Search results for "Tropomyosin receptor kinase B"

showing 10 items of 24 documents

Regulation of Dendritic Spine Morphology in Hippocampal Neurons by Copine-6.

2015

Dendritic spines compartmentalize information in the brain, and their morphological characteristics are thought to underly synaptic plasticity. Here we identify copine-6 as a novel modulator of dendritic spine morphology. We found that brain-derived neurotrophic factor (BDNF) - a molecule essential for long-term potentiation of synaptic strength - upregulated and recruited copine-6 to dendritic spines in hippocampal neurons. Overexpression of copine-6 increased mushroom spine number and decreased filopodia number, while copine-6 knockdown had the opposite effect and dramatically increased the number of filopodia, which lacked PSD95. Functionally, manipulation of post-synaptic copine-6 level…

0301 basic medicineDendritic spineVesicular Inhibitory Amino Acid Transport Proteinsdrug effects [Synapses]Tropomyosin receptor kinase BHippocampal formationgenetics [Carrier Proteins]pharmacology [Brain-Derived Neurotrophic Factor]Hippocampusmetabolism [Vesicular Inhibitory Amino Acid Transport Proteins]Mtap2 protein ratMice0302 clinical medicineNeurotrophic factorsdrug effects [Synaptic Vesicles]genetics [Nerve Tissue Proteins]Cells Culturedultrastructure [Neurons]NeuronsChemistryLong-term potentiationSynaptic Potentialsphysiology [Neurons]physiology [Dendritic Spines]Cell biologyultrastructure [Dendritic Spines]metabolism [Receptor trkB]Synaptic VesiclesFilopodiaultrastructure [Synaptosomes]Disks Large Homolog 4 ProteinMicrotubule-Associated ProteinsCognitive NeuroscienceDendritic Spinesmetabolism [Disks Large Homolog 4 Protein]Nerve Tissue Proteinsgenetics [Receptor trkB]03 medical and health sciencesCellular and Molecular NeuroscienceOrgan Culture Techniquesphysiology [Synaptic Vesicles]metabolism [Vesicular Glutamate Transport Protein 1]TrkB protein ratdrug effects [Synaptic Potentials]Synaptic vesicle recyclingAnimalsHumansReceptor trkBddc:610metabolism [Synaptosomes]metabolism [Nerve Tissue Proteins]Viaat protein ratBrain-Derived Neurotrophic Factormetabolism [Microtubule-Associated Proteins]Rats030104 developmental biologygenetics [Synaptic Potentials]nervous systemcytology [Hippocampus]Synaptic plasticityultrastructure [Synapses]SynapsesVesicular Glutamate Transport Protein 1CPNE6 protein ratphysiology [Synapses]Carrier Proteins030217 neurology & neurosurgerymetabolism [Carrier Proteins]SynaptosomesCerebral cortex (New York, N.Y. : 1991)
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The TrkB agonist 7,8-dihydroxyflavone changes the structural dynamics of neocortical pyramidal neurons and improves object recognition in mice

2018

This is a pre-print of an article published in Brain Structure and Function. The final authenticated version is available online at: https://doi.org/10.1007/s00429-018-1637-x. BDNF and its receptor TrkB have important roles in neurodevelopment, neural plasticity, learning, and memory. Alterations in TrkB expression have been described in different CNS disorders. Therefore, drugs interacting with TrkB, specially agonists, are promising therapeutic tools. Among them, the recently described 7,8-dihydroxyflavone (DHF), an orally bioactive compound, has been successfully tested in animal models of these diseases. Recent studies have shown the influence of this drug on the structure of pyramidal …

0301 basic medicineMaleDendritic spineTrkB receptorNeocortexTropomyosin receptor kinase B78-Dihydroxyflavoneaxonal dynamicsMice0302 clinical medicineReceptorMembrane GlycoproteinsGeneral NeurosciencePyramidal CellsProtein-Tyrosine Kinases2-Photonbarrel cortexFemaleMicrogliaAnatomyAgonistHistologymedicine.drug_classDendritic SpinesMice TransgenicBiologyspine dynamicsrecognition memory03 medical and health sciencesBacterial ProteinsNeuroplasticitymedicinepyramidal neuronAnimalsMaze LearningParenchymal TissueRecognition memoryAnalysis of VarianceRecognition PsychologyBarrel cortexFlavonesAxonsLuminescent Proteins030104 developmental biologynervous systemAstrocytesen passant boutonsThy-1 AntigensNeuroscience030217 neurology & neurosurgery
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Sex hormones modulate pathogenic processes in experimental traumatic brain injury.

2018

Clinical and animal studies have revealed sex-specific differences in histopathological and neurological outcome after traumatic brain injury (TBI). The impact of perioperative administration of sex steroid inhibitors on TBI is still elusive. Here, we subjected male and female C57Bl/6N mice to the controlled cortical impact (CCI) model of TBI and applied pharmacological inhibitors of steroid hormone synthesis, that is, letrozole (LET, inhibiting estradiol synthesis by aromatase) and finasteride (FIN, inhibiting dihydrotestosterone synthesis by 5α-reductase), respectively, starting 72 h prior CCI, and continuing for a further 48 h after CCI. Initial gene expression analyses showed that andro…

