Search results for "Excitatory Amino Acid Agonists"

showing 10 items of 29 documents

Involvement of putative glutamate receptors in plant defence signaling and NO production

2011

International audience; Ionotropic glutamate receptors (iGluRs) are non-selective cation channels permeable to calcium, present in animals and plants. In mammals, glutamate is a well-known neurotransmitter and recently has been recognized as an immunomodulator. As animals and plants share common mechanisms that govern innate immunity with calcium playing a key role in plant defence activation, we have checked the involvement of putative iGluRs in plant defence signaling. Using tobacco cells, we first provide evidence supporting the activity of iGluRs as calcium channels and their involvement in NO production as reported in animals. Thereafter, iGluRs were shown to be activated in response t…

0106 biological sciencesHypersensitive responsebiochemistry and molecular biologyplant defenceglutamate receptorCell Culture TechniquesGlutamic AcidBiologycalcium signaling01 natural sciencesBiochemistrytobaccoFungal Proteins03 medical and health sciencesnitric oxideelicitorsExcitatory Amino Acid Agonists[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologyrésistance végétalePlant Proteins030304 developmental biologyCalcium signaling0303 health sciencesVoltage-dependent calcium channelAlgal ProteinsGlutamate receptorGeneral MedicineGlutamic acidImmunity InnateElicitortabacReceptors GlutamateBiochemistryMetabotropic glutamate receptorNMDA receptorCalciumExcitatory Amino Acid Antagonists010606 plant biology & botany
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Choline is a Selective Agonist of α7 Nicotinic Acetylcholine Receptors in the Rat Brain Neurons

1998

In the present study, we demonstrate that choline, a precursor of acetylcholine (ACh) and a product of acetylcholine hydrolysis by acetylcholinesterase (AChE), acts as an efficient and relatively selective agonist of alpha7-containing nicotinic acetylcholine receptors (nAChR) in neurons cultured from the rat hippocampus, olfactory bulb and thalamus as well as in PC12 cells. Choline was able to activate postsynaptic and presynaptic alpha7 nAChRs, with the latter action resulting in the release of other neurotransmitters. Although choline was approximately one order of magnitude less potent than ACh (EC50 of 1.6 mM for choline and 0.13 mM for ACh), it acted as a full agonist at alpha7 nAChRs.…

AgonistN-MethylaspartatePatch-Clamp Techniquesmedicine.drug_classNicotinic AntagonistsMecamylaminePharmacologyHippocampusPC12 Cellscomplex mixturesCholineRats Sprague-DawleyMethylamineschemistry.chemical_compoundThalamusPostsynaptic potentialExcitatory Amino Acid AgonistsmedicineAnimalsCholineNicotinic AgonistsNootropic AgentsAcetylcholine receptorNeuronsGeneral NeuroscienceBungarotoxinsOlfactory BulbCholine acetyltransferaseAcetylcholinesteraseAcetylcholineRatsNicotinic agonistnervous systemchemistryBiochemistryDimethylphenylpiperazinium IodideAcetylcholinemedicine.drugEuropean Journal of Neuroscience
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Activation of phospholipases C and D by the novel metabotropic glutamate receptor agonist tADA.

1997

Abstract In hippocampal slices taken from 8-day-old rats, trans-azetidine-2,4-dicarboxylic acid (tADA), a novel glutamatergic agonist acting preferentially at class I mGluR receptors, activates phosphoinositide and phosphatidylcholine hydrolysis with widely different potencies. Inositol phosphate formation was maximally increased at 10 μM tADA ( ec 50: 1.2 μM), while phospholipase D activation was observed at a tADA concentration of 1 mM. This is the first report of a tADA-induced phospholipase D activity. © 1997 Elsevier Science Ltd. All rights reserved.

