Search results for "GLUTAMATE"

showing 10 items of 434 documents

Neurotransmitters and Behavioral Alterations Induced by Nickel Exposure.

2020

Background:: Nickel ions (Ni2+) are a heavy metal with wide industrial uses. Environmental and occupational exposures to Ni are potential risk factors for brain dysfunction and behavioral and neurological symptoms in humans. Methods: We reviewed the current evidence about neurochemical and behavioral alterations associated with Ni exposure in laboratory animals and humans. Results: Ni2+ exposure can alter (both inhibition and stimulation) dopamine release and inhibit glutamate NMDA receptors. Few reports claim an effect of Ni2+ at the level of GBA and serotonin neurotransmission. At behavioral levels, exposure to Ni2+ in rodents alters motor activity, learning and memory as well as anxiety…

0301 basic medicinemedicine.medical_specialtyEndocrinology Diabetes and MetabolismPopulationStimulationEnvironmental Illness03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNeurochemicalDopamineNickelInternal medicineImmunology and AllergyMedicineAnimalsHumanseducationNeurotransmittereducation.field_of_studyBehaviorNeurotransmitter Agentsbusiness.industryMental DisordersGlutamate receptorEnvironmental Exposure030104 developmental biologyEndocrinologychemistryNMDA receptorSerotoninbusiness030217 neurology & neurosurgerymedicine.drugEndocrine, metabolicimmune disorders drug targets
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Chronic aspartame intake causes changes in the trans-sulphuration pathway, glutathione depletion and liver damage in mice

2017

No-caloric sweeteners, such as aspartame, are widely used in various food and beverages to prevent the increasing rates of obesity and diabetes mellitus, acting as tools in helping control caloric intake. Aspartame is metabolized to phenylalanine, aspartic acid, and methanol. Our aim was to study the effect of chronic administration of aspartame on glutathione redox status and on the trans-sulphuration pathway in mouse liver. Mice were divided into three groups: control; treated daily with aspartame for 90 days; and treated with aspartame plus N-acetylcysteine (NAC). Chronic administration of aspartame increased plasma alanine aminotransferase (ALT) and aspartate aminotransferase activities…

0301 basic medicinemedicine.medical_specialtyGlutamate-Cysteine LigaseClinical BiochemistryPhenylalanineBiochemistryMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineAspartic acidmedicineAnimalsHumansCysteineAspartamelcsh:QH301-705.5lcsh:R5-920S-adenosylmethionineMethioninebiologyAspartameChemistryOrganic ChemistryCystathionine gamma-LyaseMethionine AdenosyltransferaseGlutathioneGlutathioneCystathionine beta synthaseN-acetylcysteineAcetylcysteine030104 developmental biologyEndocrinologyGCLCGene Expression RegulationLiverlcsh:Biology (General)BiochemistrySweetening Agents030220 oncology & carcinogenesisbiology.proteinChemical and Drug Induced Liver Injurylcsh:Medicine (General)Research PaperCysteineRedox Biology
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Altered synaptic phospholipid signaling in PRG-1 deficient mice induces exploratory behavior and motor hyperactivity resembling psychiatric disorders.

2017

Abstract Plasticity related gene 1 (PRG-1) is a neuron specific membrane protein located at the postsynaptic density of glutamatergic synapses. PRG-1 modulates signaling pathways of phosphorylated lipid substrates such as lysophosphatidic acid (LPA). Deletion of PRG-1 increases presynaptic glutamate release probability leading to neuronal over-excitation. However, due to its cortical expression, PRG-1 deficiency leading to increased glutamatergic transmission is supposed to also affect motor pathways. We therefore analyzed the effects of PRG-1 function on exploratory and motor behavior using homozygous PRG-1 knockout (PRG-1−/−) mice and PRG-1/LPA2–receptor double knockout (PRG-1−/−/LPA2−/−)…

