI: 10.1523/jneurosci.20-23-08604.2000.Peer-Reviewed Original ResearchConceptsNigrostriatal dopamine neuronsDopamine neuronsParkinson's diseaseSubstantia nigraDopamine cellsTyrosine hydroxylase-expressing neuronsTyrosine hydroxylase-immunoreactive cellsNigral dopamine systemsEstrogen replacement therapyNew treatment strategiesUnbiased stereological analysisTypes of neuronsProgression of diseaseEstrogen replacementPostmenopausal womenEstrogen deprivationReplacement therapyTreatment strategiesCompact zoneGonadal hormonesLong-term effectsDopamine systemEstrogenDiseaseNeurons
1999
Hypocretin (orexin) activation and synaptic innervation of the locus coeruleus noradrenergic system
Horvath T, Peyron C, Diano S, Ivanov A, Aston‐Jones G, Kilduff T, van den Pol A. Hypocretin (orexin) activation and synaptic innervation of the locus coeruleus noradrenergic system. The Journal Of Comparative Neurology 1999, 415: 145-159. PMID: 10545156, DOI: 10.1002/(sici)1096-9861(19991213)415:2<145::aid-cne1>3.0.co;2-2.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAnimalsChlorocebus aethiopsFemaleHypothalamusImmunohistochemistryIntracellular Signaling Peptides and ProteinsLocus CoeruleusMacaca fascicularisMaleMicroscopy, ElectronMSH Release-Inhibiting HormoneNeuropeptidesNeurotransmitter AgentsNorepinephrineOrexinsPresynaptic TerminalsRatsRats, Sprague-DawleyTetrodotoxinTyrosine 3-MonooxygenaseConceptsLocus coeruleusSynaptic innervationNoradrenergic systemAxon terminalsTyrosine hydroxylase-immunopositive cellsAsymmetrical synaptic contactsLC-noradrenergic systemParallel electrophysiological studiesLocus coeruleus noradrenergic systemPresence of tetrodotoxinMelanin-concentrating hormoneLC neuronsAutonomic centersNoradrenergic innervationDense arborizationsExcitatory responsesHypocretin cellsSubstantia nigraSynaptic contactsHypocretin-2Lateral hypothalamusZona incertaModest depolarizationCatecholamine systemsCentral regulation