Agonistmedicine.drug_classInositol PhosphatesPhospholipaseBiologyIn Vitro TechniquesReceptors Metabotropic GlutamateHippocampusRats Sprague-DawleyCellular and Molecular NeurosciencemedicineExcitatory Amino Acid AgonistsPhospholipase DPhospholipase D activityAnimalsInositol phosphatePharmacologychemistry.chemical_classificationPhospholipase CPhospholipase DRatsEnzyme ActivationMetabotropic receptorBiochemistrychemistryMetabotropic glutamate receptorType C PhospholipasesAzetidinecarboxylic AcidNeuropharmacology
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Excitotoxic Hippocampal Membrane Breakdown and its Inhibition by Bilobalide: Role of Chloride Fluxes

2003

We have previously shown that hypoxia and N-methyl-D-aspartate (NMDA) receptor activation induce breakdown of choline-containing phospholipids in rat hippocampus, a process which is mediated by calcium influx and phospholipase A (2) activation. Bilobalide, a constituent of Ginkgo biloba, inhibited this process in a potent manner (Weichel et al., Naunyn-Schmiedeberg's Arch. Pharmacol. 360, 609-615, 1999). In this study, we used fluorescence microscopy and radioactive flux measurements to show that bilobalide does not interfere with NMDA-induced calcium influx. Instead, bilobalide seems to inhibit NMDA-induced fluxes of chloride ions through ligand-operated chloride channels. In our experimen…

Calcium IsotopesMaleN-Methylaspartatemedicine.drug_classGlycineCyclopentanes44'-Diisothiocyanostilbene-22'-Disulfonic AcidIn Vitro TechniquesHippocampusChlorideCholinechemistry.chemical_compoundChloridesBilobalideFurosemideExcitatory Amino Acid AgonistsmedicineAnimalsCholineDrug InteractionsPharmacology (medical)Channel blockerRats WistarDiureticsFuransCell MembraneGeneral MedicineReceptor antagonistPyrrolidinonesRatsPsychiatry and Mental healthGinkgolidesnervous systemchemistryBiochemistryDIDSPotassiumChloride channelBiophysicsNMDA receptorCalciumDiterpenesDizocilpine MaleateExcitatory Amino Acid AntagonistsSynaptosomesmedicine.drugPharmacopsychiatry
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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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Calretinin/PSA-NCAM immunoreactive granule cells after hippocampal damage produced by kainic acid and DEDTC treatment in mouse.

2003

There is a dramatic increase in the number of lightly immunoreactive calretinin cells in the granular layer of the dentate gyrus of the mouse hippocampus 1 day after excitotoxic injury using kainic acid combined with the zinc chelator diethyldithiocarbamate. At 7 days after treatment, these cells are strongly immunoreactive for calretinin and for the polysialated form of the glycoprotein neural cell adhesion molecule (PSA-NCAM). The reexpression of calretinin and PSA-NCAM after treatment corresponds well with the loss of input from the damaged hilar mossy cells. These cells could be considered immature granule cells since they are immunoreactive to markers for immature cells such as PSA-NCA…

Kainic acidTime FactorsNeural Cell Adhesion Molecule L1Granular layerHippocampal formationHippocampuschemistry.chemical_compoundMiceS100 Calcium Binding Protein GExcitatory Amino Acid AgonistsAnimalsMolecular BiologyChelating AgentsNeuronsKainic AcidbiologyGeneral NeuroscienceDentate gyrusNeurogenesisDrug SynergismMolecular biologyImmunohistochemistryMicroscopy Electronnervous systemchemistryCalbindin 2Phosphopyruvate HydrataseImmunologybiology.proteinSialic AcidsNeural cell adhesion moleculeNeurology (clinical)NeuNCalretininDitiocarbDevelopmental BiologyBrain research
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Connexin-30 mRNA Is Up-Regulated in Astrocytes and Expressed in Apoptotic Neuronal Cells of Rat Brain Following Kainate-Induced Seizures

2002

Glial connexins (Cxs) make an extensively interconnected functional syncytium created by a network of gap junctions between astrocytes and oligodendrocytes. Among Cxs expressed in the brain, Cx30 is expressed in grey matter astrocytes, as shown at the protein level by immunoistochemistry. In the present study we aimed to perform a detailed study of the regional distribution of Cx30 mRNA in the adult and postnatal developing rat brain, analyzing its expression by in situ hybridization, and determining its cell type localization by double labeling. Recently, it has been suggested that neuronal activity may control the level of intercellular communication between astrocytes through gap junctio…

MaleAgingCell typeGene ExpressionConnexinApoptosisKainate receptorCell CommunicationIn situ hybridizationGrey matterBiologyConnexinsCellular and Molecular NeuroscienceStatus EpilepticusSeizuresExcitatory Amino Acid AgonistsmedicineAnimalsPremovement neuronal activityRNA MessengerRats WistarMolecular BiologyNeuronsSyncytiumKainic AcidGap junctionBrainCell BiologyImmunohistochemistryRatsUp-RegulationCell biologymedicine.anatomical_structureAnimals NewbornAstrocytesNeuroscienceMolecular and Cellular Neuroscience
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Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate-induced seizures and expression in apoptotic neuronal ce…

