2016
Isolation and Culture of Adult Zebrafish Brain-derived Neurospheres.
Lopez-Ramirez MA, Calvo CF, Ristori E, Thomas JL, Nicoli S. Isolation and Culture of Adult Zebrafish Brain-derived Neurospheres. Journal Of Visualized Experiments 2016, 53617. PMID: 26967835, PMCID: PMC4828210, DOI: 10.3791/53617.Peer-Reviewed Original ResearchConceptsAdult zebrafish brainStem/progenitor cellsZebrafish brainMolecular mechanismsRelevant model organismZebrafish adult brainProgenitor cellsSingle-cell dissociationSpecific signaling pathwaysAdult stem/progenitor cellsStem/progenitor cell proliferationNeural stem/progenitor cell proliferationProgenitor cell proliferationNeural stem/progenitor cellsModel organismsGene expressionCell dissociationSignaling pathwaysMultipotent neural stem/progenitor cellsNeurosphere assayAdult neurogenesisCell proliferationZebrafishBrain regenerationAdult brain
2014
Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1
Patterson VL, Zullo AJ, Koenig C, Stoessel S, Jo H, Liu X, Han J, Choi M, DeWan AT, Thomas JL, Kuan CY, Hoh J. Neural-Specific Deletion of Htra2 Causes Cerebellar Neurodegeneration and Defective Processing of Mitochondrial OPA1. PLOS ONE 2014, 9: e115789. PMID: 25531304, PMCID: PMC4274161, DOI: 10.1371/journal.pone.0115789.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBehavior, AnimalBlotting, WesternCell ProliferationCerebellumFemaleGTP PhosphohydrolasesHigh-Temperature Requirement A Serine Peptidase 2MaleMiceMice, Inbred C57BLMice, KnockoutMitochondriaMitochondrial ProteinsNerve DegenerationNeuronsParkinson DiseaseReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSequence DeletionSerine EndopeptidasesSignal TransductionConceptsNeural-specific deletionStriatal neuronal lossPostnatal day 18Days of ageNeuronal lossNeurological symptomsParkinson's diseaseMouse modelParkinsonian phenotypeSystemic effectsMitochondrial Opa1Day 18Premature deathMutant miceNeural contributionsMiceCerebellar neurodegenerationKey moleculesStructural anomaliesAbnormal activityAbnormal morphologyCerebellumDiseaseComplete penetranceDeath