Search results for " trkB"

showing 10 items of 16 documents

Truncated TrkB receptor-induced outgrowth of dendritic filopodia involves the p75 neurotrophin receptor.

2004

The Trk family of receptor tyrosine kinases and the p75 receptor (p75NTR) mediate the effects of neurotrophins on neuronal survival, differentiation and synaptic plasticity. The neurotrophin BDNF and its cognate receptor tyrosine kinase, TrkB.FL, are highly expressed in neurons of the central nervous system. At later stages in postnatal development the truncated TrkB splice variants (TrkB.T1, TrkB.T2) become abundant. However, the signalling and function of these truncated receptors remained largely elusive.We show that overexpression of TrkB.T1 in hippocampal neurons induces the formation of dendritic filopodia, which are known precursors of synaptic spines. The induction of filopodia by T…

Time FactorsGreen Fluorescent ProteinsReceptors Nerve Growth FactorTropomyosin receptor kinase ATransfectionTropomyosin receptor kinase CHippocampusModels BiologicalPC12 CellsReceptor Nerve Growth FactorReceptor tyrosine kinaseLow-affinity nerve growth factor receptorAnimalsReceptor trkBNerve Growth FactorsPseudopodiaCloning MolecularNeuronsbiologyDose-Response Relationship Drugmusculoskeletal neural and ocular physiologyCell DifferentiationCell BiologyDendritesImmunohistochemistryDendritic filopodiaCell biologyProtein Structure TertiaryRatsnervous systemMicroscopy FluorescenceTrk receptorembryonic structuresNeurotrophin bindingCOS Cellsbiology.proteinsense organsNeurotrophinProtein BindingSignal TransductionJournal of cell science
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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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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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Brothers in arms: proBDNF/BDNF and sAPPα/Aβ-signaling and their common interplay with ADAM10, TrkB, p75NTR, sortilin, and sorLA in the progression of…

2021

Abstract Brain-derived neurotrophic factor (BDNF) is an important modulator for a variety of functions in the central nervous system (CNS). A wealth of evidence, such as reduced mRNA and protein level in the brain, cerebrospinal fluid (CSF), and blood samples of Alzheimer’s disease (AD) patients implicates a crucial role of BDNF in the progression of this disease. Especially, processing and subcellular localization of BDNF and its receptors TrkB and p75 are critical determinants for survival and death in neuronal cells. Similarly, the amyloid precursor protein (APP), a key player in Alzheimer’s disease, and its cleavage fragments sAPPα and Aβ are known for their respective roles in neuropro…

ADAM10Clinical BiochemistryNerve Tissue ProteinsTropomyosin receptor kinase BReceptors Nerve Growth FactorBiochemistryNeuroprotectionADAM10 ProteinAmyloid beta-Protein PrecursorNeurotrophic factorsAlzheimer DiseaseAmyloid precursor proteinHumansReceptor trkBMolecular BiologyLDL-Receptor Related ProteinsAmyloid beta-PeptidesMembrane GlycoproteinsbiologyBrain-Derived Neurotrophic FactorMembrane ProteinsMembrane Transport ProteinsAdaptor Proteins Vesicular Transportnervous systembiology.proteinSignal transductionAmyloid Precursor Protein SecretasesNeuroscienceAmyloid precursor protein secretaseNeurotrophinBiological chemistryReferences
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Abnormal development of pacinian corpuscles in double trkB;trkC knockout mice.

2006

Pacinian corpuscles depend on either Aalpha or Abeta nerve fibers of the large- and intermediate-sized sensory neurons for the development and maintenance of the structural integrity. These neurons express TrkB and TrkC, two members of the family of signal transducing neurotrophin receptors, and mice lacking TrkB and TrkC lost specific neurons and the sensory corpuscles connected to them. The impact of single or double targeted mutations in trkB and trkC genes in the development of Pacinian corpuscles was investigated in 25-day-old mice using immunohistochemistry and ultrastructural techniques. Single mutations on trkB or trkC genes were without effect on the structure and S100 protein expr…

medicine.medical_specialtyanimal structuresTropomyosin receptor kinase BBiologyTropomyosin receptor kinase CS100 proteinMiceMicroscopy Electron TransmissionInternal medicinemedicineLow-affinity nerve growth factor receptorAnimalsReceptor trkBReceptor trkCReceptorMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceImmunohistochemistryCell biologyMice Inbred C57BLEndocrinologynervous systemAnimals NewbornTrk receptorembryonic structuresKnockout mousebiology.proteinPacinian CorpusclesNeurotrophinNeuroscience letters
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Impact of NTRK2, DRD2 and ACE polymorphisms on prolactin levels in antipsychotic-treated patients with first-episode psychosis.

