Search results for "Glutamic Acid"

showing 10 items of 168 documents

Cell type-specific circuits of cortical layer IV spiny neurons

2003

Sensory signal processing in cortical layer IV involves two major morphological classes of excitatory neurons: spiny stellate and pyramidal cells. It is essentially unknown how these two cell types are integrated into intracortical networks and whether they play different roles in cortical signal processing. We mapped their cell-specific intracortical afferents in rat somatosensory cortex through a combination of whole-cell patch-clamp recordings and caged glutamate photolysis. Spiny stellate cells received monosynaptic excitation and inhibition originating almost exclusively from neurons located within the same barrel. Pyramidal cells, by contrast, displayed additional excitatory inputs fr…

MaleCell typePatch-Clamp TechniquesModels NeurologicalGlutamic AcidNeural InhibitionSensory systemBiologybiocytinSomatosensory systemInhibitory postsynaptic potentiallayer IVsomatosensoryinhibitory inputsddc:590morphologyAnimalsPatch clampRats WistarARTICLEslicesCells CulturedNeuronspyramidal cellAfferent Pathwayscaged glutamatePyramidal CellsGeneral Neurosciencespiny stellate cellfunctional connectivityExcitatory Postsynaptic PotentialsNeural InhibitionSomatosensory CortexelectrophysiologyJRatsexcitatory inputsExcitatory postsynaptic potentialHepatic stellate cellbarrel cortexNeuroscience
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High-performance liquid chromatography with fluorimetric detection in biological tissues of the 4-bromomethyl-7-methoxycoumarin ester derivative of 5…

1985

MaleChemical PhenomenaMetaboliteCarboxylic acidPeptideKidneyHigh-performance liquid chromatographyMicechemistry.chemical_compoundDrug StabilityAnimalsUmbelliferonesChromatography High Pressure LiquidBrain Chemistrychemistry.chemical_classificationChromatographyGeneral ChemistryGlutamic acid4-bromomethyl-7-methoxycoumarinPyrrolidinonesPyrrolidonecarboxylic AcidChemistrySpectrometry FluorescenceLiverchemistryIndicators and ReagentsDerivative (chemistry)Journal of Chromatography B: Biomedical Sciences and Applications
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Delayed post-ischemic administration of CDP-choline increases EAAT2 association to lipid rafts and affords neuroprotection in experimental stroke

2007

Glutamate transport is the only mechanism for maintaining extracellular glutamate concentrations below excitotoxic levels. Among glutamate transporters, EAAT2 is responsible for up to 90% of all glutamate transport and has been reported to be associated to lipid rafts. In this context, we have recently shown that CDP-choline induces EAAT2 translocation to the membrane. Since CDP-choline preserves membrane stability by recovering levels of sphingomyelin, a glycosphingolipid present in lipid rafts, we have decided to investigate whether CDP-choline increases association of EAAT2 transporter to lipid rafts. Flotillin-1 was used as a marker of lipid rafts due to its known association to these m…

MaleCytidine Diphosphate CholineTime FactorsIschemiaGlutamic AcidContext (language use)PharmacologyBiologyCell FractionationNeuroprotectionlcsh:RC321-571chemistry.chemical_compoundMembrane MicrodomainsIschemiamedicineAnimalsCholineLipid raftlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGlutamate transportersGlutamate receptorInfarction Middle Cerebral ArteryGlutamic acidmedicine.diseaseRats Inbred F344Ratscarbohydrates (lipids)Disease Models AnimalNeuroprotective AgentsExcitatory Amino Acid Transporter 2Gene Expression RegulationNeurologyBiochemistrychemistrylipids (amino acids peptides and proteins)GlutamateSphingomyelinNeurobiology of Disease
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Hampered long-term depression and thin spine loss in the nucleus accumbens of ethanol-dependent rats.

