2023
Restorative effect of NitroSynapsin on synaptic plasticity in an animal model of depression
Tse W, Pochwat B, Szewczyk B, Misztak P, Bobula B, Tokarski K, Worch R, Czarnota-Bojarska M, Lipton S, Zaręba-Kozioł M, Bijata M, Wlodarczyk J. Restorative effect of NitroSynapsin on synaptic plasticity in an animal model of depression. Neuropharmacology 2023, 241: 109729. PMID: 37797736, DOI: 10.1016/j.neuropharm.2023.109729.Peer-Reviewed Original ResearchConceptsMedial prefrontal cortexLong-term potentiationChronic restraint stress mouse modelSynaptic plasticityN-methyl-D-aspartate receptor antagonistRestraint stress mouse modelMale C57BL/6J miceAntidepressant-like activityTail suspension testStress mouse modelFunctional synaptic plasticityMajor depressive disorderAntidepressant potentialPharmacological treatmentPsychotomimetic effectsReceptor antagonistC57BL/6J miceDepressive behaviorSucrose preferenceDepressive disorderNitroSynapsinMouse modelSuspension testBehavioral disturbancesCerebrocortical neurons
2021
α-Synuclein Oligomers Induce Glutamate Release from Astrocytes and Excessive Extrasynaptic NMDAR Activity in Neurons, Thus Contributing to Synapse Loss
Trudler D, Sanz-Blasco S, Eisele Y, Ghatak S, Bodhinathan K, Akhtar M, Lynch W, Piña-Crespo J, Talantova M, Kelly J, Lipton S. α-Synuclein Oligomers Induce Glutamate Release from Astrocytes and Excessive Extrasynaptic NMDAR Activity in Neurons, Thus Contributing to Synapse Loss. Journal Of Neuroscience 2021, 41: 2264-2273. PMID: 33483428, PMCID: PMC8018774, DOI: 10.1523/jneurosci.1871-20.2020.Peer-Reviewed Original ResearchConceptsLewy body dementiaExtrasynaptic NMDA receptorsSynaptic damageParkinson's diseaseNeuronal lossLewy bodiesNMDAR activityDisease progressionΑSyn oligomersPotential disease-modifying interventionsNeurodegenerative diseasesΑ-synucleinExtrasynaptic NMDAR activitySynaptic NMDAR activityDisease-modifying interventionsPatch-clamp recordingsMajor neuropathological characteristicsSynaptic lossAstrocytic glutamateGlutamate releaseSynapse lossSpine lossExtrasynaptic NMDARsFemale miceHippocampal slices
2014
Cognitive deficits associated with combined HIV gp120 expression and chronic methamphetamine exposure in mice
Kesby J, Markou A, Semenova S, Grant I, Ellis R, Letendre S, Achim C, Woods S, Carr A, Letendre S, Ellis R, Schrier R, Heaton R, Atkinson J, Cherner M, Marcotte T, Morgan E, Brown G, Jernigan T, Dale A, Liu T, Scadeng M, Fennema-Notestine C, Archibald S, Achim C, Masliah E, Lipton S, Soontornniyomkij V, Gamst A, Cushman C, Abramson I, Vaida F, Deutsch R, Umlauf A, Atkinson J, Marquie-Beck J, Minassian A, Perry W, Geyer M, Henry B, Young J, Grethe A, Paulus M, Ellis R, Morris S, Smith D, Grant I, Semenova S, Markou A, Kesby J, Kaul M. Cognitive deficits associated with combined HIV gp120 expression and chronic methamphetamine exposure in mice. European Neuropsychopharmacology 2014, 25: 141-150. PMID: 25476577, PMCID: PMC4289653, DOI: 10.1016/j.euroneuro.2014.07.014.