Search results for " glutamate"

showing 10 items of 97 documents

The endocannabinoid system controls key epileptogenic circuits in the hippocampus.

2006

SummaryBalanced control of neuronal activity is central in maintaining function and viability of neuronal circuits. The endocannabinoid system tightly controls neuronal excitability. Here, we show that endocannabinoids directly target hippocampal glutamatergic neurons to provide protection against acute epileptiform seizures in mice. Functional CB1 cannabinoid receptors are present on glutamatergic terminals of the hippocampal formation, colocalizing with vesicular glutamate transporter 1 (VGluT1). Conditional deletion of the CB1 gene either in cortical glutamatergic neurons or in forebrain GABAergic neurons, as well as virally induced deletion of the CB1 gene in the hippocampus, demonstrat…

MaleVesicular glutamate transporter 1HUMDISEASEHippocampusGene ExpressionHippocampal formationHippocampusMembrane Potentialschemistry.chemical_compoundMice0302 clinical medicineReceptor Cannabinoid CB1Premovement neuronal activitygamma-Aminobutyric Acid0303 health sciencesKainic AcidbiologyBehavior AnimalReverse Transcriptase Polymerase Chain Reactionmusculoskeletal neural and ocular physiologyGeneral NeurosciencePyramidal CellsCalcium Channel BlockersEndocannabinoid systemlipids (amino acids peptides and proteins)psychological phenomena and processesmedicine.drugKainic acidNeuroscience(all)MorpholinesGlutamic AcidMice TransgenicNaphthalenesMOLNEUROgamma-Aminobutyric acid03 medical and health sciencesGlutamatergicCannabinoid Receptor ModulatorsmedicineAnimals030304 developmental biologyAnalysis of VarianceEpilepsyBenzoxazinesMice Inbred C57BLnervous systemchemistryCalcium-Calmodulin-Dependent Protein KinasesVesicular Glutamate Transport Protein 1biology.proteinNerve NetSYSNEUROCalcium-Calmodulin-Dependent Protein Kinase Type 2Neuroscience030217 neurology & neurosurgeryEndocannabinoidsNeuron
researchProduct

AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders.

2019

AMPA receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits encoded by GRIA1-4 genes. GluA2 has an especially important role because, following post-transcriptional editing at the Q607 site, it renders heteromultimeric AMPARs Ca2+-impermeable, with a linear relationship between current and trans-membrane voltage. Here, we report heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abnormalities including autism spectrum disorder (ASD), Rett syndrome-like features, and seizures or developmental epileptic encephalopathy (DEE). In functional expression studies, mutations lead to a dec…

Male[SDV.GEN] Life Sciences [q-bio]/GeneticsIon channels in the nervous systemCohort Studiesfluids and secretionsLoss of Function MutationReceptorsAMPAAMPA receptorlcsh:ScienceChildreproductive and urinary physiologyAMPA receptor GluA2 neurodevelopmental disorders autism spectrum disorder glutamatergic synaptic transmission GRIA2neurodevelopmental disordersDevelopmental disordersQNeurodevelopmental disordersBrainMagnetic Resonance ImagingSettore MED/26 - NEUROLOGIAGluA2Child PreschoolFemaleAdultHeterozygoteAdolescentScienceautism spectrum disorderArticleYoung Adult[SDV.MHEP.PED] Life Sciences [q-bio]/Human health and pathology/PediatricsMESH: Intellectual Disability/genetics; Neurodevelopmental Disorders/genetics; Receptors AMPA/genetics; HeterozygoteIntellectual Disabilitymental disordersAdolescent; Adult; Brain; Child; Child Preschool; Cohort Studies; Female; Heterozygote; Humans; Infant; Intellectual Disability; Loss of Function Mutation; Magnetic Resonance Imaging; Male; Neurodevelopmental Disorders; Receptors AMPA; Young AdultHumansReceptors AMPAGRIA2PreschoolIon channel in the nervous system Developmental disorders Synaptic development NG sequencing[SDV.GEN]Life Sciences [q-bio]/Genetics[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/Pediatricsglutamatergic synaptic transmission[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceInfantNG sequencingSynaptic developmentIon channel in the nervous systemNext-generation sequencinglcsh:Q
researchProduct

Acute ammonia toxicity is mediated by the NMDA type of glutamate receptors

1992

AbstractPrevious experiments in our laboratory suggested that ammonium toxicity could be mediated by the NMDA type of glutamate receptors. To assess this hypothesis we tested if MK-801, a specific antagonist of the NMDA receptor, is able to prevent ammonium toxicity. Mice and rats were injected i.p. with 12 and 7 mmol/kg of ammonium acetate, respectively, 73% of the mice and 70% of the rats died. However, when the animals were injected i.p. with 2 mg/kg of MK-801, 15 min before ammonium injection, only 5% of the mice and 15% of the rats died. The remarkable protection afforded by MK-801 indicates that ammonia toxicity is mediated by the NMDA receptor.

