Search results for "neurotrophic factors"

showing 10 items of 88 documents

''Effect of stroke on arginase expression and localization in the rat brain''

2013

Quirie, Aurore | Demougeot, C. Eline | Bertrand, Nathalie | Mossiat, Claude | Garnier, Philippe | Marie, Christine | Prigent-Tessier, Anne; International audience; ''Because arginase and nitric oxide (NO) synthases (NOS) compete to degrade l-arginine, arginase plays a crucial role in the modulation of NO production. Moreover, the arginase 1 isoform is a marker of M2 phenotype macrophages that play a key role in tissue remodeling and resolution of inflammation. While NO has been extensively investigated in ischemic stroke, the effect of stroke on the arginase pathway is unknown. The present study focuses on arginase expression/activity and localization before and after (1, 8, 15 and 30days) …

MaleGene Expressionchemistry.chemical_compound0302 clinical medicineNeurotrophic factorsMACROPHAGESIN-VIVONeuronsAXONAL REGENERATION0303 health sciencesGlial fibrillary acidic proteinGeneral NeuroscienceBrainGLIAL RESPONSESCerebral InfarctionStrokeNitric oxide synthaseArginasemedicine.anatomical_structureBiochemistry[ SCCO.NEUR ] Cognitive science/NeuroscienceARGININE METABOLISMmedicine.symptom2'-DIPYRIDYLmedicine.medical_specialtyCentral nervous systemIRON CHELATOR 2InflammationBiologyFOCAL ISCHEMIANitric oxideLesion03 medical and health sciencesInternal medicineGlial Fibrillary Acidic ProteinmedicineAnimalsRats WistarNITRIC-OXIDE SYNTHASE030304 developmental biologyArginaseCEREBRAL-ISCHEMIABrain-Derived Neurotrophic Factor[SCCO.NEUR]Cognitive science/NeuroscienceCENTRAL-NERVOUS-SYSTEM''NITRIC-OXIDE SYNTHASERatsEndocrinologychemistryAstrocytesbiology.proteinMACROPHAGES''030217 neurology & neurosurgery
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Transcription factor gene expression profiling after acute intermittent nicotine treatment in the rat cerebral cortex

2004

Several studies in different in vitro and in vivo models have demonstrated neuroprotective effects of nicotinic receptor agonists and indirect trophic actions of nicotine on brain are suggested from observations describing nicotine as a cognitive enhancer by increasing vigilance and improving learning and memory. While an increasing number of studies have given evidence of neuroprotective and neurotrophic effects of nicotine treatment, the molecular mechanism mediating the neurotrophic effects of nicotine are not fully understood. Previously in an analysis of several neurotrophic factors as possible mediators of nicotine-induced neuroprotection and/or neurotrophic effects we could reveal th…

MaleNicotineGene ExpressionBiologyNeuroprotectionNicotineCerebral Cortex/drug effectNeurotrophic factorsmedicineAnimalsNicotinic AgonistsRats WistarIn Situ HybridizationOligonucleotide Array Sequence AnalysisCerebral CortexMicroarray analysis techniquesGene Expression ProfilingGeneral NeuroscienceRatsGene expression profilingNicotinic agonistNicotine/pharmacology Nicotinic Agonistsbiology.proteinGene Expression/drug effectImmediate early geneNeuroscienceTranscription Factorsmedicine.drugNeurotrophinNeuroscience
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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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Time-course of GDNF and its receptor expression after brain injury in the rat

2008

Abstract The aim of the present work was to perform, by in situ hybridization, a time-course analysis of the glial cell line-derived neurotrophic factor (GDNF) and its receptor mRNA expression in two models of brain injury in the rat: (a) excitotoxic lesion by ibotenic acid injection in the hippocampal formation; (b) mechanical lesion by needle insertion through the cerebral cortex including the white matter of the corpus callosum. The time-course analysis, ranging from 6 h to 8 days, showed that the GDNF and its receptor (RET, GFRα-1 and GFRα-2) mRNA expressions were differentially up-regulated in both models of lesion. This in vivo regulation of the GDNF and its receptor mRNA expression i…

MalePathologymedicine.medical_specialtyGlial Cell Line-Derived Neurotrophic Factor ReceptorsTime FactorsReceptor expressionCentral nervous systemBiologyHippocampal formationSettore BIO/09 - FisiologiaLesionchemistry.chemical_compoundNeurotrophic factorsGlial cell line-derived neurotrophic factormedicineAnimalsGlial Cell Line-Derived Neurotrophic FactorRNA MessengerRats WistarIbotenic AcidGeneral NeuroscienceGDNF RET GFRalfa-1 GFRalfa-2 Brain injury In situ hybridizationRatsmedicine.anatomical_structureGene Expression Regulationnervous systemchemistryCerebral cortexBrain Injuriesbiology.proteinAutoradiographymedicine.symptomIbotenic acidNeuroscience Letters
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Exogenous t-PA Administration Increases Hippocampal Mature BDNF Levels. Plasmin- or NMDA-Dependent Mechanism?