2014

Alcoholism involves long-term cognitive deficits, including memory impairment, resulting in substantial cost to society. Neuronal refinement and stabilization are hypothesized to confer resilience to poor decision making and addictive-like behaviors, such as excessive ethanol drinking and dependence. Accordingly, structural abnormalities are likely to contribute to synaptic dysfunctions that occur from suddenly ceasing the use of alcohol after chronic ingestion. Here we show that ethanol-dependent rats display a loss of dendritic spines in medium spiny neurons of the nucleus accumbens (Nacc) shell, accompanied by a reduction of tyrosine hydroxylase immunostaining and postsynaptic density 95…

MaleDendritic spineDendritic SpinesGlutamic AcidNucleus accumbensNeurotransmissionMedium spiny neuronSynaptic TransmissionNucleus AccumbensOrgan Culture TechniquesAnimalsRats WistarLong-term depressionLong-Term Synaptic Depressiondopamine synaptic plasticity Golgi glutamateMultidisciplinaryNeuronal PlasticityEthanolDopaminergic NeuronsLong-Term Synaptic DepressionCentral Nervous System DepressantsRatsAlcoholismPNAS PlusSynaptic plasticitySettore BIO/14 - FarmacologiaPsychologyNeurosciencePostsynaptic densityProceedings of the National Academy of Sciences of the United States of America
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Anti-B-50 (GAP-43) antibodies decrease exocytosis of glutamate in permeated synaptosomes.

1999

Abstract The involvement of the protein kinase C substrate, B-50 (GAP-43), in the release of glutamate from small clear-cored vesicles in streptolysin-O-permeated synaptosomes was studied by using anti-B-50 antibodies. Glutamate release was induced from endogenous as well as 3 H -labelled pools in a [Ca2+]-dependent manner. This Ca2+-induced release was partially ATP dependent and blocked by the light-chain fragment of tetanus toxin, demonstrating its vesicular nature. Comparison of the effects of anti-B-50 antibodies on glutamate and noradrenaline release from permeated synaptosomes revealed two major differences. Firstly, Ca2+-induced glutamate release was decreased only partially by anti…

MaleGlutamic AcidBiologyIn Vitro TechniquesSynaptic vesicleExocytosisExocytosischemistry.chemical_compoundNorepinephrineAdenosine TriphosphateGAP-43 ProteinAnimalsEnzyme InhibitorsRats WistarNeurotransmitterProtein kinase CProtein Kinase CPharmacologySynaptosomeVesicleGlutamate receptorAntibodies MonoclonalIntracellular MembranesRatschemistryBiochemistryStreptolysinsBiophysicsLiberationCalciumSynaptosomesEuropean journal of pharmacology
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Understanding Cannabinoid Psychoactivity with Mouse Genetic Models

2007

Marijuana and its main psychotropic ingredient Δ9-tetrahydrocannabinol (THC) exert a plethora of psychoactive effects through the activation of the neuronal cannabinoid receptor type 1 (CB1), which is expressed by different neuronal subpopulations in the central nervous system. The exact neuroanatomical substrates underlying each effect of THC are, however, not known. We tested locomotor, hypothermic, analgesic, and cataleptic effects of THC in conditional knockout mouse lines, which lack the expression of CB1 in different neuronal subpopulations, including principal brain neurons, GABAergic neurons (those that release γ aminobutyric acid), cortical glutamatergic neurons, and neurons expres…