0301 basic medicinemedicine.medical_specialtyGlutamic AcidNerve Tissue ProteinsBiologyHyperkinesisHippocampusOpen field03 medical and health sciencesBehavioral NeuroscienceGlutamatergicchemistry.chemical_compoundMice0302 clinical medicineLysophosphatidic acidmedicineAnimalsReceptors Lysophosphatidic AcidPsychiatryMice KnockoutNeuronsMental DisordersGlutamate receptorSomatosensory CortexMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurechemistrySynapsesExploratory BehaviorGABAergicCalmodulin-Binding ProteinsFemaleNeuronSignal transductionLysophospholipidsPostsynaptic density030217 neurology & neurosurgerySignal TransductionBehavioural brain research
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Obesity as a Risk Factor for Alzheimer’s Disease: Implication of Leptin and Glutamate

2019

Obesity is known to induce leptin and insulin resistance. Leptin is a peptide hormone synthesized in adipose tissue that mainly regulates food intake. It has been shown that insulin stimulates the production of leptin when adipocytes are exposed to glucose to encourage satiety; while leptin, via a negative feedback, decreases the insulin release and enhances tissue sensitivity to it, leading to glucose uptake for energy utilization or storage. Therefore, resistance to insulin is closely related to leptin resistance. Obesity in middle age has also been related to Alzheimer’s disease (AD). In recent years, the relation between impaired leptin signaling pathway and the onset of AD has been stu…

0301 basic medicinemedicine.medical_specialtyMini Reviewmedicine.medical_treatmentGlucose uptakeExcitotoxicityAdipose tissuemedicine.disease_causelcsh:RC321-57103 medical and health sciences0302 clinical medicineInsulin resistanceInternal medicinemedicineoverweightleptin-resistanceReceptorlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrybusiness.industryGeneral NeuroscienceInsulinLeptindigestive oral and skin physiologyGlutamate receptormedicine.disease030104 developmental biologyEndocrinologyLTPbusinessexcitotoxicity030217 neurology & neurosurgeryhormones hormone substitutes and hormone antagonistsNeurosciencedementiaFrontiers in Neuroscience
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Reducing Peripheral Inflammation with Infliximab Reduces Neuroinflammation and Improves Cognition in Rats with Hepatic Encephalopathy

2016

Inflammation contributes to cognitive impairment in patients with hepatic encephalopathy (HE). However, the process by which peripheral inflammation results in cognitive impairment remains unclear. In animal models, neuroinflammation and altered neurotransmission mediate cognitive impairment. Taking into account these data, we hypothesized that in rats with HE: (1) peripheral inflammation is a main contributor to neuroinflammation; (2) neuroinflammation in hippocampus impairs spatial learning by altering AMPA and/or NMDA receptors membrane expression; (3) reducing peripheral inflammation with infliximab (anti-TNF-a) would improve spatial learning; (4) this would be associated with reduced n…

0301 basic medicinemedicine.medical_specialtyTNF-ahepatic encephalopathyHippocampusMorris water navigation taskInflammationAMPA receptorNeurotransmissionlcsh:RC321-571neuroinflammation03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineInternal medicinemedicineneurotransmissionlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyNeuroinflammationOriginal Researchcognitive impairmentbusiness.industryGlutamate receptor030104 developmental biologyEndocrinologynervous systemNMDA receptormedicine.symptombusinessNeuroscience030217 neurology & neurosurgeryNeuroscience
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Modulation of Neocortical Development by Early Neuronal Activity: Physiology and Pathophysiology.

2017

Animal and human studies revealed that patterned neuronal activity is an inherent feature of developing nervous systems. This review summarizes our current knowledge about the mechanisms generating early electrical activity patterns and their impact on structural and functional development of the cerebral cortex. All neocortical areas display distinct spontaneous and sensory-driven neuronal activity patterns already at early phases of development. At embryonic stages, intermittent spontaneous activity is synchronized within small neuronal networks, becoming more complex with further development. This transition is accompanied by a gradual shift from electrical to chemical synaptic transmiss…

0301 basic medicinesomatosensory cortexReviewBiologylcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineSubplatemedicinePremovement neuronal activityhumanddc:610Neurotransmitterlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrydevelopmentspontaneous activityNeocortexGlutamate receptorrodentChemical synaptic transmission030104 developmental biologymedicine.anatomical_structureElectrical SynapseschemistryCerebral cortexsubplatecerebral cortexNeuroscience030217 neurology & neurosurgeryNeuroscience
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2013

