2019
Dopamine Deficiency Reduces Striatal Cholinergic Interneuron Function in Models of Parkinson’s Disease
McKinley JW, Shi Z, Kawikova I, Hur M, Bamford IJ, Sudarsana Devi SP, Vahedipour A, Darvas M, Bamford NS. Dopamine Deficiency Reduces Striatal Cholinergic Interneuron Function in Models of Parkinson’s Disease. Neuron 2019, 103: 1056-1072.e6. PMID: 31324539, PMCID: PMC7102938, DOI: 10.1016/j.neuron.2019.06.013.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAmphetamineAnimalsCholinergic NeuronsCyclic AMP-Dependent Protein KinasesDisease Models, AnimalDopamineDopamine AgentsDopamine Plasma Membrane Transport ProteinsHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsInterneuronsMiceNeostriatumParkinson DiseasePatch-Clamp TechniquesReceptors, Dopamine D1Receptors, Dopamine D2Transcription, GeneticConceptsParkinson's diseaseDA deficiencyACh availabilityD1-type DA receptorsHyperpolarization-activated cation channelsRelease of acetylcholineStriatal acetylcholineDA receptorsStriatal interneuronsMotor deficitsDopamine deficiencyDA releasePharmacological treatmentResidual axonsStriatal synapsesMotor functionInterneuron functionAcetylcholineCognitive functionHCN channelsDiseaseCation channelsDopamineSpike timingDeficiency
2013
Acetylcholine Encodes Long-Lasting Presynaptic Plasticity at Glutamatergic Synapses in the Dorsal Striatum after Repeated Amphetamine Exposure
Wang W, Darvas M, Storey GP, Bamford IJ, Gibbs JT, Palmiter RD, Bamford NS. Acetylcholine Encodes Long-Lasting Presynaptic Plasticity at Glutamatergic Synapses in the Dorsal Striatum after Repeated Amphetamine Exposure. Journal Of Neuroscience 2013, 33: 10405-10426. PMID: 23785153, PMCID: PMC3685836, DOI: 10.1523/jneurosci.0014-13.2013.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcholineAdrenergic Uptake InhibitorsAmphetamineAnimalsCholine O-AcetyltransferaseDependovirusElectrophysiological PhenomenaExcitatory Postsynaptic PotentialsGenetic VectorsGlutamic AcidInterneuronsLocomotionMaleMaze LearningMiceMice, Inbred C57BLMice, KnockoutMotor ActivityNeostriatumNeuronal PlasticityPostural BalanceReceptors, Dopamine D1Receptors, Dopamine D2Receptors, PresynapticSynapsesConceptsGlutamate releaseCorticostriatal activityDirect pathway medium spiny neuronsMedium spiny neuronsCorticostriatal terminalsAcetylcholine releaseAmphetamine treatmentAmphetamine challengePresynaptic depressionAmphetamine exposurePresynaptic potentiationChronic decreaseSpiny neuronsDrug challengeLocomotor sensitizationGlutamatergic synapsesBrain slicesCorticostriatal signalingParkinson's diseaseDorsal striatumLocomotor responseDopamine regulationDrug dependenceStriatal activityActive interneurons
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 abuse