Search results for "plasticity"

showing 10 items of 765 documents

Memantine blocks sensitization to the rewarding effects of morphine

2009

Knowledge regarding the specific brain changes and neural plasticity processes produced by repeated drug exposure may be used to advance the understanding of the neurobiology of addiction in order to design appropriate medications. In the present study, the influence of N-methyl-d-aspartate (NMDA) glutamatergic receptors on sensitization to the motor and rewarding effects of morphine was evaluated. The effects of pre-exposure to saline or 20 mg/kg morphine plus the NMDA receptor antagonist memantine (10 or 20 mg/kg) on motor activity and place conditioning induced by a low dose of morphine (2 mg/kg) were assessed. The dose of 2 mg/kg of morphine was ineffective in mice pre-exposed to saline…

MaleNarcoticsMotor ActivityPharmacologyReceptors N-Methyl-D-AspartateMiceGlutamatergicRewardMemantineConditioning PsychologicalNeuroplasticityAnimalsMedicineMolecular BiologySensitizationAnalysis of VarianceMotivationDose-Response Relationship DrugMorphinebusiness.industryGeneral NeuroscienceGlutamate receptorMemantineConditioned place preferencemedicine.anatomical_structureMorphineNMDA receptorNeurology (clinical)businessExcitatory Amino Acid AntagonistsDevelopmental Biologymedicine.drugBrain Research
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Memantine presents different effects from MK-801 in motivational and physical signs of morphine withdrawal

2003

Adaptive changes in neural systems due to chronic opiate exposure are related to the neural plasticity phenomenon, NMDA receptors being implicated in these processes, e.g. tolerance, dependence or withdrawal. In this work, we investigated the effect of two non-competitive NMDA antagonists, memantine and MK-801, in motivational (Conditioned Place Aversion paradigm, CPA) and physical aspects of morphine withdrawal. After the induction of morphine dependence, animals in which the CPA was studied, received memantine (5 and 10 mg/kg) or MK-801 (0.3-0.006 mg/kg) either during the acquisition (conditioning) or expression (test) phase of this procedure. Both drugs were capable of inhibiting conditi…

MaleNarcoticsTime FactorsNarcotic AntagonistsMotor ActivityPharmacologyMiceBehavioral NeuroscienceMemantineConditioning PsychologicalNeuroplasticitymedicineAnimalsDrug InteractionsBehavior AnimalDose-Response Relationship DrugMorphineNaloxoneKindlingMemantineSubstance Withdrawal SyndromeBlockadeMorphineNMDA receptorConditioningDizocilpine MaleateOpiatePsychologyExcitatory Amino Acid AntagonistsMorphine Dependencemedicine.drugBehavioural Brain Research
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The Polysialylated Form of the Neural Cell Adhesion Molecule (PSA-NCAM) Is Expressed in a Subpopulation of Mature Cortical Interneurons Characterized…

2010

Principal neurons in the adult cerebral cortex undergo synaptic, dendritic, and spine remodeling in response to different stimuli, and several reports have demonstrated that the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) participates in these plastic processes. However, there is only limited information on the expression of this molecule on interneurons and on its role in the structural plasticity of these cells. We have found that PSA-NCAM is expressed in mature interneurons widely distributed in all the extension of the cerebral cortex and have excluded the expression of this molecule in most principal cells. Although PSA-NCAM expression is generally considered a …

MaleNeurogenesisCognitive NeuroscienceCellular differentiationNeural InhibitionNeural Cell Adhesion Molecule L1BiologyInhibitory postsynaptic potentialRats Sprague-DawleyCellular and Molecular NeuroscienceInterneuronsNeural PathwaysNeuroplasticitymedicineAnimalsCell ShapeCerebral CortexNeuronal PlasticityEmbryogenesisNeurogenesisCell DifferentiationNeural InhibitionRatsmedicine.anatomical_structurenervous systemCerebral cortexSialic AcidsNeural cell adhesion moleculeNeuroscienceCerebral Cortex
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D1/D5 modulation of synaptic NMDA receptor currents.

2009

Converging evidence suggests that salience-associated modulation of behavior is mediated by the release of monoamines and that monoaminergic activation of D1/D5receptors is required for normal hippocampal-dependent learning and memory. However, it is not understood how D1/D5modulation of hippocampal circuits can affect salience-associated learning and memory. We have observed in CA1 pyramidal neurons that D1/D5receptor activation elicits a bidirectional long-term plasticity of NMDA receptor-mediated synaptic currents with the polarity of plasticity determined by NMDA receptor, NR2A/B subunit composition. This plasticity results in a decrease in the NR2A/NR2B ratio of subunit composition. Sy…

