Search results for "d-a"

showing 10 items of 426 documents

Behavioural parameters in aged rats are related to LTP and gene expression of ChAT and NMDA-NR2 subunits in the striatum.

2004

Striatal parameters were assessed for their relevance to age-related behavioural decline. Forty aged rats (28-30 months) were tested in the water maze and open field. Of these, seven superior and seven inferior learners were compared with each other in terms of levels of in vitro short- and long-term potentiation (STP and LTP), and gene expression of choline acetyltransferase (ChAT) as well as of the NMDA-NR2A-C subunits assessed by quantitative RT-PCR. Results revealed that the superior as compared with the inferior learners had higher levels of ChAT mRNA in the striatum. For the superior group, ChAT mRNA was correlated with escape on to the cued platform in the water maze, whereas level o…

Malemedicine.medical_specialtyAgingeducationLong-Term PotentiationStriatumWater mazeReceptors N-Methyl-D-AspartateOpen fieldCholine O-AcetyltransferaseInternal medicineGene expressionmedicineAnimalsRNA MessengerRats WistarMaze LearningGeneral NeuroscienceLong-term potentiationCholine acetyltransferaseCorpus StriatumRatsEndocrinologynervous systemGene Expression RegulationSynaptic plasticityExploratory BehaviorNMDA receptorPsychologyNeuroscienceThe European journal of neuroscience
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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
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Midterm follow-up after DC-BEAD™-TACE of Hepatocellular Carcinoma (HCC)

2012

Abstract Aim To determine local response, its predictors and survival and complication rates after DC-Bead™-TACE in patients with hepatocellular carcinoma (HCC). Materials and methods DC-Beads™ are non-resorbable, polyvinyl-alcoholic hydrophilic microspheres. They release high amounts of chemotherapeutics directly into the tumour. Delivery is sustained over time, tumour feeders are embolised. We used beads from 100–300 to 500–700 μm loaded with Doxorubicin (max. 150 mg/4 ml). Fifty patients (mean age: 68.5 ± 8.8 years) with HCC were analysed. DC-Bead™-TACE was performed once or repeated in two-month intervals. Imaging scans (CT or MRI) were done one-month following each procedure. To evalua…

Malemedicine.medical_specialtyCarcinoma HepatocellularPleural effusionAntineoplastic AgentsComorbidityGastroenterologyRisk FactorsGermanyInternal medicinePrevalencemedicineCarcinomaHumansRadiology Nuclear Medicine and imagingChemoembolization TherapeuticSurvival rateSurvival analysisAgedUltrasonographybusiness.industryLiver NeoplasmsGeneral Medicinemedicine.diseaseSurvival AnalysisSurgerySurvival RateTreatment OutcomeDoxorubicinDelayed-Action PreparationsHepatocellular carcinomaFemaleLiver functionbusinessProgressive diseaseFollow-Up StudiesLiver abscessEuropean Journal of Radiology
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Role of N-methyl-D-aspartate receptors in the long-term effects of repeated social defeat stress on the rewarding and psychomotor properties of cocai…

2019

Abstract Exposure to social stress increases the vulnerability of experimental animals to the rewarding effects of cocaine and it has been suggested that the glutamatergic system could be involved in these effects of stress. The aim of this work is to determine the role of N-methyl- d -aspartate (NMDA) glutamate receptors in the influence of social stress on the conditioned place preference and locomotor sensitization induced by cocaine. Mice treated with saline or NMDA antagonist memantine (5 or 10 mg/kg) underwent repeated social defeat or were kept in the exploration control condition. After three weeks, all groups (SAL + RSD, M5 + RSD, M10 + RSD, SAL + EXP, M5 + EXP and M10 + EXP) were …

Malemedicine.medical_specialtyConditioning ClassicalMice Inbred StrainsReceptors N-Methyl-D-AspartateSocial defeat03 medical and health sciencesBehavioral NeuroscienceGlutamatergicMice0302 clinical medicineCocaineRewardMemantineInternal medicinemedicineAnimalsSocial BehaviorSensitization030304 developmental biologySocial stress0303 health sciencesBehavior Animalbusiness.industryMemantineGlutamate receptorConditioned place preferencemedicine.anatomical_structureEndocrinologyPsychological DistanceNMDA receptorbusiness030217 neurology & neurosurgeryStress Psychologicalmedicine.drugBehavioural brain research
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NMDA receptor antagonist felbamate reduces behavioral deficits and blood-brain barrier permeability changes after experimental subarachnoid hemorrhag…