MaleMESH: Body TemperatureCannabinoid receptormedicine.medical_treatmentGene ExpressionMESH: Receptor Cannabinoid CB1NeocortexMESH: gamma-Aminobutyric AcidMESH: CatalepsyPharmacologyHippocampusMESH: Mice KnockoutMESH: Corpus StriatumBody TemperatureMESH: Autonomic Nervous SystemMESH: NeocortexMice0302 clinical medicineReceptor Cannabinoid CB1MESH: Behavior AnimalCannabinoid receptor type 1MESH: AnimalsMESH: Gene SilencingDronabinolMESH: NociceptorsBiology (General)gamma-Aminobutyric AcidMice Knockout0303 health sciencesBehavior Animalmusculoskeletal neural and ocular physiologyGeneral NeuroscienceMESH: Pain ThresholdNociceptorsMESH: Glutamic AcidMESH: InterneuronsMESH: Motor Activity3. Good healthGABAergicMESH: TetrahydrocannabinolGeneral Agricultural and Biological SciencesResearch Articlemedicine.drugPain ThresholdMESH: Gene ExpressionMESH: Psychotropic DrugsQH301-705.5Glutamic AcidMotor ActivityBiologyAutonomic Nervous SystemGeneral Biochemistry Genetics and Molecular Biologygamma-Aminobutyric acid03 medical and health sciencesGlutamatergicDopamine receptor D1InterneuronsCannabinoid Receptor Modulatorsmental disorders[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineAnimalsGenetic Predisposition to Disease[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyGene SilencingTetrahydrocannabinolMESH: MiceAnesthesiology and Pain Management030304 developmental biologyPharmacologyCatalepsyPsychotropic DrugsModels GeneticGeneral Immunology and MicrobiologyCannabinoidsIllicit Drugsorganic chemicalsMESH: MaleCorpus StriatumPrimerDisease Models Animalnervous systemCannabinoidNervous System Diseases030217 neurology & neurosurgeryNeurosciencePLoS Biology
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Prenatal exposure to the CB1 receptor agonist WIN 55,212-2 causes learning disruption associated with impaired cortical NMDA receptor function and em…

2005

The aim of this study was to investigate whether prenatal exposure to the cannabinoid CB1 receptor agonist WIN 55,212-2 (WIN) at a daily dose devoid of overt signs of toxicity and/or gross malformations (0.5 mg/kg, gestation days 5-20), influences cortical glutamatergic neurotransmission, learning and emotional reactivity in rat offspring. Basal and K+-evoked extracellular glutamate levels were significantly lower in cortical cell cultures obtained from pups exposed to WIN during gestation with respect to those measured in cultures obtained from neonates born from vehicle-treated dams. The addition of NMDA to cortical cell cultures from neonates born from vehicle-treated dams concentration-…

MaleMarijuana AbuseCannabinoid receptoractive avoidance behaviour; basal and K+-evoked glutamate levels; cortical cell cultures; homing behaviour; maternal marijuana consumption; ultrasonic vocalizationEmotionsReceptor Cannabinoid CB1Pregnancyactive avoidance behaviourWIN 55212-2Cells CulturedCerebral CortexBehavior AnimalGlutamate receptorBraincortical cell culturesCalcium Channel Blockersactive avoidance behaviour; basal and k plus -evoked glutamate levels; basal and k+-evoked glutamate levels; cortical cell cultures; homing behaviour; maternal marijuana consumption; ultrasonic vocalizationPrenatal Exposure Delayed EffectsChloratesNMDA receptorbasal and K+-evoked glutamate levelsFemaleMicrotubule-Associated Proteinsmedicine.drugAgonistmedicine.medical_specialtyOffspringmedicine.drug_classCognitive NeuroscienceMorpholinesGlutamic Acidmaternal marijuana consumptionNeurotransmissionBiologyNaphthalenesReceptors N-Methyl-D-AspartateCellular and Molecular NeuroscienceGlutamatergicInternal medicinemedicineAvoidance LearningAnimalsRats WistarBenzoxazinesRatsultrasonic vocalizationEndocrinologyAnimals Newbornhoming behaviourVocalization AnimalExtracellular SpaceNeuroscience
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Neuroprotection and glutamate attenuation by acetylsalicylic acid in temporary but not in permanent cerebral ischemia.

2007

To assess the effects of acetylsalicylic acid (ASA) on glutamate and interleukin-6 (IL-6) release in the striatum of rats suffering from cerebral ischemia, we used the microdialysis technique with probes implanted 2 h prior to stroke onset. A total of 36 rats were randomly assigned to either temporary (90 min, n = 18) or permanent (n = 18) middle cerebral artery occlusion (MCAO). Animals received either a bolus of 40 mg/kg ASA or saline as control 30 min after stroke onset. Permanent MCAO led to large infarct volumes with no differences between treatment with ASA (239.8 ± 4.1 mm3) and saline (230.1 ± 3.9 mm3, p = 0.15). In contrast, ASA therapy in temporary ischemia (87.2 ± 6.2 mm3) reduced…

