2022
Mispatterning and interneuron deficit in Tourette Syndrome basal ganglia organoids
Brady M, Mariani J, Koca Y, Szekely A, King R, Bloch M, Landeros-Weisenberger A, Leckman J, Vaccarino F. Mispatterning and interneuron deficit in Tourette Syndrome basal ganglia organoids. Molecular Psychiatry 2022, 27: 5007-5019. PMID: 36447010, PMCID: PMC9949887, DOI: 10.1038/s41380-022-01880-5.Peer-Reviewed Original ResearchConceptsTourette syndromeInterneuron deficitsGABAergic interneuronsHealthy controlsNeurodevelopmental underpinningsNeuropathological deficitsBG circuitryNeuropsychiatric disordersDecreased differentiationT patientsInterneuronsAltered expressionPotential mechanismsCilia disruptionSonic hedgehogOrganoidsStem cellsTS individualsPluripotent stem cellsGli transcription factorsDeficitsOrganoid differentiationEarly stagesCholinergicPatientsCellular and Molecular Pathology in Tourette Syndrome
Fasching L, Brady M, Vaccarino F. Cellular and Molecular Pathology in Tourette Syndrome. 2022, 171-183. DOI: 10.1093/med/9780197543214.003.0012.ChaptersTourette syndromeBasal gangliaAminobutyric acid-ergic interneuronsActive cholinergic interneuronsPathophysiology of TSCholinergic interneuronsPathological findingsMicroglial cellsTic disordersCaudate nucleusCortical hemispherePathogenic mechanismsInterneuronsSyndromeMolecular pathologyGangliaProminent increaseAvailable literatureInflammationPathophysiologyPutamenFindingsPathology
2015
Targeted ablation of cholinergic interneurons in the dorsolateral striatum produces behavioral manifestations of Tourette syndrome
Xu M, Kobets A, Du JC, Lennington J, Li L, Banasr M, Duman RS, Vaccarino FM, DiLeone RJ, Pittenger C. Targeted ablation of cholinergic interneurons in the dorsolateral striatum produces behavioral manifestations of Tourette syndrome. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 893-898. PMID: 25561540, PMCID: PMC4311862, DOI: 10.1073/pnas.1419533112.Peer-Reviewed Original ResearchConceptsTourette syndromeCholinergic interneuronsDorsolateral striatumSensorimotor gatingD-amphetamine challengeLarge cholinergic interneuronsSpecific cell ablationInterneuron deficitsStriatal interneuronsAcute administrationGABAergic markersDopaminergic drugsAvailable treatmentsPostmortem studiesPrepulse inhibitionTic disordersSevere diseaseHuman putamenMotor coordinationInterneuronsTargeted ablationSevere endStriatumAcute stressGilles de
2014
Fgfr1 Inactivation in the Mouse Telencephalon Results in Impaired Maturation of Interneurons Expressing Parvalbumin
Smith KM, Maragnoli ME, Phull PM, Tran KM, Choubey L, Vaccarino FM. Fgfr1 Inactivation in the Mouse Telencephalon Results in Impaired Maturation of Interneurons Expressing Parvalbumin. PLOS ONE 2014, 9: e103696. PMID: 25116473, PMCID: PMC4130531, DOI: 10.1371/journal.pone.0103696.Peer-Reviewed Original ResearchConceptsGanglionic eminenceSoma sizeCortical interneuronsAstrocytes of miceCortex of adultCortical GABAergic neuronsParvalbumin-positive cortical interneuronsRadial glial cellsSmaller soma sizeMedial ganglionic eminenceFibroblast growth factorDeficient astrocytesLocomotor hyperactivityGABAergic cellsGABAergic neuronsInterneuron maturationGlial cellsCortical astrocytesPostnatal periodAdult CNSPostnatal brainInterneuron markersInterneuronsImmunopositive interneuronsAstrocytesNeurobiology of premature brain injury
