Search results for "Glutamate receptor"

showing 10 items of 219 documents

Functional genomics indicate that schizophrenia may be an adult vascular-ischemic disorder

2015

AbstractIn search for the elusive schizophrenia pathway, candidate genes for the disorder from a discovery sample were localized within the energy-delivering and ischemia protection pathway. To test the adult vascular-ischemic (AVIH) and the competing neurodevelopmental hypothesis (NDH), functional genomic analyses of practically all available schizophrenia-associated genes from candidate gene, genome-wide association and postmortem expression studies were performed. Our results indicate a significant overrepresentation of genes involved in vascular function (P<0.001), vasoregulation (that is, perivascular (P<0.001) and shear stress (P<0.01), cerebral ischemia (P<0.001), neurode…

Candidate genemedicine.medical_specialtyPostmortem studiesLong-Term PotentiationBiologySynaptic TransmissionBrain IschemiaBrain ischemiaCellular and Molecular NeuroscienceInternal medicinemedicineHumansGenetic Predisposition to Diseaseddc:610Biological PsychiatryNeuronal PlasticityNeurogenesisGlutamate receptorLong-term potentiationGenomicsmedicine.diseasePsychiatry and Mental healthEndocrinologySchizophreniaSynaptic plasticitySchizophreniaOriginal ArticleNeuroscienceGenome-Wide Association Study
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Cell type‐specific genetic reconstitution of CB1 receptor subsets to assess their role in exploratory behaviour, sociability, and memory

2021

Several studies support the notion that exploratory behaviour depends on the functionality of the cannabinoid type 1 (CB1) receptor in a cell type-specific manner. Mice lacking the CB1 receptor in forebrain GABAergic or dorsal telencephalic glutamatergic neurons have served as essential tools revealing the necessary CB1 receptor functions in these two neuronal populations. However, whether these specific CB1 receptor populations are also sufficient within the endocannabinoid system for wild-type-like exploratory behaviour has remained unknown. To evaluate cell-type-specific sufficiency of CB1 receptor signalling exclusively in dorsal telencephalic glutamatergic neurons (Glu-CB1-RS) or in fo…

Cannabinoid receptormedicine.medical_treatmentBiologyMice03 medical and health sciencesGlutamatergic0302 clinical medicineReceptor Cannabinoid CB1medicineAnimalsGABAergic NeuronsReceptorgamma-Aminobutyric Acid030304 developmental biologyMice Knockout0303 health sciencesmusculoskeletal neural and ocular physiologyGeneral NeuroscienceGlutamate receptorfood and beveragesEndocannabinoid systemMice Inbred C57BLnervous systemForebrainExploratory BehaviorGABAergiclipids (amino acids peptides and proteins)CannabinoidNeurosciencepsychological phenomena and processes030217 neurology & neurosurgeryEndocannabinoidsEuropean Journal of Neuroscience
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Galantamine modulates nicotinic receptor and blocks Aβ-enhanced glutamate toxicity

2004

Galantamine is a plant alkaloid that is used in the treatment of Alzheimer's disease. We have studied the effects of galantamine on beta-amyloid-enhanced glutamate toxicity using primary rat cultured cortical neurons. Nicotine and galantamine alone, and in combination, protected neurons against this neurotoxicity. The protection was not blocked by alpha4beta2 nicotinic acetylcholine receptor (nAChR) antagonists, but was partially blocked by alpha7 nAChR antagonists. Galantamine induced phosphorylation of Akt, an effector of phosphatidylinositol 3-kinase (PI3K), while PI3K inhibitors blocked the protective effect and Akt phosphorylation. The antibody FK1, which selectively blocks the alloste…

Cell SurvivalBiophysicsGlutamic AcidReceptors NicotinicPharmacologycomplex mixturesBiochemistryNeuroprotectionmedicineGalantamineAnimalsDrug InteractionsMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCerebral CortexNeuronsAmyloid beta-PeptidesDose-Response Relationship DrugGalantamineChemistryGlutamate receptorNeurotoxicityCell Biologymedicine.diseaseRatsNeuroprotective AgentsNicotinic agonistnervous systemPhosphorylationmedicine.drugBiochemical and Biophysical Research Communications
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Cellular physiology of the neonatal rat cerebral cortex.

