Search results for "3-dione"

showing 10 items of 34 documents

Palladium Catalyzed [3+2] Cycloaddition of Vinyl Aziridine and Indane-1,3-diones: Diastereo- and Enantioselective Access to Spiro-Pyrrolidines

2020

A mild and efficient palladium-catalyzed [3+2] cycloaddition of vinylaziridine and indane-1,3-diones has been realized. The resulting spiro-pyrrolidines were provided in excellent yields and, with the introduction of the leucine-derived phosphine ligand, moderate to good enantio­- and diastereoselectivities.

010405 organic chemistryLigandOrganic Chemistryasymmetric synthesisIndaneEnantioselective synthesischemistry.chemical_elementspriopyrrolidines010402 general chemistry01 natural sciencesMedicinal chemistryCatalysisCycloaddition0104 chemical sciencesCatalysis3-dioneschemistry.chemical_compoundchemistryaziridinesinsane-1palladium catalysis; asymmetric synthesis; spriopyrrolidines; aziridines; insane-13-dionespalladium catalysisPhosphinePalladium
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CCDC 1456785: Experimental Crystal Structure Determination

2016

Related Article: Beáta Fekete, Márta Palkó, István Mándity, Matti Haukka, Ferenc Fülöp|2016|Eur.J.Org.Chem.|2016|3519|doi:10.1002/ejoc.201600434

12-hydroxy-312-diazapentacyclo[13.2.1.0214.0311.0510]octadeca-57916-tetraene-413-dione monohydrateSpace GroupCrystallographyCrystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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CCDC 127015: Experimental Crystal Structure Determination

2000

Related Article: S.E.Mallakpour, H.Kolshorn, D.Schollmeyer, R.Stadler|1997|Macromol.Chem.Phys.|198|251|doi:10.1002/macp.1997.021980203

2-Phenyl-5-(4-phenyl-124-triazolin-35-dione)-47-etheno-perhydro-23a7a-triazaindane-13-dioneSpace GroupCrystallographyCrystal SystemCrystal StructureCell ParametersExperimental 3D Coordinates
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Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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Altered morphological and electrophysiological properties of Cajal-Retzius cells in cerebral cortex of embryonic Presenilin-1 knockout mice

2004

Mutations of Presenilin-1 are the major cause of familial Alzheimer's disease. Presenilin-1 knockout (PS1-/-) mice develop severe cortical dysplasia related to human type 2 lissencephaly. This overmigration syndrome has been attributed to the premature loss of Cajal-Retzius cells (CRcs), pioneer neurons required for the termination of radial neuronal migration. To elucidate the potential cellular mechanisms responsible for this premature neuronal loss, we investigated the morphological and electrophysiological properties of visually identified CRcs of wild-type (WT) and PS1-/- mouse brains at embryonic day 16.5. The density of CRcs was substantially reduced in the cerebral cortex of PS1-/-.…

Cell Adhesion Molecules NeuronalNerve Tissue ProteinsBiologyBicucullineMembrane PotentialsGABA AntagonistsMicemental disordersExcitatory Amino Acid AgonistsPresenilin-1medicineAnimalsneoplasms6-Cyano-7-nitroquinoxaline-23-dioneCerebral CortexMice KnockoutNeuronsMembrane potentialExtracellular Matrix ProteinsGABAA receptorStem CellsGeneral NeuroscienceSerine EndopeptidasesExcitatory Postsynaptic PotentialsMembrane ProteinsCortical dysplasiaBicucullineEmbryo Mammalianmedicine.diseaseImmunohistochemistryElectric Stimulationdigestive system diseasesnervous system diseasesCell biologyReelin ProteinElectrophysiologymedicine.anatomical_structure2-Amino-5-phosphonovaleratenervous systemCerebral cortexKnockout mouseExcitatory postsynaptic potentialExcitatory Amino Acid AntagonistsNeurosciencemedicine.drugEuropean Journal of Neuroscience
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Temporally precise control of single-neuron spiking by juxtacellular nanostimulation