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, OcularAnalysis of VarianceAnimalsBody WeightCentral Nervous System StimulantsCognition DisordersDisease Models, AnimalGene Expression RegulationGlial Fibrillary Acidic ProteinHIV Envelope Protein gp120MaleMaze LearningMethamphetamineMiceMice, Inbred C57BLMice, TransgenicReaction TimeRecognition, PsychologyConceptsGp120-tg miceCognitive domainsBarnes mazeMethamphetamine exposureCognitive deficitsSpatial learningAssociative recognition memoryDiscrete cognitive domainsMethamphetamine abuseHuman immunodeficiency virusRecognition memoryExecutive functionBarnes maze testCognitive performanceChronic methamphetamine exposureCognitive functionGp120 expressionAcquisition trialsGreater deficitsHIV infectionPlace testStrategy scoresNeurocognitive outcomesMethamphetamine usersSpatial strategies
2006
HIV-1 coreceptors CCR5 and CXCR4 both mediate neuronal cell death but CCR5 paradoxically can also contribute to protection
Kaul M, Ma Q, Medders K, Desai M, Lipton S. HIV-1 coreceptors CCR5 and CXCR4 both mediate neuronal cell death but CCR5 paradoxically can also contribute to protection. Cell Death & Differentiation 2006, 14: 296-305. PMID: 16841089, DOI: 10.1038/sj.cdd.4402006.Peer-Reviewed Original ResearchConceptsHuman immunodeficiency virus-1Neuronal cell deathStromal cell-derived factor-1HIV-1 envelope glycoprotein gp120Cell-derived factor-1Cell deathHIV-1 coreceptor CCR5Chemokine receptor CCR5Immunodeficiency virus-1Brain-derived cellsEnvelope glycoprotein gp120Intracellular free Ca2Gp120 neurotoxicityCCR5 ligandsHIV coreceptorsP38 mitogen-activated protein kinaseCCR5 agonistsNeuroprotective pathwaysReceptor CCR5Heterologous desensitizationCoreceptor CCR5CXCR4 agonistCCR5Glial culturesGlycoprotein gp120
2000
Expression of GABAC receptor ρ1 and ρ2 subunits during development of the mouse retina
Greka A, Lipton S, Zhang D. Expression of GABAC receptor ρ1 and ρ2 subunits during development of the mouse retina. European Journal Of Neuroscience 2000, 12: 3575-3582. PMID: 11029627, DOI: 10.1046/j.1460-9568.2000.00247.x.Peer-Reviewed Original ResearchConceptsRetinal developmentGamma-aminobutyric acid type C receptorMouse retinaRho subunitsReceptor-mediated currentsPostnatal day 6Type C receptorsBipolar cell differentiationMouse retinal developmentΡ2 subunitsBipolar cellsC receptorRho2 subunitsRho1 subunitDay 6ReceptorsEye openingSubunit transcriptionSubunit messageAdulthoodRetinaFuture studiesCompetitive PCRCell differentiationP9Functional role and therapeutic implications of neuronal caspase-1 and -3 in a mouse model of traumatic spinal cord injury
Li M, Ona V, Chen M, Kaul M, Tenneti L, Zhang X, Stieg P, Lipton S, Friedlander R. Functional role and therapeutic implications of neuronal caspase-1 and -3 in a mouse model of traumatic spinal cord injury. Neuroscience 2000, 99: 333-342. PMID: 10938439, DOI: 10.1016/s0306-4522(00)00173-1.Peer-Reviewed Original ResearchConceptsSpinal cord injuryCord injuryCaspase-1Acute central nervous system insultLesion sizeCentral nervous system insultsTraumatic spinal cord injuryVehicle-treated miceSham-operated miceNervous system insultsCaspase-3Spinal cord samplesNon-neuronal cellsN-benzyloxycarbonyl-ValCaspase-1 activityCaspase-3 expressionCell deathNeurological dysfunctionCord samplesMotor functionTissue injuryMouse modelTherapeutic implicationsTransgenic miceTissue damage
1999
The contribution of various NOS gene products to HIV-1 coat protein (gp120)-mediated retinal ganglion cell injury.