2014

International audience; Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular attention has been paid to the link between tissue plasminogen activator (tPA)/plasmin system and BDNF metabolism. However, t-PA via its action on different N-methyl-D-aspartate (NMDA) receptor subunits is also considered as a neuromodulator of glutamatergic transmission. In this context, the aim of our study was to investigate the effect of recombinant (r)t-PA administration on brain BDNF metabo…

MalePlasminlcsh:MedicineTropomyosin receptor kinase BBiochemistryMechanical Treatment of SpecimensHippocampusTissue plasminogen activator[SCCO]Cognitive scienceCell SignalingNeurotrophic factorsNeurobiology of Disease and RegenerationMedicine and Health SciencesMembrane Receptor SignalingFibrinolysinBRAINlcsh:ScienceMultidisciplinaryNeuromodulationNeurotransmitter Receptor SignalingNeurochemistryLong-term potentiationNeurotransmittersDENDRITIC GROWTHNEURONAL DEATHRECEPTORSElectroporationNeurologySpecimen DisruptionTranexamic AcidTissue Plasminogen ActivatorACTIVATORTPANMDA receptor[ SCCO ] Cognitive scienceLONG-TERM POTENTIATIONResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyN-MethylaspartateResearch and Analysis MethodsNeuropharmacologyDevelopmental NeuroscienceInternal medicinemedicineAnimalsReceptor trkBProtein PrecursorsRats WistarSPATIAL MEMORYBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factorlcsh:RBiology and Life SciencesCell BiologySYNAPTIC-PLASTICITYRetractionEndocrinologynervous systemSpecimen Preparation and TreatmentSynaptic plasticitylcsh:QMolecular NeuroscienceDizocilpine MaleateNEUROTROPHIC FACTORNeuroscienceSynaptic PlasticityPLoS ONE
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Brain-Derived Neurotrophic Factor But Not Forced Arm Use Improves Long-Term Outcome After Photothrombotic Stroke and Transiently Upregulates Binding …

2008

Background and Purpose— Both application of neurotrophic factors like brain-derived neurotrophic factor (BDNF) and constraint-induced movement therapy like forced arm use have been shown to potentially improve outcome after stroke. The aim of the present study was to check whether postischemic long-term outcome correlates to specific modifications in the abundance of various neurotransmitter receptors. Methods— Adult male Wistar rats were subjected to photothrombotic ischemia and assigned to various treatment groups (n=5 each) with end points at 3 and 6 weeks: (1) ischemic control (saline); (2) BDNF (ischemia, 20 μg BDNF); (3) forced arm use (ischemia, saline, and ipsilateral plaster cast …

MaleRestraint PhysicalMotor ActivityLigandsDownregulation and upregulationNeurotrophic factorsForelimbmedicineAnimalsRats WistarReceptorGABA Agonistsalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidStrokePhysical Therapy ModalitiesAdvanced and Specialized NursingBrain-derived neurotrophic factorMuscimolbusiness.industryBrain-Derived Neurotrophic FactorGlutamate receptorBrainCerebral Infarctionmedicine.diseaseRatsUp-RegulationStrokemedicine.anatomical_structureReceptors Glutamatenervous systemAnesthesiaExcitatory postsynaptic potentialAutoradiographyNeurology (clinical)Dizocilpine MaleateIntracranial ThrombosisForelimbCardiology and Cardiovascular MedicinebusinessExcitatory Amino Acid AntagonistsNeuroscienceStroke
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Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

2014

Purpose Neurotrophic deprivation is considered an important event in glaucomatous retinal ganglion cell (RGC) death. However, the mitogen-activated protein kinase (MAPK) pathway transmitting axonal neurotrophic signals in RGC has not been identified. We investigated the involvement of ERK5 and ERK1/2 in retrograde axonal neurotrophic signaling in rats. Methods Adult Sprague-Dawley rats were used. Retinal immunostaining for ERK5 and MEK5 was performed. Levels of total and phosphorylated ERK5 and ERK1/2 were analyzed in retinal lysate by quantitative Western blotting. The effects of age, brain-derived neurotrophic factor (BDNF) stimulation at RGC soma (intravitreal injection) or axon ending (…

MaleRetinal Ganglion Cellsmedicine.medical_specialtyAgingSuperior ColliculiMAP Kinase Signaling SystemBlotting WesternRetinal ganglionRetinaRats Sprague-Dawley03 medical and health sciences0302 clinical medicineNeurotrophic factorsInternal medicinemedicineAnimalsAxonPhosphorylationMitogen-Activated Protein Kinase 7030304 developmental biologyBrain-derived neurotrophic factorMitogen-Activated Protein Kinase 10303 health sciencesRetinaMitogen-Activated Protein Kinase 3biologyChemistryBrain-Derived Neurotrophic FactorBrainAnatomyRatsmedicine.anatomical_structureEndocrinologynervous systemRetinal ganglion cellTrk receptorOptic Nerve InjuriesIntravitreal Injectionsbiology.proteinsense organsNeuroglia030217 neurology & neurosurgeryNeurotrophinInvestigative ophthalmologyvisual science
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Physical training and hypertension have opposite effects on endothelial brain-derived neurotrophic factor expression