2017

Temporal patterns of action potentials influence a variety of activity-dependent intra- and intercellular processes and play an important role in theories of neural coding. Elucidating the mechanisms underlying these phenomena requires imposing spike trains with precisely defined patterns, but this has been challenging due to the limitations of existing stimulation techniques. Here we present a new nanostimulation method providing control over the action potential output of individual cortical neurons. Spikes are elicited through the juxtacellular application of short-duration fluctuating currents (“kurzpulses”), allowing for the sub-millisecond precise and reproducible induction of arbitr…

Male0301 basic medicine2-amino-5-phosphopentanoic acidPatch-Clamp TechniquesTime FactorsPhysiologyComputer scienceAction Potentialsgenetics [Luminescent Proteins]pharmacology [Valine]metabolism [Cytoskeletal Proteins]Mice0302 clinical medicineCortex (anatomy)physiology [Action Potentials]genetics [Nerve Tissue Proteins]6-Cyano-7-nitroquinoxaline-23-dioneNeuronsGeneral Neurosciencepharmacology [Excitatory Amino Acid Antagonists]Valinephysiology [Neurons]medicine.anatomical_structurepharmacology [6-Cyano-7-nitroquinoxaline-23-dione]FemaleSpike (software development)Neuroinformaticsgenetics [Synapsins]Models NeurologicalBiophysicsMice TransgenicNerve Tissue ProteinsOptogenetics03 medical and health sciencesmedicinedrug effects [Neurons]Animalsmetabolism [Synapsins]ddc:610metabolism [Luminescent Proteins]activity regulated cytoskeletal-associated proteingenetics [Cytoskeletal Proteins]analogs & derivatives [Valine]metabolism [Nerve Tissue Proteins]drug effects [Action Potentials]Somatosensory CortexSynapsinsElectric StimulationOptogeneticsCytoskeletal ProteinsLuminescent Proteins030104 developmental biologynervous systemInnovative Methodologycytology [Somatosensory Cortex]NeuronWhole cellExcitatory Amino Acid AntagonistsNeuroscience030217 neurology & neurosurgeryJournal of Neurophysiology
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Mild systemic inflammation and moderate hypoxia transiently alter neuronal excitability in mouse somatosensory cortex

2016

During the perinatal period, the brain is highly vulnerable to hypoxia and inflammation, which often cause white matter injury and long-term neuronal dysfunction such as motor and cognitive deficits or epileptic seizures. We studied the effects of moderate hypoxia (HYPO), mild systemic inflammation (INFL), or the combination of both (HYPO + INFL) in mouse somatosensory cortex induced during the first postnatal week on network activity and compared it to activity in SHAM control animals. By performing in vitro electrophysiological recordings with multi-electrode arrays from slices prepared directly after injury (P8–10), one week after injury (P13–16), or in young adults (P28–30), we investig…

Male0301 basic medicineAction PotentialsKainate receptorStimulationPotassium ChlorideMicechemistry.chemical_compound0302 clinical medicineHypoxia6-Cyano-7-nitroquinoxaline-23-dioneNeuronsAge FactorsInterleukin-1βElectrophysiologyEpileptiform activityNeurologyAnesthesiaCNQXNMDA receptorFemalemedicine.symptommedicine.drugmedicine.medical_specialtyAMPA receptorIn Vitro TechniquesBiologyBicucullineMulti-electrode arrayArticlelcsh:RC321-57103 medical and health sciencesInternal medicinemedicineAnimalsGABA-A Receptor Antagonistslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryInflammationSystemic inflammationSomatosensory CortexHypoxia (medical)BicucullineBarrel cortexMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology2-Amino-5-phosphonovalerateGene Expression Regulationchemistrynervous systemExploratory BehaviorExcitatory Amino Acid Antagonists030217 neurology & neurosurgeryNeurobiology of Disease
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Role of AMPA glutamate receptors in the conditioned rewarding effects of MDMA in mice

