2019
Corticostriatal plasticity in the nucleus accumbens core
Bamford NS, Wang W. Corticostriatal plasticity in the nucleus accumbens core. Journal Of Neuroscience Research 2019, 97: 1559-1578. PMID: 31298422, PMCID: PMC6801067, DOI: 10.1002/jnr.24494.Peer-Reviewed Original ResearchConceptsPrefrontal cortical projectionsCortical projectionsNAc coreDrug reinstatementSaline-treated miceSpiny projection neuronsMotor learningNew therapeutic targetsNucleus accumbens coreUse of amphetaminesStriatal glutamateGlutamate releaseCortical stimulationPresynaptic depressionProjection neuronsStriatal circuitryD1 receptorsDrug challengeLocomotor sensitizationMale miceCorticostriatal plasticityGlutamatergic boutonsDopamine releaseNucleus accumbensParadoxical excitationChondrodysplasia Punctata: A Clue to the Zellweger Spectrum Disorders
Bamford NS. Chondrodysplasia Punctata: A Clue to the Zellweger Spectrum Disorders. Pediatric Neurology 2019, 95: 84-85. PMID: 30898411, DOI: 10.1016/j.pediatrneurol.2019.01.013.Peer-Reviewed Original Research
2018
Pearls & Oy-sters
Dhakar MB, Bamford NS. Pearls & Oy-sters. Neurology 2018, 91: 47-49. PMID: 29967203, DOI: 10.1212/wnl.0000000000005745.Peer-Reviewed Original Research
2016
Nicotine Modifies Corticostriatal Plasticity and Amphetamine Rewarding Behaviors in Mice1,2,3
Storey GP, Gonzalez-Fernandez G, Bamford IJ, Hur M, McKinley JW, Heimbigner L, Minasyan A, Walwyn WM, Bamford NS. Nicotine Modifies Corticostriatal Plasticity and Amphetamine Rewarding Behaviors in Mice1,2,3. ENeuro 2016, 3: eneuro.0095-15.2015. PMID: 26866057, PMCID: PMC4745180, DOI: 10.1523/eneuro.0095-15.2015.Peer-Reviewed Original ResearchMeSH KeywordsAction PotentialsAlpha7 Nicotinic Acetylcholine ReceptorAmphetamineAnimalsCentral Nervous System StimulantsCholinergic NeuronsConditioning, OperantCorpus StriatumDrug-Seeking BehaviorFemaleMaleMiceMice, Inbred C57BLMotor ActivityMotor CortexNeural PathwaysNeuronal PlasticityNicotineNicotinic AgonistsReceptors, NicotinicRewardSelf AdministrationConceptsCorticostriatal activityAmphetamine challengeGlutamate releaseLocomotor sensitizationDirect pathway medium spiny neuronsAmphetamine-induced locomotor sensitizationActive cholinergic interneuronsAmphetamine-seeking behaviorSubsequent drug challengeMedium spiny neuronsActivity ex vivoNicotinic acetylcholine receptorsDrug-seeking behaviorPeriod of abstinenceSelf-administer amphetamineDrugs of abuseSelf-administering miceDrug-taking behaviorDwelling catheterAmphetamine withdrawalCholinergic interneuronsGlutamatergic activityPresynaptic depressionPotentiating responseSpiny neurons
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 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 inhibitionHyperactivityMiceNeuronsReceptorsRegulation of prefrontal excitatory neurotransmission by dopamine in the nucleus accumbens core
Wang W, Dever D, Lowe J, Storey GP, Bhansali A, Eck EK, Nitulescu I, Weimer J, Bamford NS. Regulation of prefrontal excitatory neurotransmission by dopamine in the nucleus accumbens core. The Journal Of Physiology 2012, 590: 3743-3769. PMID: 22586226, PMCID: PMC3476631, DOI: 10.1113/jphysiol.2012.235200.Peer-Reviewed Original ResearchMeSH KeywordsAdenosineAmphetamineAnimalsDopamineEndocannabinoidsGreen Fluorescent ProteinsMaleMiceMice, TransgenicNucleus AccumbensOptical ImagingPrefrontal CortexPresynaptic TerminalsPyridinium