2003

The identification of connexins (Cxs) expressed in neuronal cells represents a crucial step for understanding the direct communication between neurons and between neuron and glia. In the present work, using a double-labelling method combining in situ hybridization for Cx mRNAs with immunohistochemical detection for neuronal markers, we provide evidence that, among cerebral connexins (Cx26, Cx32, Cx36, Cx37, Cx40, Cx43, Cx45 and Cx47), only Cx45 and Cx36 mRNAs are localized in neuronal cells in both developing and adult rat brain. In order to establish whether connexin expression is influenced in vivo by abnormal neuronal activity, we examined the short-term effects of kainate-induced seizur…

MaleAgingTime FactorsgliaHippocampusConnexinbrain developmentKainate receptorApoptosisIn situ hybridizationBiologyConnexinsgap junctionbrain development; gap junction; gliaSeizuresTubulinmedicineExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingPremovement neuronal activityAnimalsRNA MessengerOrganic ChemicalsRats WistarIn Situ HybridizationFluorescent DyesNeuronsMessenger RNAKainic AcidReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceGap junctionBrainGene Expression Regulation DevelopmentalFluoresceinsImmunohistochemistryCell biologyRatsmedicine.anatomical_structurenervous systemAnimals NewbornPhosphopyruvate HydrataseAutoradiographysense organsNeuronNeuroscienceDensitometryThe European journal of neuroscience
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CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity

2003

Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protecti…

MaleCannabinoid receptorReceptors Drugmedicine.medical_treatment2-ArachidonoylglycerolExcitotoxicityHippocampal formationmedicine.disease_causeHippocampusMicechemistry.chemical_compoundPiperidinesCannabinoid receptor type 1Excitatory Amino Acid AgonistsReceptors Cannabinoidgamma-Aminobutyric AcidMice KnockoutNeuronsKainic AcidMultidisciplinaryBrainEndocannabinoid systemNeuroprotective AgentsMitogen-Activated Protein KinasesRimonabantSignal Transductionmedicine.medical_specialtyKainic acidPolyunsaturated AlkamidesGlutamic AcidMice TransgenicArachidonic AcidsIn Vitro TechniquesBiologyGlyceridesProsencephalonInternal medicinemedicineAnimalsFuransGenes Immediate-EarlyEpilepsyCannabinoidsBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsMice Inbred C57BLEndocrinologyGene Expression Regulationnervous systemchemistryMutationPyrazolesCannabinoidNeuroscienceEndocannabinoidsScience
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Role of GABAergic antagonism in the neuroprotective effects of bilobalide

2006

Bilobalide, a constituent of Ginkgo biloba, has neuroprotective properties. Its mechanism of action is unknown but it was recently found to block GABA(A) receptors. The goal of this study was to test the potential role of a GABAergic mechanism for the neuroprotective activity of bilobalide. In rat hippocampal slices exposed to NMDA, release of choline indicates breakdown of membrane phospholipids. NMDA-induced choline release was almost completely blocked in the presence of bilobalide (10 microM) and under low-chloride conditions. Bicuculline (100 microM), a competitive antagonist at GABA(A) receptors, reduced NMDA-induced choline release to a small extent (-23%). GABA (100 microM) partiall…

MaleN-MethylaspartateBrain EdemaCyclopentanesIn Vitro TechniquesPharmacologyBicucullineInhibitory postsynaptic potentialHippocampusArticlegamma-Aminobutyric acidCholineGABA AntagonistsRats Sprague-Dawleychemistry.chemical_compoundBilobalideExcitatory Amino Acid AgonistsmedicineAnimalsPicrotoxinDrug InteractionsFuransMolecular Biologygamma-Aminobutyric AcidChemistryGABAA receptorGeneral NeuroscienceBicucullineGABA receptor antagonistBridged Bicyclo Compounds HeterocyclicRatsGinkgolidesNeuroprotective Agentsnervous systemNonlinear DynamicsMechanism of actionArea Under CurveGABAergicNeurology (clinical)medicine.symptomSynaptosomesDevelopmental Biologymedicine.drugBrain Research
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