Search results for "Brain-derived neurotrophic factor"

showing 10 items of 85 documents

Sexually Dimorphic Behavioral Profile in a Transgenic Model Enabling Targeted Recombination in Active Neurons in Response to Ketamine and (2R,6R)-Hyd…

2020

Background: Rapid-acting antidepressants ketamine and (2R,6R)-hydroxynorketamine ((2R,6R)-HNK) have overcome some of the major limitations of classical antidepressants. However, little is known about sex-specific differences in the behavioral and molecular effects of ketamine and (2R,6R)-HNK in rodents. Methods: We treated mice with an intraperitoneal injection of either saline, ketamine (30 mg kg&minus

Male0301 basic medicineHydroxynorketaminemedicine.medical_treatmentAntidepressantAnxietyHippocampuslcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5Salineactivated neuronsSpectroscopyNeuronsRecombination GeneticSex CharacteristicsBehavior AnimalhydroxynorketamineGeneral MedicineComputer Science ApplicationsActivated neuronsAntidepressantFemaleKetaminemedicine.drugmedicine.medical_specialtyketamineMemory Episodicsex differenceGreen Fluorescent ProteinsIntraperitoneal injectionMice TransgenicIn situ hybridizationBiologyHydroxynorketamineArticleCatalysisInorganic Chemistry03 medical and health sciencesInternal medicineketamine ; sex difference ; activated neurons ; antidepressant ; behavior ; BDNF ; rapid-acting ; hydroxynorketaminemedicineAnimalsKetamineRapid-actingPhysical and Theoretical ChemistrySocial BehaviorMolecular BiologyCell NucleusBehaviorantidepressantbehaviorBrain-Derived Neurotrophic FactorOrganic ChemistrySex differencerapid-actingSexual dimorphismDisease Models AnimalBDNF030104 developmental biologyEndocrinologylcsh:Biology (General)lcsh:QD1-999030217 neurology & neurosurgeryBehavioural despair test
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Compromised Neurotrophic and Angiogenic Regenerative Capability during Tendon Healing in a Rat Model of Type-II Diabetes

2017

Metabolic diseases such as diabetes mellitus type-II (DM-II) may increase the risk of suffering painful connective tissue disorders and tendon ruptures. The pathomechanisms, however, by which diabetes adversely affects connective tissue matrix metabolism and regeneration, still need better definition. Our aim was to study the effect of DM-II on expressional changes of neuro- and angiotrophic mediators and receptors in intact and healing Achilles tendon. The right Achilles tendon was transected in 5 male DM-II Goto-Kakizaki (GK) and 4 age-matched Wistar control rats. The left Achilles tendons were left intact. At week 2 post-injury, NGF, BDNF, TSP, and receptors TrkA, TrkB and Nk1 gene expre…

Male0301 basic medicinePhysiologyGene Expressionlcsh:MedicineSubstance PCardiovascular PhysiologyTendonsEndocrinology0302 clinical medicineNerve Growth FactorMedicine and Health SciencesHomeostasisMedicinelcsh:ScienceMammalsAchilles tendonMultidisciplinarybiologyAnimal ModelsAnatomyReceptors Neurokinin-1musculoskeletal systemTendonmedicine.anatomical_structureExperimental Organism SystemsConnective TissueVertebratesAnatomyResearch ArticleNeurotrophinmedicine.medical_specialtyWistar RatsEndocrine DisordersNeovascularization PhysiologicConnective tissueResearch and Analysis MethodsRodentsAchilles Tendon03 medical and health sciencesModel OrganismsTendon InjuriesInternal medicineTissue RepairDiabetes MellitusGeneticsAnimalsReceptor trkBRats WistarReceptor trkABrain-derived neurotrophic factorWound Healingbusiness.industryBrain-Derived Neurotrophic Factorlcsh:RScleraxisOrganismsBiology and Life SciencesRatsTenomodulinDisease Models AnimalBiological Tissue030104 developmental biologyNerve growth factorEndocrinologyDiabetes Mellitus Type 2Metabolic DisordersAmniotesbiology.proteinlcsh:QAngiogenesisPhysiological Processesbusiness030217 neurology & neurosurgeryDevelopmental BiologyPLOS ONE
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Oxytocin prevents the increase of cocaine-related responses produced by social defeat

2019

The neuropeptide oxytocin (OXT) plays a critical role in the regulation of social and emotional behaviors. OXT plays a role in stress response and in drug reward, but to date no studies have evaluated its implication in the long-lasting increase of the motivational effects of cocaine induced by repeated social defeat (RSD). During the social defeat procedure, 1 mg/kg of OXT was administered 30 min before each episode of RSD. Three weeks after the last defeat, the effects of cocaine on the conditioned place preference (CPP), locomotor sensitization and the self-administration (SA) paradigms were evaluated. The influence of OXT on the levels of BDNF in the prefrontal cortex (PFC), striatum an…

