ATP Synthase c-Subunit Leak Causes Aberrant Cellular Metabolism in Fragile X Syndrome
Licznerski P, Park HA, Rolyan H, Chen R, Mnatsakanyan N, Miranda P, Graham M, Wu J, Cruz-Reyes N, Mehta N, Sohail S, Salcedo J, Song E, Effman C, Effman S, Brandao L, Xu GN, Braker A, Gribkoff VK, Levy RJ, Jonas EA. ATP Synthase c-Subunit Leak Causes Aberrant Cellular Metabolism in Fragile X Syndrome. Cell 2020, 182: 1170-1185.e9. PMID: 32795412, PMCID: PMC7484101, DOI: 10.1016/j.cell.2020.07.008.Peer-Reviewed Original ResearchConceptsFragile X syndromeC subunitAberrant synaptic developmentHuman fragile X syndromeATP synthase enzymeMental retardation proteinX syndromeATP production efficiencyMRNA translation rateAberrant cellular metabolismATP synthaseMRNA translationTranslation rateCellular metabolismSynaptic growthSynthase enzymeMouse neuronsSynapse maturationSynaptic developmentPharmacological inhibitionLeak channelsSynaptic maturationMembrane leakMaturationMetabolismRemodeling of axo-spinous synapses in the pathophysiology and treatment of depression
Licznerski P, Duman RS. Remodeling of axo-spinous synapses in the pathophysiology and treatment of depression. Neuroscience 2012, 251: 33-50. PMID: 23036622, PMCID: PMC3566360, DOI: 10.1016/j.neuroscience.2012.09.057.Peer-Reviewed Original ResearchConceptsAxo-spinous synapsesAlters spine morphologyPathophysiology of depressionTreatment of depressionLimbic brain regionsEffective therapeutic agentExpression of prePlasticity-related proteinsStress-related illnessesBasic research studiesSynaptic machineryBehavioral deficitsDendritic spinesPsychiatric disordersAnimal modelsFunctional alterationsSynaptic plasticityBrain regionsSpine morphologyPrefrontal cortexTherapeutic agentsStress exposureNeuronal communicationBrain imagingSpine architectureDecreased expression of synapse-related genes and loss of synapses in major depressive disorder
Kang HJ, Voleti B, Hajszan T, Rajkowska G, Stockmeier CA, Licznerski P, Lepack A, Majik MS, Jeong LS, Banasr M, Son H, Duman RS. Decreased expression of synapse-related genes and loss of synapses in major depressive disorder. Nature Medicine 2012, 18: 1413-1417. PMID: 22885997, PMCID: PMC3491115, DOI: 10.1038/nm.2886.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsCalmodulinCell LineDepressive Disorder, MajorGATA1 Transcription FactorGene Expression ProfilingGene Expression RegulationHumansMicroarray AnalysisMicroscopy, ElectronPrefrontal CortexRab3A GTP-Binding ProteinRab4 GTP-Binding ProteinsRatsReverse Transcriptase Polymerase Chain ReactionSynapsesSynapsinsTubulinNeuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress
Son H, Banasr M, Choi M, Chae SY, Licznerski P, Lee B, Voleti B, Li N, Lepack A, Fournier NM, Lee KR, Lee IY, Kim J, Kim JH, Kim YH, Jung SJ, Duman RS. Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 11378-11383. PMID: 22733766, PMCID: PMC3396528, DOI: 10.1073/pnas.1201191109.Peer-Reviewed Original ResearchConceptsChronic unpredictable stressAntidepressant actionAtrophy of dendritesDepressive-like behaviorAntidepressant treatment responseSymptoms of depressionExpression of neuritinActivity-dependent genesAntidepressant treatmentLimbic structuresHippocampal expressionUnpredictable stressTreatment responseMood disordersBehavioral deficitsNeuronal plasticityTreatment reversesAnxiety behaviorChronic stressNeuritinDendrite branchingUnique actionHippocampusNeuroplasticityModel of stress