Salmaso N, Jablonska B, Scafidi J, Vaccarino FM, Gallo V. Neurobiology of premature brain injury. Nature Neuroscience 2014, 17: 341-346. PMID: 24569830, PMCID: PMC4106480, DOI: 10.1038/nn.3604.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus Statements
2013
Hypoxia-Induced Developmental Delays of Inhibitory Interneurons Are Reversed by Environmental Enrichment in the Postnatal Mouse Forebrain
Komitova M, Xenos D, Salmaso N, Tran KM, Brand T, Schwartz ML, Ment L, Vaccarino FM. Hypoxia-Induced Developmental Delays of Inhibitory Interneurons Are Reversed by Environmental Enrichment in the Postnatal Mouse Forebrain. Journal Of Neuroscience 2013, 33: 13375-13387. PMID: 23946395, PMCID: PMC3742925, DOI: 10.1523/jneurosci.5286-12.2013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Adhesion Molecules, NeuronalCerebral CortexChromatography, High Pressure LiquidDisease Models, AnimalExtracellular Matrix ProteinsGene Knock-In TechniquesHousing, AnimalHypoxiaImmunohistochemistryInterneuronsMiceMice, Inbred C57BLMice, TransgenicNerve Tissue ProteinsParvalbuminsProsencephalonReelin ProteinSerine EndopeptidasesSomatostatinConceptsCortical interneuronsNormoxic controlsMarker expressionPostnatal cortical developmentVasoactive intestinal peptidePostnatal day 3Central nervous systemTotal GABA contentImpact of hypoxicPostnatal mouse forebrainEnvironmental enrichmentIntestinal peptideGABAergic interneuronsFrontal neocortexInhibitory interneuronsCortical developmentMouse modelReelin expressionInterneuron numbersNervous systemDay 3Cognitive impairmentInterneuronsHousing miceRLN expressionCellular and Molecular Pathology in Tourette Syndrome
Vaccarino F, Kataoka-Sasaki Y, Lennington J. Cellular and Molecular Pathology in Tourette Syndrome. 2013, 205-220. DOI: 10.1093/med/9780199796267.003.0010.Chapters
2009
Decreased number of parvalbumin and cholinergic interneurons in the striatum of individuals with Tourette syndrome
Kataoka Y, Kalanithi PS, Grantz H, Schwartz ML, Saper C, Leckman JF, Vaccarino FM. Decreased number of parvalbumin and cholinergic interneurons in the striatum of individuals with Tourette syndrome. The Journal Of Comparative Neurology 2009, 518: 277-291. PMID: 19941350, PMCID: PMC2846837, DOI: 10.1002/cne.22206.Peer-Reviewed Original ResearchConceptsMedium spiny neuronsCholinergic interneuronsTourette syndromeNormal controlsCholinergic striatal interneuronsNumber of parvalbuminBrains of patientsCaudate nucleus volumeUnbiased stereological analysisStriatal interneuronsOngoing motor behaviorCholinergic cellsTotal neuronsCholine acetyltransferaseSpiny neuronsLimbic regionsStriatum of individualsTS patientsPostmortem brainsThalamic controlSensorimotor regionsInterneuronsCellular abnormalitiesNeuron firingTS subjectsPrecursors with Glial Fibrillary Acidic Protein Promoter Activity Transiently Generate GABA Interneurons in the Postnatal Cerebellum
Silbereis J, Cheng E, Ganat YM, Ment LR, Vaccarino FM. Precursors with Glial Fibrillary Acidic Protein Promoter Activity Transiently Generate GABA Interneurons in the Postnatal Cerebellum. Stem Cells 2009, 27: 1152-1163. PMID: 19418461, PMCID: PMC2903623, DOI: 10.1002/stem.18.Peer-Reviewed Original ResearchConceptsCerebellar white matterWhite matterGFAP/Inducible Cre recombinationMolecular layerGlial cell typesNSC/NPCsGABA interneuronsGFAP promoter activityGAD-67GABAergic interneuronsGlial cellsIntact cerebellumNeurogenic potentialCerebellar cortexCerebellar interneuronsInhibitory factorPostnatal cerebellumInterneuronsNeural stemProgenitor cellsDifferent neuronsCerebellumCerebellar developmentCre recombination