MaleNeuronal PlasticityGeneral Neurosciencemusculoskeletal neural and ocular physiologyReceptors Dopamine D1Long-term potentiationAMPA receptorNeurotransmissionBiologyReceptors N-Methyl-D-AspartateSynaptic TransmissionArticleMice Inbred C57BLMicenervous systemSynaptic plasticitySynapsesNMDA receptorAnimalsReceptors Dopamine D5Nerve NetReceptorLong-term depressionNeuronal memory allocationNeuroscienceThe Journal of neuroscience : the official journal of the Society for Neuroscience
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Effects of chronic fluoxetine treatment on the rat somatosensory cortex: Activation and induction of neuronal structural plasticity

2009

Recent hypotheses support the idea that disruption of normal neuronal plasticity mechanisms underlies depression and other psychiatric disorders, and that antidepressant treatment may counteract these changes. In a previous report we found that chronic fluoxetine treatment increases the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a molecule involved in neuronal structural plasticity, in the somatosensory cortex. In the present study we intended to find whether, in fact, cell activation and neuronal structural remodeling occur in parallel to changes in the expression of this molecule. Using immunohistochemistry, we found that chronic fluoxetine trea…

MaleNeuronsNeuronal PlasticityDose-Response Relationship DrugGeneral NeuroscienceCentral nervous systemHippocampusSomatosensory CortexBiologySomatosensory systemRatsRats Sprague-Dawleymedicine.anatomical_structurenervous systemFluoxetineApical dendriteNeuroplasticitymedicineAnimalsAntidepressive Agents Second-GenerationNeural cell adhesion moleculeCell activationPrefrontal cortexNeuroscienceNeuroscience Letters
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PSA-NCAM expression in the rat medial prefrontal cortex

2005

The rat medial prefrontal cortex, an area considered homologous to the human prefrontal cortex, is a region in which neuronal structural plasticity has been described during adulthood. Some plastic processes such as neurite outgrowth and synaptogenesis are known to be regulated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). Since PSA-NCAM is present in regions of the adult CNS which are undergoing structural remodeling, such as the hypothalamus or the hippocampus, we have analyzed the expression of this molecule in the medial prefrontal cortex of adult rats using immunohistochemistry. PSA-NCAM immunoreactivity was found both in cell bodies and in the neuropil of…

MaleNeuropilNeuriteInterneuronAntimetabolitesCell SurvivalSynaptophysinSynaptogenesisPrefrontal CortexHippocampusNeural Cell Adhesion Molecule L1BiologyRats Sprague-DawleyNeuroplasticityNeuropilmedicineAnimalsFluorescent Antibody Technique IndirectPrefrontal cortexNeuronsNeuronal PlasticityGlutamate DecarboxylasePyramidal CellsGeneral NeuroscienceImmunohistochemistryRatsPhenotypemedicine.anatomical_structureBromodeoxyuridinenervous systemSialic AcidsNeural cell adhesion moleculeNeuroscienceNeuroscience
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Acute intermittent nicotine treatment induces fibroblast growth factor-2 in the subventricular zone of the adult rat brain and enhances neuronal prec…

2007

Abstract Over the past years, evidence has accumulated that stem cells are present in the adult brain, and generate neurons and/or glia from two active germinal zones: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus. This study shows that acute intermittent nicotine treatment significantly enhances neuronal precursor cell proliferation in the SVZ of adult rat brain, but not in the SGZ of the hippocampus, and pre-treatment with mecamylamine, a nonselective nAChR antagonist, blocks the enhanced precursor proliferation by nicotine. This effect is supported by up-regulation of fibroblast growth factor-2 (FGF-2) mRNA …

MaleNicotinemedicine.medical_specialtyBasic fibroblast growth factorSubventricular zoneNicotinic AntagonistsReceptors NicotinicBiologyFibroblast growth factorSettore BIO/09 - FisiologiaHippocampusSubgranular zonechemistry.chemical_compoundLateral VentriclesInternal medicinePrecursor cellmedicineAnimalsPyrrolesNicotinic AgonistsRNA MessengerReceptor Fibroblast Growth Factor Type 1Rats WistarCell ProliferationNeuronsNeuronal PlasticityStem CellsGeneral NeuroscienceFibroblast growth factor receptor 1Dentate gyrusNeurogenesisCell DifferentiationNerve RegenerationRatsUp-RegulationCell biologymedicine.anatomical_structureEndocrinologynervous systemchemistryneurogenesis FGF-2 FGFR-1 subventricular zone nicotineFibroblast Growth Factor 2Neuroscience
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Chronic fluoxetine treatment alters the structure, connectivity and plasticity of cortical interneurons

2014

Novel hypotheses suggest that antidepressants, such as the selective serotonin reuptake inhibitor fluoxetine, induce neuronal structural plasticity, resembling that of the juvenile brain, although the underlying mechanisms of this reopening of the critical periods still remain unclear. However, recent studies suggest that inhibitory networks play an important role in this structural plasticity induced by fluoxetine. For this reason we have analysed the effects of a chronic fluoxetine treatment in the hippocampus and medial prefrontal cortex (mPFC) of transgenic mice displaying eGFP labelled interneurons. We have found an increase in the expression of molecules related to critical period pla…