2018

Abstract Currently, there is not an effective treatment for 3,4-methylenedioxymethamphetamine (MDMA) dependence but pharmacotherapies targeting glutamate neurotransmission are a promising strategy. Previously, we showed that blockade of glutamate NMDA and AMPA receptors impairs the conditioned rewarding effects of MDMA and cocaine, respectively. In this study we evaluated the role of AMPA receptors in the rewarding effects of MDMA in mice using the conditioned place preference (CPP) paradigm. Mice were conditioned with MDMA (1.25 mg/kg) 60 min after the treatment with saline or different doses (0.25, 1 and 5 mg/kg) of the AMPA/kainate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dion…

MaleHallucinogenMDMAmiceN-Methyl-34-methylenedioxyamphetamineAmphetamine-Related DisordersSpatial BehaviorKainate receptorAMPA receptorPharmacologyMice03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compound0302 clinical medicineRewardConditioning Psychologicalmental disordersmedicineAnimalsReceptors AMPAAMPA receptorsreward6-Cyano-7-nitroquinoxaline-23-dioneDose-Response Relationship Drugbusiness.industryGlutamate receptorMDMACNQXconditioned place preferenceConditioned place preference030227 psychiatrynervous systemchemistryHallucinogensCNQXNMDA receptorbusinessExcitatory Amino Acid Antagonistspsychological phenomena and processes030217 neurology & neurosurgerymedicine.drugBehavioural Brain Research
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Effect of memantine and CNQX in the acquisition, expression and reinstatement of cocaine-induced conditioned place preference

2006

The present study evaluates the effect of memantine, a non-competitive N-methyl-d-aspartate (NMDA) glutamate receptor antagonist and CNQX, an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptor antagonist on the rewarding effects of cocaine in mice, using the conditioned place preference (CPP) paradigm. Cocaine-induced CPP was studied pairing this drug with different memantine or CNQX doses during either the acquisition or the expression phase of the procedure. Once CPP was established, and the preference extinguished, reinstatement was induced by a priming dose of cocaine. Both antagonists, which in themselves do not present motivational actions on the preferen…

MaleKainate receptorAMPA receptorPharmacologyExtinction PsychologicalMicechemistry.chemical_compoundCocaineDopamine Uptake InhibitorsMemantineAnimalsMedicineDrug InteractionsGlutamate receptor antagonistBiological Psychiatry6-Cyano-7-nitroquinoxaline-23-dionePharmacologyBehavior AnimalDose-Response Relationship Drugbusiness.industryGlutamate receptorMemantineConditioned place preferencenervous systemchemistryCNQXConditioning OperantNMDA receptorbusinessExcitatory Amino Acid AntagonistsReinforcement Psychologypsychological phenomena and processesmedicine.drugProgress in Neuro-Psychopharmacology and Biological Psychiatry
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Effects of CNQX and MPEP on sensitization to the rewarding effects of morphine

2011

The present study was conducted to evaluate the influence of the glutamatergic receptors α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and metabotropic glutamate 5 (mGlu5) receptors on sensitization to the rewarding effects of morphine. The effects of pre-treatment with saline or 20 mg/kg morphine plus the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (5 or 10 mg/kg) or the metabotropic Glu5 receptor antagonist 6-methyl-2-(phenylethynyl)-pyridine (MPEP) (5 or 10 mg/kg) on the place conditioning induced by a low dose of morphine (2 mg/kg) were assessed. The 2 mg/kg dose of morphine was ineffective in animals pre-treated with saline but induced a clear con…

MalePyridinesmedicine.drug_classReceptor Metabotropic Glutamate 5AMPA receptorPharmacologyReceptors Metabotropic GlutamateMicechemistry.chemical_compoundRewardmedicineAnimalsReceptors AMPASensitization6-Cyano-7-nitroquinoxaline-23-dionePharmacologyDose-Response Relationship DrugMorphineAntagonistReceptor antagonistConditioned place preferencemedicine.anatomical_structureMetabotropic receptorchemistryAnesthesiaCNQXMorphineConditioning OperantExcitatory Amino Acid Antagonistsmedicine.drugEuropean Journal of Pharmacology
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