Malemedicine.medical_specialtyBiophysicsGlutamic AcidReceptors N-Methyl-D-AspartateBiochemistryAmmonia toxicityMicechemistry.chemical_compoundGlutamatesAmmoniaStructural BiologyInternal medicineGeneticsmedicineAnimalsHyperammonemiaNeurotransmitter metabolismAmmoniumReceptorMolecular BiologyMK-801Glutamate receptorRats Inbred StrainsValineCell BiologyGlutamic acidNMDA receptorRatsReceptors NeurotransmitterEndocrinologyReceptors GlutamatechemistryToxicityNMDA receptorDizocilpine MaleateAmmonium acetateFEBS Letters
researchProduct

Impaired cannabinoid receptor type 1 signaling interferes with stress-coping behavior in mice.

2007

Dysregulation of the endocannabinoid system is known to interfere with emotional processing of stressful events. Here, we studied the role of cannabinoid receptor type 1 (CB1) signaling in stress-coping behaviors using the forced swim test (FST) with repeated exposures. We compared effects of genetic inactivation with pharmacological blockade of CB1 receptors both in male and female mice. In addition, we investigated potential interactions of the endocannabinoid system with monoaminergic and neurotrophin systems of the brain. Naive CB1 receptor-deficient mice (CB1-/-) showed increased passive stress-coping behaviors as compared to wild-type littermates (CB1+/+) in the FST, independent of se…

Malemedicine.medical_specialtyCannabinoid receptormedicine.medical_treatmentBiologyPharmacologyHippocampusMicePiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid receptor type 1MonoaminergicAdaptation PsychologicalGeneticsmedicineAnimalsBiogenic MonoaminesRNA MessengerReceptorMonoamine OxidaseSwimmingPharmacologyBrain-derived neurotrophic factormusculoskeletal neural and ocular physiologyBrain-Derived Neurotrophic FactorDesipraminefood and beveragesEndocannabinoid systemMice Inbred C57BLMonoamine neurotransmitterEndocrinologynervous systemVesicular Glutamate Transport Protein 1Molecular MedicinePyrazoleslipids (amino acids peptides and proteins)FemaleCannabinoidRimonabantpsychological phenomena and processesStress PsychologicalSignal TransductionThe pharmacogenomics journal
researchProduct

Sildenafil reduces neuroinflammation and restores spatial learning in rats with hepatic encephalopathy: underlying mechanisms

2015

Background: There are no specific treatments for the neurological alterations of cirrhotic patients with minimal hepatic encephalopathy (MHE). Rats with MHE due to portacaval shunt (PCS) show impaired spatial learning. The underlying mechanisms remain unknown. The aims of this work were to assess: (a) whether PCS rats show neuroinflammation in hippocampus, (b) whether treatment with sildenafil reduces neuroinflammation and restores spatial learning in PCS rats, and (c) analyze the underlying mechanisms. Methods: Neuroinflammation was assessed by determining inflammatory markers by Western blot. Phosphorylation of MAP-kinase p38 was assessed by immunohistochemistry. Membrane expression of GA…

Malemedicine.medical_specialtyNeurologySildenafilVasodilator AgentsInterleukin-1betaImmunologyHippocampusInflammationPortacaval shuntHippocampusp38 Mitogen-Activated Protein KinasesSildenafil Citratechemistry.chemical_compoundCellular and Molecular NeuroscienceReceptors GABANeuroinflammationmedicineAnimalsRats WistarMaze LearningHepatic encephalopathyNeuroinflammationHepatic encephalopathyInflammationMicrogliaPortacaval Shunt SurgicalTumor Necrosis Factor-alphabusiness.industryResearchGeneral NeuroscienceMacrophage Activationmedicine.diseasehumanitiesSildenafil treatmentRatscGMPmedicine.anatomical_structureCognitive impairmentReceptors Glutamatechemistrynervous systemNeurologyHepatic EncephalopathyMicrogliamedicine.symptombusinesshuman activitiesNeuroscience
researchProduct

Binge drinking upregulates accumbens mGluR5-Homer2-PI3K signaling: functional implications for alcoholism.

2009

The glutamate receptor-associated protein Homer2 regulates alcohol-induced neuroplasticity within the nucleus accumbens (NAC), but the precise intracellular signaling cascades involved are not known. This study examined the role for NAC metabotropic glutamate receptor (mGluR)-Homer2-phosphatidylinositol 3-kinase (PI3K) signaling in regulating excessive alcohol consumption within the context of the scheduled high alcohol consumption (SHAC) model of binge alcohol drinking. Repeated bouts of binge drinking ( approximately 1.5 g/kg per 30 min) elevated NAC Homer2a/b expression and increased PI3K activity in this region. Virus-mediated knockdown of NAC Homer2b expression attenuated alcohol intak…