2007

Increased levels of glutamate and aspartate have been detected after subarachnoid hemorrhage (SAH) that correlate with neurological status. The NMDA receptor antagonist felbamate (FBM; 2-phenyl-1,3-propanediol dicarbamate) is an anti-epileptic drug that elicits neuroprotective effects in different experimental models of hypoxia-ischemia. The aim of this dose-response study was to evaluate the effect of FBM after experimental SAH in rats on (1) behavioral deficits (employing a battery of assessment tasks days 1-5 post-injury) and (2) blood-brain barrier (BBB) permeability changes (quantifying microvascular alterations according to the extravasation of protein-bound Evans Blue by a spectropho…

Malemedicine.medical_specialtyExcitotoxicityPhenylcarbamatesBehavioral deficitsmedicine.disease_causeCisterna magnaBlood–brain barrierNeuroprotectionReceptors N-Methyl-D-AspartateFelbamateRats Sprague-Dawleychemistry.chemical_compoundInternal medicinemedicineAnimalsAnimals; Blood-Brain Barrier; Rats; Subarachnoid Hemorrhage; Evans Blue; Behavioral deficits; Cognitive deficits; NMDA receptor; FelbamatePostural BalanceEvans BlueBehavior AnimalDose-Response Relationship Drugbusiness.industryCognitive deficitsMicrocirculationBody WeightGlutamate receptorSubarachnoid HemorrhageNMDA receptorFelbamateRatsEndocrinologymedicine.anatomical_structureNeuroprotective AgentsSpectrometry FluorescencechemistryBlood-Brain BarrierPropylene GlycolsAnesthesiaCerebrovascular CirculationNMDA receptorNeurology (clinical)businessmedicine.drugEvans BlueJournal of neurotrauma
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Nitric oxide and glutamate interaction in the control of cortical and hippocampal excitability.

1999

Summary: Purpose: We investigated the role of nitric oxide (NO) as a new neurotransmitter in the control of excitability of the hippocampus and the cerebral cortex, as well as the possible functional interaction between NO and the glutamate systems. Methods: The experiments were performed on anesthetized rats. The bioelectrical activities of the somatosensory cortex and the CA1 region of the hippocampus of these rats were recorded. Pharmacologic inhibition of NO synthase (NOS) through the nonselective and brain-selective inhibitors, N-nitro-L-arginine methyl ester (l-NAME) and 7-nitroindazole (7-NI), was performed. Results: The treatments caused the appearance of an interictal discharge act…

Malemedicine.medical_specialtyHippocampusGlutamic AcidHippocampal formationNeurotransmissionBiologyNitric OxideHippocampusReceptors N-Methyl-D-Aspartatechemistry.chemical_compoundInternal medicinemedicineAnimalsRats WistarNeurotransmitterCerebral CortexEpilepsyGlutamate receptorSomatosensory CortexRatsEndocrinologyNeurologychemistryCNQXExcitatory postsynaptic potentialNMDA receptorNeurology (clinical)Epilepsia
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Dose-dependent effect of S(+) ketamine on post-ischemic endogenous neurogenesis in rats.

2009

Background: Ketamine is a non-competitive antagonist at N-methyl-d-aspartate (NMDA) receptors and reduces neuronal injury after cerebral ischemia by blocking the excitotoxic effects of glutamate. However, cerebral regeneration by means of endogenous neurogenesis may be impaired with blockade of NMDA receptors. The effects of S(+) ketamine on post-ischemic neurogenesis are unknown and investigated in this study. Methods: Thirty-two male Sprague–Dawley rats were randomly assigned to the following treatment groups with intravenous S(+) ketamine anesthesia: S(+) ketamine 0.75 mg/kg/min with or without cerebral ischemia and S(+) ketamine 1.0 mg/kg/min with or without cerebral ischemia. Eight non…

Malemedicine.medical_specialtyNeurogenesisIschemiaHippocampusReceptors N-Methyl-D-AspartateBrain IschemiaRats Sprague-DawleyInternal medicinemedicineAnimalsKetamineDose-Response Relationship Drugbusiness.industryDentate gyrusNeurogenesisAntagonistGlutamate receptorGeneral Medicinemedicine.diseaseRatsAnesthesiology and Pain MedicineEndocrinologyAnesthesiaNMDA receptorKetaminebusinessExcitatory Amino Acid Antagonistsmedicine.drugActa anaesthesiologica Scandinavica
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Pregnenolone sulfate, a naturally occurring excitotoxin involved in delayed retinal cell death.

