Search results for "MDA"

showing 10 items of 275 documents

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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Platelet-activating factor contributes to the induction of long-term potentiation in the rat somatosensory cortex in vitro

2007

The contribution of platelet-activating factor (PAF) to the induction of neocortical LTP was examined in rat brain slices containing the primary somatosensory cortex (SI). Field potentials evoked by single pulse stimulation in cortical layer IV were recorded from layer II/III. In control experiments, tetanic high frequency stimulation (HFS) resulted in input-specific, NMDA receptor-dependent LTP (21.1+/-3.2%; mean+/-SEM; n=15; P0.001). BN-52021 (5 microM), an antagonist at the extracellular PAF receptor, weakened the HFS-induced LTP to 12.4+/-2.7% (n=11; P0.05). In contrast, HFS-induced LTP was significantly enhanced to 29.4+/-2.3% (n=11; P0.05) when brain slices were superfused with ACSF c…

Malemedicine.medical_specialtyLong-Term PotentiationCentral nervous systemStimulationIn Vitro TechniquesBiologySomatosensory systemRats Sprague-Dawleychemistry.chemical_compoundInternal medicineExcitatory Amino Acid AgonistsmedicineAnimalsPlatelet Activating FactorMolecular BiologyPlatelet-activating factorGeneral NeuroscienceValineLong-term potentiationSomatosensory CortexElectric StimulationIn vitroRatsmedicine.anatomical_structureEndocrinologychemistrySynaptic plasticityNMDA receptorNeurology (clinical)NeuroscienceDevelopmental BiologyBrain Research
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Effects of excitatory amino acids and neuropeptide Y on the discharge activity of suprachiasmatic neurons in rat brain slices

1997

Effects of L-glutamate, AMPA, NMDA and NPY on the discharge activity of neurons located in the ventral subdivision of the suprachiasmatic nucleus were examined in submerged coronal slices of the rat hypothalamus. All substances were bath applied. Application of L-glutamate (14 neurons examined) induced an excitatory response in 8 suprachiasmatic neurons (+248.9 +/- 122.24%, mean +/- S.E.M.; P0.001). A biphasic response, i.e. an initial transient excitation (+54.3 +/- 8.21%; P0.001) succeeded by an inhibition (-66.2 +/- 9.31%; P0.001), was observed in 6 neurons. Application of AMPA (36 neurons examined) resulted in an excitation of 31 neurons (+209.2 +/- 58.58%; P0.0001). Application of NMDA…

Malemedicine.medical_specialtyN-MethylaspartateGlutamic AcidAMPA receptorInhibitory postsynaptic potentialRats Sprague-Dawleychemistry.chemical_compoundOrgan Culture TechniquesInternal medicineExcitatory Amino Acid AgonistsmedicineAnimalsNeuropeptide Yalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidMolecular BiologyGlycine receptorNeuronsDose-Response Relationship DrugChemistrySuprachiasmatic nucleusGeneral NeuroscienceGlycine AgentsStrychnineStrychninehumanitiesCircadian RhythmRatsElectrophysiologyEndocrinologynervous systemHypothalamusExcitatory postsynaptic potentialNMDA receptorSuprachiasmatic NucleusNeurology (clinical)NeuroscienceDevelopmental BiologyBrain Research
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Hippocampal dopamine receptors modulate cFos expression in the rat nucleus accumbens evoked by chemical stimulation of the ventral hippocampus

2005

Recently, we have shown that D1 and D2 receptors in the ventral hippocampus (VH) modulate both the locomotor activation and the increase in dopamine (DA) levels in the rat nucleus accumbens (NAc) induced by NMDA stimulation of the VH. In the present study we analyze the possible role of VH D1 and D2 receptors in the modulation of the cFos expression in NAc (core and shell subregions) and in dorsal striatum. This was assessed by immunohistochemical analysis of cFos expression in the rat brains after retro-dialysis application of NMDA (50mM, 10 min) into VH, in absence and in presence of either the D1/D5 receptor antagonist SCH 23390 (100 and 250 microM, 60 min) or the D2 receptor antagonist …

Malemedicine.medical_specialtyN-Methylaspartatenucleus accumbensMicrodialysisStriatumNucleus accumbensHippocampusNucleus AccumbensReceptors DopamineCellular and Molecular Neurosciencechemistry.chemical_compoundDopamineDopamine receptor D2Internal medicinemedicineExcitatory Amino Acid AgonistsAnimalsRats WistarPharmacologyRacloprideSCH-23390ChemistryGenes fosBenzazepinesImmunohistochemistryStimulation ChemicalRatsNeostriatumcFosEndocrinologyD2Gene Expression Regulationnervous systemD1NMDADopamine receptorRacloprideNMDA receptorDopamine Antagonistsdopamineventral hippocampusmedicine.drug
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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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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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Different postischemic protein expression of the GABA_{A} receptor α2 subunit and the plasticity-associated protein MAP1B after treatment with BDNF v…

2009

Purpose Recent data indicate that both brain-derived neurotrophic factor (BDNF) and granulocyte-colony stimulating factor (G-CSF) exert substantial neuroregenerative effects and improve functional outcome after ischemic stroke. In the present study, we checked for potential differences in the postischemic modulation of various excitatory and inhibitory neurotransmitter receptors as well as various marker molecules for structural plasticity by BDNF versus G-CSF. Methods Adult male Wistar rats were subjected to photothrombotic ischemia and subsequently treated with NaCl, BDNF or G-CSF, respectively. After 6 weeks, postischemic protein expression of the NR1, GluR1 and alpha2 subunit of the NMD…

Malemedicine.medical_specialtyProtein subunitSynaptophysinHippocampusAMPA receptorFunctional LateralityRandom AllocationDevelopmental NeuroscienceNeurotrophic factorsInternal medicineGranulocyte Colony-Stimulating FactormedicineAnimalsRats WistarReceptorAnalysis of VariancebiologyChemistryGABAA receptorBrain-Derived Neurotrophic FactorBrainReceptors GABA-ARatsStrokeDisease Models AnimalEndocrinologyGene Expression Regulationnervous systemNeurologySynaptophysinbiology.proteinNMDA receptorNeurology (clinical)Intracranial ThrombosisMicrotubule-Associated ProteinsRestorative Neurology and Neuroscience
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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
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