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
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
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
1996
Varicella-zoster Virus Retrobulbar Optic Neuritis in a Patient With Human Immunodeficiency Virus
Shayegani A, Odel J, Kazim M, Hall L, Bamford N, Schubert H. Varicella-zoster Virus Retrobulbar Optic Neuritis in a Patient With Human Immunodeficiency Virus. American Journal Of Ophthalmology 1996, 122: 586-588. PMID: 8862063, DOI: 10.1016/s0002-9394(14)72127-0.Peer-Reviewed Original ResearchConceptsProgressive outer retinal necrosisRetrobulbar optic neuritisHuman immunodeficiency virusOuter retinal necrosisBilateral retrobulbar optic neuritisOptic neuritisRetinal necrosisImmunodeficiency virusVaricella-zoster virusCerebrospinal fluid samplesViral culturePolymerase chain reactionRadiologic examinationNeuritisInfectious diseasesPatientsNecrosisChain reactionFluid samplesVirusCauseRheumatologicNeurologistsOphthalmologistsDisease