2003

The early development of the cerebral cortex is characterized by neurogenesis, neuronal migration, cellular differentiation and programmed cell death. Cajal-Retzius cells, developing cortical plate neurons and subplate cells form a transient synaptic circuit which may serve as a template for the formation of cortical layers and columns. These three neuronal cell types show distinct electrophysiological properties and synaptic inputs. Endogenous or exogenous harmful disturbances during this developmental period may lead to the preservation of early cortical circuits, which may act as trigger zones for the initiation of pathophysiological activity.

Cell physiologyCerebral CortexNeuronsCell typeGeneral NeuroscienceCellular differentiationNeurogenesisGlutamate receptorAction PotentialsBiologyCell Physiological PhenomenaRatsElectrophysiologymedicine.anatomical_structureAnimals NewbornCerebral cortexSubplatemedicineAnimalsNeuroscienceBrain research bulletin
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Multifaceted effects of oligodendroglial exosomes on neurons: impact on neuronal firing rate, signal transduction and gene regulation.

2014

Exosomes are small membranous vesicles of endocytic origin that are released by almost every cell type. They exert versatile functions in intercellular communication important for many physiological and pathological processes. Recently, exosomes attracted interest with regard to their role in cell–cell communication in the nervous system. We have shown that exosomes released from oligodendrocytes upon stimulation with the neurotransmitter glutamate are internalized by neurons and enhance the neuronal stress tolerance. Here, we demonstrate that oligodendroglial exosomes also promote neuronal survival during oxygen–glucose deprivation, a model of cerebral ischaemia. We show the transfer from…

Cell typeCell signalingEndocytic cycleBlotting WesternAction PotentialsCell CommunicationNeurotransmissionBiologyExosomesReal-Time Polymerase Chain ReactionExosomeSynaptic TransmissionGeneral Biochemistry Genetics and Molecular BiologyMiceAnimalsPhosphorylationCells CulturedNeuronsSuperoxide DismutaseGlutamate receptorCatalaseMicroarray AnalysisPart III: Intercellular communication—basic insightImmunohistochemistryMicrovesiclesCell HypoxiaCell biologyMice Inbred C57BLOligodendrogliaGlucoseGene Expression RegulationSignal transductionGeneral Agricultural and Biological SciencesSignal TransductionPhilosophical transactions of the Royal Society of London. Series B, Biological sciences
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NG2-positive cells in CNS function and the pathological role of antibodies against NG2 in demyelinating diseases

2005

NG2 is expressed by a variety of immature glia in the CNS including oligodendrocyte progenitor cells, paranodal astrocytes and perisynaptic glia. The protein has a large extracellular domain with two LNS/Lam G domains at the N-terminus and a short intracellular tail with a PDZ-recognition domain at the C-terminus. Experiments suggest that the protein plays a role in migration. The PDZ protein GRIP was identified as an intracellular binding partner of NG2 in immature glial cells. A complex is formed between GRIP, NG2 and the AMPA class of glutamate receptors: this may position these glial receptors towards sites of neuronal glutamate release at synapses and during myelination. Identification…

Central Nervous SystemCentral nervous systemPDZ domainGlutamate receptorAMPA receptorBiologyModels BiologicalAntibodiesOligodendrocytemedicine.anatomical_structurenervous systemNeurologySynapsesmedicineAnimalsHumansNeurogliaProteoglycansNeurology (clinical)AntigensRemyelinationReceptorNeurogliaNeuroscienceDemyelinating DiseasesJournal of the Neurological Sciences
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Possible Pathomechanisms Responsible for Injury to the Central Nervous System in the Settings of Chronic Cerebrospinal Venous Insufficiency

2012

The discovery of stenoses in the azygous and internal jugular veins, the so-called chronic cerebrospinal venous insufficiency that accompanies multiple sclerosis, has enabled the reinterpretation of knowledge about this neurologic dis- ease. Pathologic venous outflow from the central nervous system appears to lead to two main problems. Firstly, it disas- sembles the blood-brain barrier and may allow the penetration of nervous parenchyma by glutamate and leukocytes. Sec- ondly, it may result in significant hypoperfusion of the brain and spinal cord. These two overlapping pathologies are likely to trigger plaques through caspase-1-driven pyroptosis of oligodendrocytes and to evoke neurodegene…