Male0301 basic medicinemedicine.medical_specialtyConditioning ClassicalPrefrontal CortexHippocampusSelf AdministrationStriatumAnxietyOxytocinHippocampusSocial defeatMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineCocaineRewardSocial defeatInternal medicinemedicineAnimalsPrefrontal cortexPharmacologybusiness.industryBrain-Derived Neurotrophic FactorSelf-administrationExtinction (psychology)Conditioned place preferenceCorpus StriatumConditioned place preferenceDisease Models AnimalBDNF030104 developmental biologyEndocrinologyOxytocinConditioning OperantSelf-administrationbusinessReinforcement PsychologyStress Psychologicalhormones hormone substitutes and hormone antagonists030217 neurology & neurosurgerymedicine.drugNeuropharmacology
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Brain BDNF levels are dependent on cerebrovascular endothelium-derived nitric oxide

2016

International audience; Scientific evidence continues to demonstrate a link between endothelial function and cognition. Besides, several studies have identified a complex interplay between nitric oxide (NO) and brain-derived neurotrophic factor (BDNF), a neurotrophin largely involved in cognition. Therefore, this study investigated the link between cerebral endothelium-derived NO and BDNF signaling. For this purpose, levels of BDNF and the phosphorylated form of endothelial NO synthase at serine 1177 (p-eNOS) were simultaneously measured in the cortex and hippocampus of rats subjected to either bilateral common carotid occlusion (n=6), physical exercise (n=6) or a combination of both (n=6) …

Male0301 basic medicinemedicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumHippocampusPhysical exerciseTropomyosin receptor kinase BHippocampusNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemphysical exercisenitric oxideNeurotrophic factorsPhysical Conditioning AnimalInternal medicinemedicineAnimalsReceptor trkBRats WistarCerebral CortexBrain-derived neurotrophic factorbiologyChemistry[SCCO.NEUR]Cognitive science/NeuroscienceGeneral Neurosciencebrain-derived neurotrophic factorTrkB[ SDV.MHEP.CSC ] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemRatsCerebrovascular Disorders030104 developmental biologyEndocrinologymedicine.anatomical_structurecarotid arteries occlusionnervous system[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinEndothelium VascularNeuroscience030217 neurology & neurosurgeryNeurotrophinEuropean Journal of Neuroscience
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''Comparative Effect of Treadmill Exercise on Mature BDNF Production in Control versus Stroke Rats''

2012

Quirie, Aurore | Hervieu, Marie | Garnier, Philippe | Demougeot, Celine | Mossiat, Claude | Bertrand, Nathalie | Martin, Alain | Marie, Christine | Prigent-Tessier, Anne; International audience; ''Physical exercise constitutes an innovative strategy to treat deficits associated with stroke through the promotion of BDNF-dependent neuroplasticity. However, there is no consensus on the optimal intensity/duration of exercise. In addition, whether previous stroke changes the effect of exercise on the brain is not known. Therefore, the present study compared the effects of a clinically-relevant form of exercise on cerebral BDNF levels and localization in control versus stroke rats. For this purpo…

MaleBEHAVIORAL RECOVERYTropomyosin receptor kinase BBiochemistryHippocampus0302 clinical medicineNerve Growth FactorHippocampus (mythology)StrokeCerebral Cortex0303 health sciencesNeuronal PlasticityMultidisciplinaryMOTOR RECOVERYQRTRKBNeurochemistryStrokemedicine.anatomical_structureNeurologyOrgan SpecificityCerebral cortex[ SCCO.NEUR ] Cognitive science/NeuroscienceMedicineNeurochemicalsmedicine.symptomResearch ArticleEXPRESSIONmedicine.medical_specialtyHIPPOCAMPAL PLASTICITYCORTEXCerebrovascular DiseasesAnimal TypesScienceBlotting WesternSynaptophysinEnzyme-Linked Immunosorbent AssayPhysical exerciseCONTROLLED-TRIALLesion03 medical and health sciencesPhysical Conditioning AnimalInternal medicineNeuroplasticitymedicineAnimalsLaboratory AnimalsSports and Exercise MedicineProtein PrecursorsRats WistarBiologyIschemic Stroke030304 developmental biologyBrain-derived neurotrophic factorbusiness.industry[SCCO.NEUR]Cognitive science/NeuroscienceBrain-Derived Neurotrophic FactorTRKB''AXONAL-TRANSPORTmedicine.diseaseCorpus StriatumRatsDisease Models AnimalEndocrinology''FOCAL BRAIN ISCHEMIAnervous systemFOCAL BRAIN ISCHEMIAExercise TestPhysical therapyBlood VesselsVeterinary ScienceEndothelium Vascularbusiness030217 neurology & neurosurgerySynaptic PlasticityNeuroscienceNEUROTROPHIC FACTOR
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CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity

2003

Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protecti…

MaleCannabinoid receptorReceptors Drugmedicine.medical_treatment2-ArachidonoylglycerolExcitotoxicityHippocampal formationmedicine.disease_causeHippocampusMicechemistry.chemical_compoundPiperidinesCannabinoid receptor type 1Excitatory Amino Acid AgonistsReceptors Cannabinoidgamma-Aminobutyric AcidMice KnockoutNeuronsKainic AcidMultidisciplinaryBrainEndocannabinoid systemNeuroprotective AgentsMitogen-Activated Protein KinasesRimonabantSignal Transductionmedicine.medical_specialtyKainic acidPolyunsaturated AlkamidesGlutamic AcidMice TransgenicArachidonic AcidsIn Vitro TechniquesBiologyGlyceridesProsencephalonInternal medicinemedicineAnimalsFuransGenes Immediate-EarlyEpilepsyCannabinoidsBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsMice Inbred C57BLEndocrinologyGene Expression Regulationnervous systemchemistryMutationPyrazolesCannabinoidNeuroscienceEndocannabinoidsScience
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Early life stress stimulates hippocampal reelin gene expression in a sex-specific manner: Evidence for corticosterone-mediated action

2010

Early life stress predisposes to the development of psychiatric disorders. In this context the hippocampal formation is of particular interest, because it is affected by stress on the structural and cognitive level. Since little is known how early life stress is translated on the molecular level, we mimicked early life stress in mouse models and analyzed the expression of the glycoprotein Reelin, a master molecule for development and differentiation of the hippocampus. From postnatal day 1 (P1) to P14, mouse pups were subjected to one of the following treatments: nonhandling (NH), handling (H), maternal separation (MS), and early deprivation (ED) followed by immediate (P15) or delayed (P70)…

MaleCell Adhesion Molecules NeuronalCognitive NeuroscienceGene ExpressionCell CountNerve Tissue ProteinsContext (language use)Hippocampal formationHippocampusMiceCajal–Retzius cellchemistry.chemical_compoundSex FactorsCorticosteronemedicineAnimalsRNA MessengerReelinBrain-derived neurotrophic factorExtracellular Matrix ProteinsMaternal deprivationbiologyMaternal DeprivationSerine EndopeptidasesDAB1Reelin Proteinmedicine.anatomical_structurenervous systemchemistrybiology.proteinFemaleCorticosteroneNeuroscienceStress PsychologicalHippocampus
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BDNF contributes to the facilitation of hippocampal synaptic plasticity and learning enabled by environmental enrichment

2014

Sensory, motor, and cognitive stimuli, resulting from interactions with the environment, play a key role in optimizing and modifying the neuronal circuitry required for normal brain function. An experimental animal model for this phenomenon comprises environmental enrichment (EE) in rodents. EE causes profound changes in neuronal and signaling levels of excitation and plasticity throughout the entire central nervous system and the hippocampus is particularly affected. The mechanisms underlying these changes are not yet fully understood. As brain-derived neurotrophic factor (BDNF) supports hippocampal long-term potentiation (LTP), we explored whether it participates in the facilitation of sy…

MaleCognitive NeuroscienceCentral nervous systemHippocampusMice TransgenicStimulationEnvironmentHippocampal formationHippocampusMiceNeurotrophic factorsmedicineAnimalsLearningEnvironmental enrichmentNeuronal PlasticityBehavior AnimalBrain-Derived Neurotrophic FactorRecognition PsychologyLong-term potentiationMice Inbred C57BLmedicine.anatomical_structurenervous systemSynaptic plasticityFemalePsychologyNeuroscienceHippocampus
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''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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Loss of striatal type 1 cannabinoid receptors is a key pathogenic factor in Huntington's disease.

2010

Endocannabinoids act as neuromodulatory and neuroprotective cues by engaging type 1 cannabinoid receptors. These receptors are highly abundant in the basal ganglia and play a pivotal role in the control of motor behaviour. An early downregulation of type 1 cannabinoid receptors has been documented in the basal ganglia of patients with Huntington's disease and animal models. However, the pathophysiological impact of this loss of receptors in Huntington's disease is as yet unknown. Here, we generated a double-mutant mouse model that expresses human mutant huntingtin exon 1 in a type 1 cannabinoid receptor-null background, and found that receptor deletion aggravates the symptoms, neuropatholog…

MaleHuntingtinCannabinoid receptorCell Survivalmedicine.medical_treatmentBlotting WesternMice TransgenicBiologyMotor ActivityGrowth Hormone-Releasing HormoneMiceReceptor Cannabinoid CB1medicineCannabinoid receptor type 2AnimalsDronabinolReceptorBrain-derived neurotrophic factorNeuronsAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionEndocannabinoid systemMagnetic Resonance ImagingCorpus StriatumHuntington DiseaseRotarod Performance TestGPR18Neurology (clinical)CannabinoidNeuroscienceBrain : a journal of neurology
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