MaleMicrodialysisTime Factorsmedicine.medical_treatmentIschemiaGlutamic AcidEnzyme-Linked Immunosorbent AssayNeuroprotectionBrain IschemiaBrain ischemiaBolus (medicine)Developmental NeurosciencemedicineAnimalscardiovascular diseasesRats WistarSalinePeroxidaseAnalysis of VarianceAspirinbusiness.industryInterleukin-6PenumbraGlutamate receptorCerebral Infarctionmedicine.diseaseRatsDisease Models AnimalNeuroprotective AgentsNeurologyGene Expression RegulationIschemic Attack TransientAnesthesiabusinessProto-Oncogene Proteins c-fosExperimental neurology
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Effects of a small acute subdural hematoma following traumatic brain injury on neuromonitoring, brain swelling and histology in pigs.

2011

An acute subdural hematoma (ASDH) induces pathomechanisms which worsen outcome after traumatic brain injury, even after a small hemorrhage. Synergistic effects of a small ASDH on brain damage are poorly understood, and were studied here using neuromonitoring for 10 h in an injury model of controlled cortical impact (CCI) and ASDH. Pigs (n = 32) were assigned to 4 groups: sham, CCI (2.5 m/s), ASDH (2 ml) and CCI + ASDH. Intracranial pressure was significantly increased above sham levels by all injuries with no difference between groups. CCI and ASDH reduced ptiO<sub>2</sub> by a maximum of 36 ± 9 and 26 ± 11%, respectively. The combination caused a 31 ± 11% drop. ASDH alone and i…

MaleMicrodialysisanimal structuresIntracranial PressureTraumatic brain injurySus scrofaGlutamic AcidBrain EdemaBrain damageEvoked Potentials SomatosensorymedicineAnimalsHematoma Subdural AcuteLactic AcidIntracranial pressureMonitoring Physiologicbusiness.industryGlutamate receptorHistologymedicine.diseasenervous system diseasesDisease Models AnimalSomatosensory evoked potentialAnesthesiaBrain InjuriesCerebrovascular CirculationSurgerymedicine.symptombusinessAcute subdural hematomapsychological phenomena and processesEuropean surgical research. Europaische chirurgische Forschung. Recherches chirurgicales europeennes
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Nitric oxide-active compounds modulate the intensity of glutamate-evoked responses in the globus pallidus of the rat

2011

Abstract Aim The effects of local applied NO-active compounds on glutamate (GLU)-evoked responses were investigated in globus pallidus (GP) neurons. Main methods Extracellularly recorded single units from anesthetized rats were treated with GLU before and during the microiontophoretic application of S-nitrosoglutathione (SNOG), a NO donor, and Nω-nitro- l -arginine methyl ester (L-NAME), a NOS inhibitor. Key findings Most GP cells were excited by SNOG whereas administration of L-NAME induced decrease of GP neurons activity. Nearly all neurons responding to SNOG and/or L-NAME showed significant modulation of their excitatory responses to the administration of iontophoretic GLU. In these cell…

MaleNOS inhibitorGlutamic AcidNitric oxide - Microiontophoresis - ElectrophysiologyBiologyPharmacologyGlobus PallidusNitric OxideSettore BIO/09 - FisiologiaGeneral Biochemistry Genetics and Molecular BiologyNitric oxidechemistry.chemical_compoundGlutamatergicNitric oxide; Basal ganglia; Single unit electrophysiology; MicroiontophoresisBasal gangliaSingle unit electrophysiologyAnimalsNitric Oxide DonorsRats WistarGeneral Pharmacology Toxicology and PharmaceuticsEvoked PotentialsNeuronsMicroiontophoresisIontophoresisGlutamate receptorExcitatory Postsynaptic PotentialsGeneral MedicineIontophoresisRatsNG-Nitroarginine Methyl EsterGlobus pallidusBiochemistrychemistryBasal gangliaExcitatory postsynaptic potentialNitric Oxide SynthaseMicroelectrodesLife Sciences
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