2013

AIMS: Changes in circulating brain-derived neurotrophic factor (BDNF) levels were reported in patients with or at risk for cardiovascular diseases associated with endothelial dysfunction, suggesting a link between BDNF and endothelial functionality. However, little is known on cardiovascular BDNF. Our aim was to investigate levels/localization, function, and relevance of cardiovascular BDNF. METHODS AND RESULTS: BDNF levels (western blotting) and localization (immunostaining) were assessed in the heart and aorta from rats with impaired (spontaneously hypertensive rats [SHR]), normal (Wistar Kyoto rats [WKY]), and improved (SHR and WKY subjected to physical training) endothelial function. BD…

MaleTime FactorsPhysiologyAorta ThoracicRats Inbred WKYVentricular Function Left0302 clinical medicineNeurotrophic factorsRats Inbred SHRMedicineEndothelial dysfunctionCells CulturedComputingMilieux_MISCELLANEOUS0303 health sciences[SDV.BA]Life Sciences [q-bio]/Animal biologyCoronary VesselsVasodilationmedicine.anatomical_structureHypertensioncardiovascular systemCardiology and Cardiovascular Medicinemedicine.medical_specialtyCell typeEndotheliumContractility03 medical and health sciencesCoronary CirculationPhysical Conditioning AnimalPhysiology (medical)Internal medicinemedicine.arteryVentricular PressureAnimals030304 developmental biologyBrain-derived neurotrophic factorAortabusiness.industryBrain-Derived Neurotrophic FactorEndothelial Cellsmedicine.diseaseMyocardial ContractionRatsDisease Models AnimalEndocrinologynervous systemRegional Blood FlowStress Mechanicalbusiness030217 neurology & neurosurgeryImmunostaining
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Ipsilateral versus contralateral spontaneous post-stroke neuroplastic changes: involvement of BDNF?

2013

International audience; Stroke is a leading cause of death and disability in industrialized countries. Although surviving patients exhibit a certain degree of restoration of function attributable to brain plasticity, the majority of stroke survivors has to struggle with persisting deficits. In order to potentiate post-stroke recovery, several rehabilitation therapies have been undertaken and many experimental studies have reported that brain-derived neurotrophic factor (BDNF) is central to many facets of neuroplastic processes. However, although BDNF role in brain plasticity is well characterized through strategies that manipulate its content, the involvement of this neurotrophin in spontan…

MaleTime FactorsSynaptophysinHippocampusTropomyosin receptor kinase BHippocampal formationBrain Ischemia03 medical and health sciences0302 clinical medicineNeurotrophic factorsNeuroplasticitymedicineAnimalsRats WistarStroke030304 developmental biology0303 health sciencesNeuronal PlasticitybiologyGeneral NeuroscienceBrain-Derived Neurotrophic Factor[SCCO.NEUR]Cognitive science/NeuroscienceBrainmedicine.diseaseRatsStrokenervous system[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinSynaptophysinPsychologyNeuroscience030217 neurology & neurosurgeryNeurotrophin
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Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats.

2010

International audience; Although brain-derived neurotrophic factor (BDNF) plays a central role in recovery after cerebral ischemia, little is known about cells involved in BDNF production after stroke. The present study testes the hypothesis that neurons are not the unique source of neosynthesized BDNF after stroke and that non neuronal-BDNF producing cells differ according to the delay after stroke induction. For this purpose, cellular localization of BDNF and BDNF content of each hemisphere were analysed in parallel before and after (4h, 24h and 8d) ischemic stroke in rats. Stroke of different severities was induced by embolization of the brain with variable number of calibrated microsphe…

MaleTime Factorsmedicine.medical_treatmentCentral nervous systemIschemiaBDNF productionFunctional LateralityBrain IschemiaBrain ischemia03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineNeurotrophic factorsGlial Fibrillary Acidic ProteinmedicineAnimalsRats WistarStrokeCellular localization030304 developmental biologyBrain-derived neurotrophic factorBrain ChemistryNeurons0303 health sciencesbusiness.industryBDNF localization[SCCO.NEUR]Cognitive science/NeuroscienceBrain-Derived Neurotrophic Factor[SCCO.NEUR] Cognitive science/NeuroscienceBrainCell BiologyCerebral Infarctionmedicine.diseaseRatsStrokemedicine.anatomical_structurenervous systemIntracranial Embolism[ SCCO.NEUR ] Cognitive science/NeurosciencebusinessStroke recoveryNeuroscience030217 neurology & neurosurgeryNeurochemistry international
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