2018

Background: Hyperprolactinemia is a common side-effect of antipsychotics (APs), which may trigger serious secondary problems and compromise the adherence to treatment which is crucial for prognosis, especially in patients presenting with a first-episode of psychosis (FEP). Aims: We evaluated, in some cases for the first time, the effect of polymorphisms in multiple candidate genes on serum prolactin (PRL) levels in an AP-treated FEP cohort recruited in the multicenter PEPs study (Phenotype − genotype and environmental interaction; Application of a predictive model in first psychotic episodes). Methods: PRL concentration was measured in serum from 222 patients. A total of 167 polymorphisms w…

AdultMalePsychosismedicine.medical_specialtyCandidate geneSerotoninSide effectAdolescentmedicine.medical_treatmentDopaminePeptidyl-Dipeptidase A03 medical and health sciencesYoung Adult0302 clinical medicineDopaminePolymorphism (computer science)Internal medicinemedicineHumansReceptor trkBPharmacology (medical)AntipsychoticPharmacologyMembrane GlycoproteinsPolymorphism Geneticbusiness.industryReceptors Dopamine D2medicine.diseaseProlactin030227 psychiatryProlactinHyperprolactinemiaPsychiatry and Mental healthEndocrinologyPsychotic DisordersCohortFemalebusiness030217 neurology & neurosurgerymedicine.drugAntipsychotic AgentsJournal of psychopharmacology (Oxford, England)
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Astrocytes in culture express the full-length Trk-B receptor and respond to brain derived neurotrophic factor by changing intracellular calcium level…

2000

Abstract Although cultured astroglial cells were reported to express exclusively the truncated non-catalytic Trk B receptor for brain-derived neurotrophic factor (BDNF), we detect here, using a sensitive ribonuclease protection assay, mRNAs for both truncated (TrkB–T) and the full length catalytic (TrkB–fl) form of BDNF receptor in developing cortical astrocytes and neurons in culture. Cortical neurons and immature astroglia, such as radial glia and proliferating astrocytes, express both the protein and mRNAs for TrkB-fl and TrkB-T, whereas the differentiation of astrocytes leads to a decrease in the trkB-fl mRNA, being the truncated TrkB the predominant receptor in differentiating and conf…

Tropomyosin receptor kinase BBiologyFetusNeurotrophic factorsmedicineAnimalsReceptor trkBRNA MessengerReceptorCells CulturedBrain-derived neurotrophic factorEthanolmusculoskeletal neural and ocular physiologyGeneral NeuroscienceBrain-Derived Neurotrophic FactorCentral Nervous System DepressantsGene Expression Regulation DevelopmentalCell DifferentiationCell biologyRatsmedicine.anatomical_structurenervous systemAstrocytesembryonic structuresbiology.proteinNeurogliaCalciumSignal transductionNeuroscienceNeurotrophinAstrocyteNeuroscience letters
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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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Spatial shaping of cochlear innervation by temporally regulated neurotrophin expression.

2001

Previous work suggested qualitatively different effects of neurotrophin 3 (NT-3) in cochlear innervation patterning in different null mutants. We now show that all NT-3 null mutants have a similar phenotype and lose all neurons in the basal turn of the cochlea. To understand these longitudinal deficits in neurotrophin mutants, we have compared the development of the deficit in the NT-3 mutant to the spatial–temporal expression patterns of brain-derived neurotrophic factor (BDNF) and NT-3, using lacZ reporters in each gene and with expression of the specific neurotrophin receptors, trkB and trkC. In the NT-3 mutant, almost normal numbers of spiral ganglion neurons form, but fiber outgrowth t…

HeterozygoteCell SurvivalCell CountNeurotrophin-3Tropomyosin receptor kinase BTropomyosin receptor kinase CArticleMiceNeurotrophin 3Neurotrophic factorsGenes ReportermedicineAnimalsReceptor trkBReceptor trkCNeurons AfferentCochleaSpiral ganglionBrain-derived neurotrophic factorAfferent PathwaysbiologyGeneral NeuroscienceBrain-Derived Neurotrophic FactorHomozygoteGene Expression Regulation DevelopmentalImmunohistochemistryMice Mutant StrainsCochleamedicine.anatomical_structurePhenotypenervous systemAnimals NewbornLac OperonMutationbiology.proteinSpiral GanglionNeuroscienceNeurotrophin
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BDNF, but not NT-4, is necessary for normal development of Meissner corpuscles.

2005

Abstract Meissner corpuscles are rapidly adapting cutaneous mechanoreceptors depending for development on TrkB expressing sensory neurons, but it remains to be established which of the known TrkB ligands, BDNF or NT-4, is responsible of this dependence. In this study we analyze Meissner corpuscles in the digital pads of mice with target mutations in the genes encoding for either BDNF or NT-4, using immunohistochemistry and transmission-electron microscopy, and they were identified based on their morphology and expression of S100 protein. All wild-type animals as well as NT-4 −/− animals and BDNF and NT4 heterozygous animals have Meissner corpuscles that are normal in number and size. Howeve…

Pathologymedicine.medical_specialtyRatónTropomyosin receptor kinase BLigandsS100 proteinMicemedicineAnimalsReceptor trkBNerve Growth FactorsBrain-derived neurotrophic factorMice KnockoutbiologyChemistryGeneral NeuroscienceBrain-Derived Neurotrophic FactorCell biologyMechanoreceptorMice Inbred C57BLmedicine.anatomical_structurenervous systemMeissner Corpusclebiology.proteinImmunohistochemistryMechanoreceptorsNeurotrophinNeuroscience letters
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