CompoundsQuaternary Ammonium CompoundsReceptors, AMPAReceptors, Dopamine D1Receptors, GlutamateReceptors, N-Methyl-D-AspartateSynaptic TransmissionConceptsD2 receptor-expressing cellsReceptor-expressing cellsMedium spiny neuronsSpiny neuronsExcitatory inputsD2 receptor-expressing medium spiny neuronsReceptor-expressing medium spiny neuronsGroup 1 metabotropic glutamate receptorsActivation of NMDAReceptor null miceMetabotropic glutamate receptorsBacterial artificial chromosome transgenic miceDopamine D1 receptorsBasal ganglia pathwaysConvergence of excitatoryNucleus accumbens coreCortical terminalsGlutamate releaseGlutamatergic inputsStriatonigral pathwayInhibitory modulationGlutamatergic signalsD1 receptorsSlice preparationGlutamatergic synapses
2011
Attenuating GABAA Receptor Signaling in Dopamine Neurons Selectively Enhances Reward Learning and Alters Risk Preference in Mice
Parker JG, Wanat MJ, Soden ME, Ahmad K, Zweifel LS, Bamford NS, Palmiter RD. Attenuating GABAA Receptor Signaling in Dopamine Neurons Selectively Enhances Reward Learning and Alters Risk Preference in Mice. Journal Of Neuroscience 2011, 31: 17103-17112. PMID: 22114279, PMCID: PMC3235504, DOI: 10.1523/jneurosci.1715-11.2011.Peer-Reviewed Original ResearchConceptsDA neuronsDA neuron activityGABAA Receptor SignalingPhasic dopamine transmissionPhasic DA responsesAversive learningAppetitive learningGABAergic toneExcitatory afferentsMidbrain slicesDA releaseDopamine neuronsExcitatory driveDopamine transmissionNucleus accumbensDA responseElectrical stimulationNeuron activityDA signalingPsychiatric conditionsCompensatory upregulationMiceNeuronsReceptor signalingAppetitive task
2009
Neuromuscular hip dysplasia in Charcot–Marie–Tooth disease type 1A
BAMFORD NS, WHITE KK, ROBINETT SA, OTTO RK, GOSPE SM. Neuromuscular hip dysplasia in Charcot–Marie–Tooth disease type 1A. Developmental Medicine & Child Neurology 2009, 51: 408-411. PMID: 19388151, DOI: 10.1111/j.1469-8749.2008.03234.x.Peer-Reviewed Original ResearchConceptsNeuromuscular hip dysplasiaHip dysplasiaClinical signsCharcot-MarieType 1AInconsistent clinical signsInitial clinical signsTooth disease type 1ACMT type 1APeripheral neuropathyHip diseaseOrthopedic abnormalitiesTooth diseaseNeurological disordersCMT 1A.DysplasiaFrequent formDiseaseSignsChildrenConsiderable variabilityNeuropathySymptomsAbnormalitiesDiagnosis
2002
Congenital Guillain–Barré syndrome associated with maternal inflammatory bowel disease is responsive to intravenous immunoglobulin
Bamford NS, Trojaborg W, Sherbany AA, de Vivo DC. Congenital Guillain–Barré syndrome associated with maternal inflammatory bowel disease is responsive to intravenous immunoglobulin. European Journal Of Paediatric Neurology 2002, 6: 115-119. PMID: 11995958, DOI: 10.1053/ejpn.2002.0557.Peer-Reviewed Original ResearchConceptsGuillain-Barré syndromeIntravenous immunoglobulinMaternal inflammatory bowel diseaseSlow nerve conduction velocitiesSevere generalized hypotoniaInflammatory demyelinating polyneuropathyAcute ulcerative colitisInflammatory bowel diseaseInflammatory bowel syndromeNerve conduction velocitySpontaneous limb movementsHours of treatmentDemyelinating polyneuropathyDenervation activityAutonomic dysfunctionRespiratory failureBowel syndromeClinical improvementPreterm infantsBowel diseaseUlcerative colitisAxonal featuresGeneralized hypotoniaConduction blockConduction velocity