2023
Operant Training for Highly Palatable Food Alters Translating Messenger RNA in Nucleus Accumbens D2 Neurons and Reveals a Modulatory Role of Ncdn
Montalban E, Giralt A, Taing L, Nakamura Y, Pelosi A, Brown M, de Pins B, Valjent E, Martin M, Nairn A, Greengard P, Flajolet M, Hervé D, Gambardella N, Roussarie J, Girault J. Operant Training for Highly Palatable Food Alters Translating Messenger RNA in Nucleus Accumbens D2 Neurons and Reveals a Modulatory Role of Ncdn. Biological Psychiatry 2023, 95: 926-937. PMID: 37579933, PMCID: PMC11059129, DOI: 10.1016/j.biopsych.2023.08.006.Peer-Reviewed Original ResearchStriatal projection neuronsNucleus accumbensPalatable foodProjection neuronsNAc neuronsD2-striatal projection neuronsWild-type miceMessenger RNAConditioning-induced changesSpine densityDopamine neuronsDopamine receptorsDownregulated genesD2 neuronsModulatory roleNAc dopamineDopamine DFood altersCompensatory mechanismsRegular foodNeuronsFeeding behaviorBehavioral responsesMRNA alterationsMice
2021
Loss of Ftsj1 perturbs codon-specific translation efficiency in the brain and is associated with X-linked intellectual disability
Nagayoshi Y, Chujo T, Hirata S, Nakatsuka H, Chen C, Takakura M, Miyauchi K, Ikeuchi Y, Carlyle B, Kitchen R, Suzuki T, Katsuoka F, Yamamoto M, Goto Y, Tanaka M, Natsume K, Nairn A, Suzuki T, Tomizawa K, Wei F. Loss of Ftsj1 perturbs codon-specific translation efficiency in the brain and is associated with X-linked intellectual disability. Science Advances 2021, 7: eabf3072. PMID: 33771871, PMCID: PMC7997516, DOI: 10.1126/sciadv.abf3072.Peer-Reviewed Original ResearchTransfer RNAsTranslation efficiencyAberrant synaptic plasticityIntellectual disabilitySubset of genesPatient-derived cellsRibosome profilingKO miceSynaptic organizationSteady-state levelsKnockout miceMolecular pathogenesisSynaptic plasticityMemory deficitsSynaptic morphologyAnticodon regionPhe codonsBrainSlow decodingMechanistic insightsMiceFTSJ1GenesMethylationDisability
2018
Striatal Signaling Regulated by the H3R Histamine Receptor in a Mouse Model of tic Pathophysiology
Rapanelli M, Frick L, Jindachomthong K, Xu J, Ohtsu H, Nairn A, Pittenger C. Striatal Signaling Regulated by the H3R Histamine Receptor in a Mouse Model of tic Pathophysiology. Neuroscience 2018, 392: 172-179. PMID: 30278251, PMCID: PMC6204318, DOI: 10.1016/j.neuroscience.2018.09.035.Peer-Reviewed Original ResearchConceptsHDC-KO miceMitogen-activated protein kinaseHistamine receptorsWT animalsDorsal striatumH3R activationTic-like movementsStriatonigral medium spiny neuronsAkt phosphorylationMedium spiny neuronsWild-type miceRare genetic causeHistamine dysregulationAgonist treatmentKO miceSpiny neuronsTic disordersTic pathophysiologyStriatal signalingMouse modelNeuropsychiatric diseasesKO modelRepetitive movementsStriatumMice
2000
Severe deficiencies in dopamine signaling in presymptomatic Huntington's disease mice
Bibb J, Yan Z, Svenningsson P, Snyder G, Pieribone V, Horiuchi A, Nairn A, Messer A, Greengard P. Severe deficiencies in dopamine signaling in presymptomatic Huntington's disease mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 6809-6814. PMID: 10829080, PMCID: PMC18747, DOI: 10.1073/pnas.120166397.Peer-Reviewed Original ResearchConceptsMedium spiny neuronsDisease miceSpiny neuronsStriatal medium spiny neuronsHuntington's diseaseSevere deficiencyHuntington's disease miceHD model miceModel miceDopaminergic neurotransmissionHD miceSelective neurodegenerationHD pathologyMiceDARPP-32DopamineHuman huntingtinBehavioral phenotypesDiseaseNeuronsIon channelsTotal levelsDisease-causing formHuntingtinDeficiency
1997
Widespread Neuronal Ectopia Associated with Secondary Defects in Cerebrocortical Chondroitin Sulfate Proteoglycans and Basal Lamina in MARCKS-Deficient Mice
Blackshear P, Silver J, Nairn A, Sulik K, Squier M, Stumpo D, Tuttle J. Widespread Neuronal Ectopia Associated with Secondary Defects in Cerebrocortical Chondroitin Sulfate Proteoglycans and Basal Lamina in MARCKS-Deficient Mice. Experimental Neurology 1997, 145: 46-61. PMID: 9184108, DOI: 10.1006/exnr.1997.6475.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalBasement MembraneCerebral CortexChondroitin SulfatesFemaleGene Expression Regulation, DevelopmentalIntracellular Signaling Peptides and ProteinsLamininMaleMembrane ProteinsMiceMice, Mutant StrainsMicroscopy, Electron, ScanningMutationMyristoylated Alanine-Rich C Kinase SubstrateNeurogliaNeuronsPia MaterPregnancyProteinsProteoglycansReticulinSynaptophysinConceptsChondroitin sulfate proteoglycanNeuronal ectopiaBasal laminaSulfate proteoglycanProtein kinase CEmbryonic day 13Basal lamina proteinsReticulin stainingSubarachnoid spaceForebrain commissuresPial membraneDay 13EctopiaGross abnormalitiesRetinal laminationMiceMARCKS deficiencyAbnormalitiesPotential mechanismsNeural substratesMarginal zoneProteolytic destructionKinase CProteoglycansLamina