2002

The present study was designed to investigate the neurosteroid pregnenolone sulfate (PS), known for its ability to modulate NMDA receptors and interfere with acute excitotoxicity, in delayed retinal cell death. Three hours after exposure of the isolated and intact retina to a 30-min PS pulse, DNA fragmentation as assessed by genomic DNA gel electrophoresis and a modified in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method appeared concurrently with an increase in superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels. At 7 h, the increased amount of DNA laddering was accompanied by a higher number of TUN…

Malemedicine.medical_specialtyNeurotoxinsExcitotoxicityApoptosisDNA FragmentationDNA ladderingBiologymedicine.disease_causeBiochemistryReceptors N-Methyl-D-AspartateThiobarbituric Acid Reactive SubstancesRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundAdjuvants ImmunologicSuperoxidesInternal medicinemedicineTBARSIn Situ Nick-End LabelingAnimalsCycloheximideRats WistarProgesteroneProtein Synthesis InhibitorsTUNEL assayEstradiolL-Lactate DehydrogenaseDehydroepiandrosterone SulfateSuperoxide DismutaseRatsEndocrinologychemistryApoptosisPregnenolonePregnenoloneDNA fragmentationLipid PeroxidationPregnenolone sulfateReactive Oxygen Speciesmedicine.drugJournal of neurochemistry
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Thermal Index for early non-invasive assessment of brain injury in newborns treated with therapeutic hypothermia: preliminary report.

2021

AbstractPerinatal asphyxia (PA) is the 3rd most common cause of neonatal death and one of the most common causes of severe neurological impairments in children. Current tools and measurements mainly based on the analysis of clinical evaluation and laboratory and electrophysiological tests do not give consistent data allowing to predict the severity of hypoxic-ischemic encephalopathy (HIE) until a magnetic resonance imaging (MRI) score is performed. The aim of this work is to evaluate the usefulness of the new index, called Thermal Index (TI) in the assessment of the degree of brain damage in newborns in the course of therapeutic hypothermia (TH) due to PA. This was a prospective, observatio…

Malemedicine.medical_specialtyPhysiologyScienceEncephalopathyNeurophysiologyBrain damageThermal indexFluid-attenuated inversion recoveryIntensive Care Units PediatricArticle03 medical and health sciences0302 clinical medicineHypothermia InducedPregnancymedicineHumansMultidisciplinarymedicine.diagnostic_testbusiness.industryQRHealth careInfant NewbornBrainInfant030208 emergency & critical care medicineMagnetic resonance imagingHypothermiamedicine.diseaseMagnetic Resonance ImagingPerinatal asphyxiaBrain InjuriesHypoxia-Ischemia BrainMedicineObservational studyFemaleRadiologymedicine.symptombusiness030217 neurology & neurosurgeryNeurological disordersScientific reports
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Acute ammonia intoxication induces an NMDA receptor-mediated increase in poly(ADP-ribose) polymerase level and NAD+ metabolism in nuclei of rat brain…

2004

Acute ammonia toxicity is mediated by excessive activation of NMDA receptors. Activation of NMDA receptors leads to activation of poly(ADP-ribose) polymerase (PARP) which mediates NMDA excitotoxicity. PARP is activated following DNA damage and may lead to cell death via NAD+ and ATP depletion. The aim of the present work was to assess whether acute ammonia intoxication in vivo leads to increased PARP in brain cells nuclei and to altered NAD+ and superoxide metabolism and the contribution of NMDA receptors to these alterations. Acute ammonia intoxication increases PARP content twofold in brain cells nuclei.NAD+ content decreased by 55% in rats injected with ammonia. This was not due to decre…

Malemedicine.medical_specialtyPoly ADP ribose polymeraseExcitotoxicityBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundNAD+ NucleosidaseAmide SynthasesAmmoniaSuperoxidesInternal medicinemedicineAnimalsNeurotoxinRats WistarReceptorBrain ChemistryCell NucleusProtein Synthesis InhibitorsSuperoxideNAD+ ADP-RibosyltransferaseBrainProteinsNADMolecular biologyRatsEndocrinologychemistryTyrosineNMDA receptorNAD+ kinasePoly(ADP-ribose) PolymerasesJournal of Neurochemistry
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