MalePERINEURONAL NET EXPRESSIONTime FactorsDendritic spinePSA-NCAMCritical period plasticityHippocampusCell CountADULT BRAIN PLASTICITYTREATMENT INCREASESHippocampusMice0302 clinical medicinePharmacology (medical)Prefrontal cortexCerebral Cortex0303 health sciencesNeuronal PlasticitybiologyGlutamate DecarboxylaseMEDIAL PREFRONTAL CORTEXPOLYSIALIC ACIDmusculoskeletal neural and ocular physiologyPerineuronal net3. Good healthPsychiatry and Mental healthParvalbuminsmedicine.anatomical_structureCerebral cortexCELL-ADHESION MOLECULEAntidepressive Agents Second-GenerationDendritic SpinesGreen Fluorescent ProteinseducationMice TransgenicNerve Tissue ProteinsNeural Cell Adhesion Molecule L1Inhibitory postsynaptic potentialRAT HIPPOCAMPUS03 medical and health sciencesmedicineAnimalsPSA-NCAM EXPRESSION030304 developmental biologyPharmacologyperineuronal netsinterneuronsCENTRAL-NERVOUS-SYSTEMfluoxetine3112 NeurosciencesGene Expression Regulationnervous systemVesicular Glutamate Transport Protein 1Sialic Acidsbiology.proteinNeural cell adhesion moleculeNerve NetNeuroscience030217 neurology & neurosurgeryParvalbuminThe International Journal of Neuropsychopharmacology
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Membrane-Derived Phospholipids Control Synaptic Neurotransmission and Plasticity

2015

Synaptic communication is a dynamic process that is key to the regulation of neuronal excitability and information processing in the brain. To date, however, the molecular signals controlling synaptic dynamics have been poorly understood. Membrane-derived bioactive phospholipids are potential candidates to control short-term tuning of synaptic signaling, a plastic event essential for information processing at both the cellular and neuronal network levels in the brain. Here, we showed that phospholipids affect excitatory and inhibitory neurotransmission by different degrees, loci, and mechanisms of action. Signaling triggered by lysophosphatidic acid (LPA) evoked rapid and reversible depress…

MalePatch-Clamp TechniquesQH301-705.5NeurotransmissionBiologyInhibitory postsynaptic potentialSynaptic TransmissionGeneral Biochemistry Genetics and Molecular BiologyMicePregnancySynaptic augmentationMetaplasticityAnimalsRats WistarBiology (General)Motor Neuronsrho-Associated KinasesNeuronal PlasticityGeneral Immunology and MicrobiologyCalcineurinGeneral NeuroscienceReceptors GABA-ACell biologySynaptic fatigueBiochemistrySynapsesSynaptic plasticityExcitatory postsynaptic potentialFemalelipids (amino acids peptides and proteins)Synaptic signalingLysophospholipidsrhoA GTP-Binding ProteinGeneral Agricultural and Biological SciencesResearch Article
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Gene Expression Profiling of Facilitated L-LTP in VP16-CREB Mice Reveals that BDNF Is Critical for the Maintenance of LTP and Its Synaptic Capture

2011

Expression of VP16-CREB, a constitutively active form of CREB, in hippocampal neurons of the CA1 region lowers the threshold for eliciting the late, persistent phase of long-term potentiation (L-LTP) in the Schaffer collateral pathway. This VP16-CREB-mediated L-LTP differs from the conventional late phase of LTP in not being dependent on new transcription. This finding suggests that in the transgenic mice the mRNA transcript(s) encoding the protein(s) necessary for this form of L-LTP might already be present in CA1 neurons in the basal condition. We used high-density oligonucleotide arrays to identify the mRNAs differentially expressed in the hippocampus of transgenic and wild-type mice. We…

MalePatch-Clamp TechniquesTime FactorsTransgeneNeuroscience(all)Long-Term PotentiationNerve Tissue ProteinsDynorphinHippocampal formationCREBHippocampusSynaptic TransmissionMiceNeurotrophic factorsMHC class ImedicineAnimalsRNA MessengerIn Situ HybridizationMice KnockoutNeuronsNeuronal PlasticitybiologyReverse Transcriptase Polymerase Chain ReactionBrain-Derived Neurotrophic FactorGene Expression Profilingmusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic PotentialsHerpes Simplex Virus Protein Vmw65Long-term potentiationExonsCREB-Binding ProteinMolecular biologyCell biologymedicine.anatomical_structurenervous systemSchaffer collateralSynapsesbiology.proteinFemaleNeuron
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