Malemedicine.medical_specialtyReceptor Metabotropic Glutamate 5Binge drinkingContext (language use)Mice TransgenicNucleus accumbensReceptors Metabotropic GlutamateNucleus AccumbensArticleWortmanninchemistry.chemical_compoundMicePhosphatidylinositol 3-KinasesHomer Scaffolding ProteinsInternal medicinemental disordersmedicineAnimalsEthanolEthanolMetabotropic glutamate receptor 5business.industryGeneral NeuroscienceAntagonistUp-RegulationMice Inbred C57BLAlcoholismEndocrinologyPhenotypechemistryMetabotropic glutamate receptorbusinessCarrier ProteinsNeuroscienceSignal TransductionThe Journal of neuroscience : the official journal of the Society for Neuroscience
researchProduct

Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implicatio…

2009

Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine acting on two distinct receptor subtypes, namely p55 and p75 receptors. TNF-alpha p55 and p75 receptor knockout mice were previously shown to display a decreased or enhanced susceptibility to seizures, respectively, suggesting intrinsic modifications in neuronal excitability. We investigated whether alterations in glutamate system function occur in these naive knockout mice with perturbed cytokine signaling that could explain their different propensity to develop seizures. Using Western blot analysis of hippocampal homogenates, we found that p55(-/-) mice have decreased levels of membrane GluR3 and NR1 glutamate receptor subuni…

Malemedicine.medical_specialtyReceptors Kainic acidMicrodialysisAction PotentialsGlutamic AcidKainate receptorAMPA receptorIn Vitro TechniquesBiologyHippocampusReceptors N-Methyl-D-Aspartateelectrophysiology microiontophoresisSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundGlutamatergicReceptors Kainic AcidSeizuresInternal medicinemedicineAnimalsReceptors Tumor Necrosis Factor Type IIReceptors AMPAMice KnockoutNeuronsInflammationTumor Necrosis Factor-alphaGeneral NeuroscienceGlutamate receptorProtein SubunitsEndocrinologymedicine.anatomical_structureReceptors Glutamatenervous systemchemistryReceptors Tumor Necrosis Factor Type IMetabotropic glutamate receptorAstrocytesCytokinesNMDA receptorNBQXDisease SusceptibilityAstrocyte
researchProduct

Group II metabotropic glutamate receptor activation by agonist LY379268 treatment increases the expression of brain derived neurotrophic factor in th…

2009

A number of in vitro and in vivo studies using selective agonists have indicated a neuroprotective role for group-II metabotropic glutamate (mGlu2/3) receptors in various models of neuronal injury. Although an interplay among neurotrophic factors and mGlu2/3 receptors signalling system has been suggested as possible mechanism involved on neuroprotection, at present poor information are available concerning the in vivo regulation by mGlu2/3 receptors activation of specific neurotrophic factors. By using in situ hybridization and western blotting methods the aim of present study was to analyse the potential regulatory role of selective mGluR2/3 agonist LY379268 treatment on brain derived neur…

Malemedicine.medical_specialtyTime Factorsmedicine.drug_classTropomyosin receptor kinase BBiologyReceptors Metabotropic GlutamateHippocampusSettore BIO/09 - FisiologiaMiceNeurotrophic factorsInternal medicineExcitatory Amino Acid AgonistsmedicineAnimalsRNA MessengerAmino Acidsneurotrophic factorNeuronsBrain-derived neurotrophic factorDose-Response Relationship DrughippocampuBrain-Derived Neurotrophic FactorGeneral NeuroscienceGlutamate receptorBrainLY379268Bridged Bicyclo Compounds HeterocyclicReceptor antagonistUp-RegulationMice Inbred C57BLMetabotropic receptorEndocrinologyBDNFXanthenesMetabotropic glutamate receptorcerebral cortexMetabotropic glutamate receptor 2Excitatory Amino Acid AntagonistsmGlu2/3 receptor
researchProduct

Full Domain Closure of the Ligand-binding Core of the Ionotropic Glutamate Receptor iGluR5 Induced by the High Affinity Agonist Dysiherbaine and the …

2009

The prevailing structural model for ligand activation of ionotropic glutamate receptors posits that agonist efficacy arises from the stability and magnitude of induced domain closure in the ligand-binding core structure. Here we describe an exception to the correlation between ligand efficacy and domain closure. A weakly efficacious partial agonist of very low potency for homomeric iGluR5 kainate receptors, 8,9-dideoxyneodysiherbaine (MSVIII-19), induced a fully closed iGluR5 ligand-binding core. The degree of relative domain closure, approximately 30 degrees , was similar to that we resolved with the structurally related high affinity agonist dysiherbaine and to that of l-glutamate. The ph…

Models MolecularAgonistStereochemistrymedicine.drug_classGlutamic AcidKainate receptorCrystallography X-RayLigandsBiochemistryPartial agonistCell LineReceptors Kainic AcidmedicineHumansComputer SimulationAmino AcidsReceptorMolecular BiologyAlanineBinding SitesChemistryMechanisms of Signal TransductionGlutamate receptorHydrogen BondingCell BiologyBridged Bicyclo Compounds HeterocyclicLigand (biochemistry)Protein Structure TertiaryProtein SubunitsIonotropic glutamate receptorProtein BindingIonotropic effectJournal of Biological Chemistry
researchProduct

Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
researchProduct