Central Nervous SystemPathologymedicine.medical_specialtyCentral nervous systemExcitotoxicityglutamatemultiple sclerosismedicine.disease_causeAxonal injuryCentral Nervous System Diseasescaspase 1venous insufficiencymedicineHumansBrachiocephalic Veinsjugular veinsPharmacologybusiness.industryMultiple sclerosisazygous veinNeurodegenerationPyroptosisGlutamate receptorGeneral Medicineblood-brain barriermedicine.diseaseSpinal cordChronic cerebrospinal venous insufficiencymedicine.anatomical_structureSpinal CordbusinessReviews on Recent Clinical Trials
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Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions

2005

Steroids that activate glucocorticoid receptors (GRs) and mineralocorticoid receptors have important regulatory effects on neural development, plasticity, and the body's stress response. Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transporters glial glutamate transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) in rat primary astrocytes. The synthetic glucocorticoid dexamethasone provoked a marked increase of GLT-1 transcription and protein levels in cortical astrocytes, whereas GLAST expression remained unaffected. Up-regulation of GLT-1 expression was accompanied by an enhanced glutamate uptake, which could be blocked …

Central Nervous SystemTime FactorsAmino Acid Transport System X-AGLigandsBiochemistryDexamethasoneRats Sprague-Dawleychemistry.chemical_compoundGlucocorticoid receptorMineralocorticoid receptorAdrenal Cortex HormonesCorticosteroneCerebellumGene expressionLuciferasesReceptorDNA Modification MethylasesKainic AcidReverse Transcriptase Polymerase Chain ReactionGlutamate receptorBrainImmunohistochemistryUp-RegulationMifepristoneAzacitidineNeurogliaGlucocorticoidmedicine.drugmedicine.medical_specialtymedicine.drug_classBlotting WesternDetergentsBiologyDecitabineTransfectionMembrane MicrodomainsInternal medicinemedicineAnimalsGlucocorticoidsMolecular BiologyDNA PrimersFluorescent DyesDose-Response Relationship DrugCell BiologyDNA MethylationRatsReceptors MineralocorticoidEndocrinologychemistryMineralocorticoidAstrocytesCorticosteroneJournal of Biological Chemistry
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Glutamate Excitotoxicity in the Cerebellum Mediated by IL-1β

2013

Multiple sclerosis (MS) is the prototypic inflammatory demyelinating disorder of the CNS. Symptoms of cerebellar dysfunction, such as tremors and ataxia, are relatively common in MS, but available treatment options are generally of limited value. Although many clinical manifestations of MS are

CerebellumAtaxiabusiness.industryGeneral NeuroscienceMultiple sclerosisEncephalomyelitisExcitotoxicityGlutamate receptorTreatment optionsmedicine.disease_causemedicine.diseasemedicine.anatomical_structureImmunologymedicinemedicine.symptomDemyelinating DisorderbusinessThe Journal of Neuroscience
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Interplay between glutamatergic and GABAergic neurotransmission alterations in cognitive and motor impairment in minimal hepatic encephalopathy.

2015

The cognitive and motor alterations in hepatic encephalopathy (HE) are the final result of altered neurotransmission and communication between neurons in neuronal networks and circuits. Different neurotransmitter systems cooperate to modulate cognitive and motor function, with a main role for glutamatergic and GABAergic neurotransmission in different brain areas and neuronal circuits. There is an interplay between glutamatergic and GABAergic neurotransmission alterations in cognitive and motor impairment in HE. This interplay may occur: (a) in different brain areas involved in specific neuronal circuits; (b) in the same brain area through cross-modulation of glutamatergic and GABAergic neur…

CerebellumMinimal hepatic encephalopathyGlutamic AcidNeurotransmissionSynaptic TransmissionCellular and Molecular NeuroscienceGlutamatergicmedicineHyperammonemiaAnimalsHumansGlutamatergic neurotransmissionGABAergic neurotransmissionHepatic encephalopathygamma-Aminobutyric AcidHepatic encephalopathyGABAA receptorbusiness.industryGlutamate receptorHyperammonemiaCognitionCell Biologymedicine.diseaseMotor Skills Disordersmedicine.anatomical_structureHepatic EncephalopathyCognitive functionCognition DisordersbusinessNeuroscience
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