Reciprocal interactions between neurons and oligodendrocytes are not only crucial for myelination, but also for long-term survival of axons. Degeneration of axons occurs in several human myelin diseases, however the molecular mechanisms of axon-glia communication maintaining axon integrity are poorly understood. Here, we describe the signal-mediated transfer of exosomes from oligodendrocytes to neurons. These endosome-derived vesicles are secreted by oligodendrocytes and carry specific protein and RNA cargo. We show that activity-dependent release of the neurotransmitter glutamate triggers oligodendroglial exosome secretion mediated by Ca2+ entry through oligodendroglial NMDA and AMPA recep…

0303 health sciencesCell signalingGeneral Immunology and MicrobiologyGeneral NeuroscienceGlutamate receptorAMPA receptorBiologyExosomeGeneral Biochemistry Genetics and Molecular BiologyOligodendrocyteMicrovesiclesCell biology03 medical and health sciences0302 clinical medicinemedicine.anatomical_structurenervous systemmedicineNeuronAxonGeneral Agricultural and Biological Sciences030217 neurology & neurosurgery030304 developmental biologyPLOS Biology
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Involvement of cyclin-dependent kinase-5 in the kainic acid-mediated degeneration of glutamatergic synapses in the rat hippocampus

2011

Increased levels of glutamate causing excitotoxic damage accompany neurological disorders such as ischemia/stroke, epilepsy and some neurodegenerative diseases. Cyclin-dependent kinase-5 (Cdk5) is important for synaptic plasticity and is deregulated in neurodegenerative diseases. However, the mechanisms by which kainic acid (KA)-induced excitotoxic damage involves Cdk5 in neuronal injury are not fully understood. In this work, we have thus studied involvement of Cdk5 in the KA-mediated degeneration of glutamatergic synapses in the rat hippocampus. KA induced degeneration of mossy fiber synapses and decreased glutamate receptor (GluR)6/7 and post-synaptic density protein 95 (PSD95) levels in…

0303 health sciencesKainic acidGeneral NeuroscienceCyclin-dependent kinase 5ExcitotoxicityGlutamate receptorBiologyHippocampal formationmedicine.disease_cause3. Good healthCell biology03 medical and health sciencesGlutamatergicchemistry.chemical_compound0302 clinical medicinenervous systemchemistrySynaptic plasticitymedicineReceptorNeuroscience030217 neurology & neurosurgery030304 developmental biologyEuropean Journal of Neuroscience
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Author response: ON selectivity in the Drosophila visual system is a multisynaptic process involving both glutamatergic and GABAergic inhibition

2019

0303 health sciencesbiologyChemistrybiology.organism_classification03 medical and health sciencesGlutamatergic0302 clinical medicineGabaergic inhibitionDrosophila (subgenus)SelectivityNeuroscienceProcess (anatomy)030217 neurology & neurosurgery030304 developmental biology
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Semilunar Granule Cells Are the Primary Source of the Perisomatic Excitatory Innervation onto Parvalbumin-Expressing Interneurons in the Dentate Gyrus

2020

AbstractWe analyzed the origin and relevance of the perisomatic excitatory inputs on the parvalbumin interneurons of the granule cell layer in mouse. Confocal analysis of the glutamatergic innervation showed that it represents ∼50% of the perisomatic synapses that parvalbumin cells receive. This excitatory input may originate from granule cell collaterals, the mossy cells, or even supramammillary nucleus. First, we assessed the input from the mossy cells on parvalbumin interneurons. Axon terminals of mossy cells were visualized by their calretinin content. Using multicolor confocal microscopy, we observed that less than 10% of perisomatic excitatory innervation of parvalbumin cells could or…

6Neuronal ExcitabilityMiceGlutamatergicInterneuronsmedicineAnimalsAxonNeuronselectron microscopybiologyChemistrymusculoskeletal neural and ocular physiologyGeneral NeuroscienceDentate gyrusGeneral MedicinetracingGranule cellAxonsAnterograde tracingParvalbuminsmedicine.anatomical_structurenervous systemDentate GyrusimmunochemistryExcitatory postsynaptic potentialbiology.proteinCalretininNeuroscienceResearch Article: New ResearchmicrocircuitryParvalbumineneuro
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