Dreyer E, Zurakowski D, Gorla M, Vorwerk C, Lipton S. The contribution of various NOS gene products to HIV-1 coat protein (gp120)-mediated retinal ganglion cell injury. Investigative Ophthalmology & Visual Science 1999, 40: 983-9. PMID: 10102296.Peer-Reviewed Original ResearchConceptsNitric oxide synthaseHIV-1 coat proteinRetinal ganglion cell injuryIsoforms of NOSNitric oxideNeuronal nitric oxide synthaseGanglion cell injuryRetinal ganglion cellsPresence of nNOSNOS-deficient miceWild-type miceNeuronal lossExcitotoxic pathwayIntravitreal injectionGanglion cellsGp120 toxicityNeuronal pathologyNOS inhibitorOxide synthaseHIV-1Cell injuryControl animalsNervous systemGp120Pathologic states
1998
Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A
Das S, Sasaki Y, Rothe T, Premkumar L, Takasu M, Crandall J, Dikkes P, Conner D, Rayudu P, Cheung W, Chen H, Lipton S, Nakanishi N. Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A. Nature 1998, 393: 377-381. PMID: 9620802, DOI: 10.1038/30748.Peer-Reviewed Original ResearchConceptsNMDA receptorsReceptor subunit NR1Synaptic refinementSpine densityNMDA receptor subunit NR3ANMDA responsesNMDA subclassSmall unitary conductanceNMDAR activitySubunit NR1NMDAR subunitsCerebrocortical neuronsDendritic spinesSynaptic plasticityNR1 subunitMice resultsSingle-channel recordingsGenetic knockoutSynaptic elementsHeteromultimeric channelsNR1NR3AXenopus oocytesUnitary conductanceNMDATissue plasminogen activator (tPA) increase neuronal damage after focal cerebral ischemia in wild-type and tPA-deficient mice
Wang Y, Tsirka S, Strickland S, Stieg P, Soriano S, Lipton S. Tissue plasminogen activator (tPA) increase neuronal damage after focal cerebral ischemia in wild-type and tPA-deficient mice. Nature Medicine 1998, 4: 228-231. PMID: 9461198, DOI: 10.1038/nm0298-228.Peer-Reviewed Original ResearchConceptsTissue plasminogen activatorTPA-deficient miceWild-type miceCerebral infarctsNeuronal damageEffects of tPAIntravenous tissue plasminogen activatorRole of tPAPlasminogen activatorSmall cerebral infarctsAcute cerebral infarctsFocal cerebral ischemiaMiddle cerebral arteryIschemia/reperfusionStroke-induced injuryCerebral viabilityIntravascular filamentAcute strokeExcitotoxic damageCerebral ischemiaCerebral arteryLarge infarctsIntracerebral injectionIntravenous injectionThrombolytic agents
1997
Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice
Le D, Das S, Wang Y, Yoshizawa T, Sasaki Y, Takasu M, Nemes A, Mendelsohn M, Dikkes P, Lipton S, Nakanishi N. Enhanced neuronal death from focal ischemia in AMPA-receptor transgenic mice. Brain Research 1997, 52: 235-241. PMID: 9495544, DOI: 10.1016/s0169-328x(97)00261-1.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingAnimalsBrainCell DeathCerebral CortexCrosses, GeneticDisease SusceptibilityFemaleGenetic VariationHeterozygoteIschemic Attack, TransientMaleMiceMice, Inbred C57BLMice, Inbred CBAMice, TransgenicNeocortexNeuronsPolymerase Chain ReactionReceptors, AMPATranscription, GeneticConceptsNeuronal cell deathMiddle cerebral arteryWild-type neuronsTransgenic miceAMPA receptorsCerebral ischemiaFocal ischemiaGluR2 flipExcitatory amino acid receptorsCell deathAcute cerebral ischemiaGlobal cerebral ischemiaAmino acid receptorsAMPAR-mediated currentsGlutamate receptor antagonistsPermanent focal ischemiaGenetic mouse modelsWild-type controlsExcitotoxic damageEAA receptorsLarge infarctionCerebral arteryFocal strokeGlutamate excitotoxicityNeuronal death
1988
Characterization of GABA- and glycine-induced currents of solitary rodent retinal ganglion cells in culture
Tauck D, Frosch M, Lipton S. Characterization of GABA- and glycine-induced currents of solitary rodent retinal ganglion cells in culture. Neuroscience 1988, 27: 193-203. PMID: 3200439, DOI: 10.1016/0306-4522(88)90230-8.Peer-Reviewed Original ResearchConceptsGanglion cellsBicuculline methiodideRodent retinal ganglion cellsReversal potentialRetinal ganglion cellsWhole-cell recordingsAgonist-induced currentsRodent retinaD-tubocurarineMicroM GABAMicroM glycineReceptor desensitizationGABAPatch electrodeDesensitizationStrychnineMembrane conductancePicrotoxininMethiodideTaurineCellsSolitary cellsSpace clampTissue cultureResponse