2012
Overinhibition of corticostriatal activity following prenatal cocaine exposure
Wang W, Nitulescu I, Lewis JS, Lemos JC, Bamford IJ, Posielski NM, Storey GP, Phillips PE, Bamford NS. Overinhibition of corticostriatal activity following prenatal cocaine exposure. Annals Of Neurology 2012, 73: 355-369. PMID: 23225132, PMCID: PMC3766752, DOI: 10.1002/ana.23805.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnalysis of VarianceAnesthetics, LocalAnimalsBiophysicsCerebral CortexCocaineCorpus StriatumDopamineDopamine AgentsDopamine Uptake InhibitorsDrug InteractionsElectric StimulationEmbryo, MammalianExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsExploratory BehaviorFemaleGABA AgentsGreen Fluorescent ProteinsHindlimb SuspensionIn Vitro TechniquesInterneuronsLidocaineMaleMiceMice, Inbred C57BLMice, TransgenicNerve Tissue ProteinsNeural InhibitionNeuronal PlasticityPatch-Clamp TechniquesPregnancyPrenatal Exposure Delayed EffectsQuinoxalinesQuinpiroleReceptors, GABA-ARotarod Performance TestSodium Channel BlockersStatistics, NonparametricTetrodotoxinConceptsPrenatal cocaine exposureCocaine exposureCorticostriatal activityTonic GABA currentsGABAA receptor antagonistBasal ganglia functionDopamine-dependent behaviorsCorticostriatal terminalsGABA interneuronsCorticostriatal synapsesDopamine-dependent plasticityGABAergic mechanismsGlutamate releaseGABAB receptorsMotor abnormalitiesGanglia functionTonic inhibitionReceptor antagonistStriatal synapsesAdolescent miceGABAergic signalingGABA currentsClinical studiesD2 receptorsPolysubstance abuseLack of GPR88 enhances medium spiny neuron activity and alters motor- and cue-dependent behaviors
Quintana A, Sanz E, Wang W, Storey GP, Güler AD, Wanat MJ, Roller BA, La Torre A, Amieux PS, McKnight GS, Bamford NS, Palmiter RD. Lack of GPR88 enhances medium spiny neuron activity and alters motor- and cue-dependent behaviors. Nature Neuroscience 2012, 15: 1547-1555. PMID: 23064379, PMCID: PMC3483418, DOI: 10.1038/nn.3239.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAvoidance LearningBenzylaminesBiophysicsCells, CulturedChromonesCorpus StriatumCuesElectric StimulationEmbryo, MammalianExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsFemaleGABA AntagonistsGamma-Aminobutyric AcidGene Expression ProfilingGreen Fluorescent ProteinsIn Vitro TechniquesMaleMaze LearningMiceMice, Inbred C57BLMice, TransgenicMotor ActivityMutationNeuronsOligonucleotide Array Sequence AnalysisPhosphinic AcidsReceptors, AMPAReceptors, GABA-BReceptors, G-Protein-CoupledRotarod Performance TestConceptsMedium spiny neuronsMedium spiny neuron activityStriatal medium spiny neuronsOrphan G protein-coupled receptorPoor motor coordinationG protein-coupled receptorsProtein-coupled receptorsSpiny neuronsMotor coordinationGPR88Neuron activityFiring rateReduced inhibitionHyperactivityMiceNeuronsReceptors
2009
Age-Dependent Alterations of Corticostriatal Activity in the YAC128 Mouse Model of Huntington Disease
Joshi PR, Wu NP, André VM, Cummings DM, Cepeda C, Joyce JA, Carroll JB, Leavitt BR, Hayden MR, Levine MS, Bamford NS. Age-Dependent Alterations of Corticostriatal Activity in the YAC128 Mouse Model of Huntington Disease. Journal Of Neuroscience 2009, 29: 2414-2427. PMID: 19244517, PMCID: PMC2670193, DOI: 10.1523/jneurosci.5687-08.2009.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAgingAnalysis of VarianceAnimalsBiophysicsCadmiumCells, CulturedCerebral CortexChromosomes, Artificial, YeastCorpus StriatumDisease Models, AnimalDopamine AgentsDose-Response Relationship, DrugElectric StimulationExcitatory Amino Acid AgentsExcitatory Postsynaptic PotentialsHumansHuntington DiseaseIn Vitro TechniquesMembrane PotentialsMiceNeural PathwaysNeuronsPyridinium CompoundsQuaternary Ammonium CompoundsStatistics, NonparametricTime FactorsTrinucleotide Repeat ExpansionConceptsYAC128 mouse modelGlutamate releaseCorticostriatal pathwayHuntington's diseaseCorticostriatal activityMouse modelSynaptic currentsMedium spiny neuronsAge-dependent alterationsGenetic neurodegenerative disorderAge-dependent changesBehavioral phenotypesSpiny neuronsCortical neuronsDisease progressionReceptor modulationSynaptic dysregulationDegenerative changesBrain slicesCorticostriatal functionPresynaptic terminalsCognitive deficitsNeurodegenerative disordersDiseaseMonths
2004
Heterosynaptic Dopamine Neurotransmission Selects Sets of Corticostriatal Terminals
Bamford NS, Zhang H, Schmitz Y, Wu NP, Cepeda C, Levine MS, Schmauss C, Zakharenko SS, Zablow L, Sulzer D. Heterosynaptic Dopamine Neurotransmission Selects Sets of Corticostriatal Terminals. Neuron 2004, 42: 653-663. PMID: 15157425, DOI: 10.1016/s0896-6273(04)00265-x.Peer-Reviewed Original ResearchMeSH KeywordsAfferent PathwaysAmphetamineAnimalsCalcium SignalingCerebral CortexDopamineElectric StimulationExcitatory Postsynaptic PotentialsExocytosisFeedbackGlutamic AcidMiceMice, Inbred C57BLMice, KnockoutNeostriatumNeural InhibitionPresynaptic TerminalsPyridinium CompoundsQuaternary Ammonium CompoundsReceptors, Dopamine D2Substantia NigraSynaptic TransmissionSynaptic VesiclesConceptsMedium spiny neuronsCorticostriatal terminalsDirect presynaptic effectIndividual presynaptic terminalsStriatal dopamine releaseEffects of dopamineHigh-frequency stimulationVoluntary motor movementDrugs of abuseCorticostriatal afferentsMSN excitabilityPresynaptic effectsCorticostriatal inputsCorticostriatal synapsesActivity of subsetsInhibitory modulationSpiny neuronsD2 receptorsDopamine releaseFrequency stimulationDopamine inputPresynaptic terminalsElectrical stimulationHeterosynaptic inhibitionSynaptic connections