0301 basic medicineMalemedicine.medical_specialtyanimal structuresmedicine.drug_classmedicine.medical_treatmentTropomyosin receptor kinase BTropomyosin receptor kinase ABiochemistryNeuroprotection03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineInternal medicineBrain Injuries TraumaticmedicineAnimalsNerve Growth FactorsSex CharacteristicsbiologyEstradiolbusiness.industryEstrogen AntagonistsBrainDihydrotestosteroneAndrogennervous system diseasesMice Inbred C57BLSteroid hormoneDisease Models Animal030104 developmental biologyEndocrinologynervous systemSex steroidDihydrotestosteronebiology.proteinFemalebusiness030217 neurology & neurosurgeryNeurotrophinmedicine.drugJournal of neurochemistry
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Serotonin Heteroreceptor Complexes and Their Integration of Signals in Neurons and Astroglia—Relevance for Mental Diseases

2021

The heteroreceptor complexes present a novel biological principle for signal integration. These complexes and their allosteric receptor–receptor interactions are bidirectional and novel targets for treatment of CNS diseases including mental diseases. The existence of D2R-5-HT2AR heterocomplexes can help explain the anti-schizophrenic effects of atypical antipsychotic drugs not only based on blockade of 5-HT2AR and of D2R in higher doses but also based on blocking the allosteric enhancement of D2R protomer signaling by 5-HT2AR protomer activation. This research opens a new understanding of the integration of DA and 5-HT signals released from DA and 5-HT nerve terminal networks. The biologica…

0301 basic medicineReviewheteroreceptor complexesTropomyosin receptor kinase BReceptor tyrosine kinasechemistry.chemical_compound0302 clinical medicineG protein-coupled receptorsserotonin receptorsReceptor Serotonin 5-HT2ABiology (General)astrogliabiologyChemistryMental DisordersBrainGeneral MedicineAntidepressive AgentsdepressionG protein-coupled receptors; astroglia; depression; heteroreceptor complexes; rapid antidepressant drugs; receptor tyrosine kinase; serotonin receptors.medicine.symptomAntipsychotic AgentsSerotonergic NeuronsSignal TransductionProto-oncogene tyrosine-protein kinase Srcserotonin receptorheteroreceptor complexeQH301-705.5Astroglia; Depression; G protein-coupled receptors; Heteroreceptor complexes; Rapid antidepressant drugs; Receptor tyrosine kinase; Serotonin receptors;Allosteric regulationserotonin receptors heteroreceptor complexes depression astroglia receptor tyrosine kinase rapid antidepressant drugs G protein-coupled receptors.depression astroglia receptor tyrosine kinase rapid antidepressant drugs G protein-coupled receptorsHeteroreceptorNO03 medical and health sciencesmedicineAnimalsHumansReceptor Fibroblast Growth Factor Type 1rapid antidepressant drugsG protein-coupled receptorReceptors Dopamine D2Dopaminergic NeuronsTyrosine phosphorylationReceptor Cross-TalkReceptor Galanin Type 1Receptor Galanin Type 2030104 developmental biologyMechanism of actionAstrocytesreceptor tyrosine kinasebiology.proteinReceptors Serotonin 5-HT1Neuroscience030217 neurology & neurosurgeryCells
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Optical activation of TrkB neurotrophin receptor in mouse ventral hippocampus promotes plasticity and facilitates fear extinction

2021

AbstractSuccessful extinction of traumatic memories depends on neuronal plasticity in the fear extinction network. However, the mechanisms involved in the extinction process remain poorly understood. Here, we investigated the fear extinction network by using a new optogenetic technique that allows temporal and spatial control of neuronal plasticity in vivo. We optimized an optically inducible TrkB (CKII-optoTrkB), the receptor of the brain-derived neurotrophic factor, which can be activated upon blue light exposure to increase plasticity specifically in pyramidal neurons. The activation of CKII-optoTrkB facilitated the induction of LTP in Schaffer collateral-CA1 synapses after brief theta-b…

0303 health sciencesHippocampusLong-term potentiationExtinction (psychology)Tropomyosin receptor kinase BOptogeneticsBiology03 medical and health sciences0302 clinical medicinenervous systemNeurotrophic factorsNeuroplasticitybiology.proteinNeuroscience030217 neurology & neurosurgery030304 developmental biologyNeurotrophin
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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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Modulatory effects of the novel TrkB receptor agonist 7,8-dihydroxyflavone on synaptic transmission and intrinsic neuronal excitability in mouse visu…

2013

7,8-Dihydroxyflavone (7,8 DHF) is a new recently identified TrkB receptor agonist, which possesses a potent neurotrophic activity and shares many physiological properties with the neurotrophin "Brain Derived Neurotrophic Factor" (BDNF). However, its precise mechanism of action at the cellular level has not been clarified yet. In the present study we explored the effects of this agent on synaptic and intrinsic neuronal properties by performing whole-cell patch clamp recordings from layer 2/3 pyramidal neurons. Incubation of acute cortical slices with 7,8-DHF (20 µM) for 30 min caused a selective reduction in the strength of GABAergic inhibition. The amplitude of evoked inhibitory postsynapti…

Agonistmedicine.drug_classNerve Tissue ProteinsTropomyosin receptor kinase BNeurotransmissionIn Vitro Techniques78-DihydroxyflavoneInhibitory postsynaptic potentialSynaptic TransmissionGlutamatergicMicemedicineElectric ImpedanceAnimalsReceptor trkBGABA-A Receptor AntagonistsGABAergic NeuronsProtein Kinase InhibitorsCells CulturedNootropic AgentsVisual CortexPharmacologyBrain-derived neurotrophic factorbiologyPyramidal CellsNeural InhibitionFlavonesReceptors GABA-AMice Inbred C57BLKineticsNeuroprotective Agentsbiology.proteinEvoked Potentials VisualNeuroscienceNeurotrophinEuropean journal of pharmacology
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Subtype-specific endothelin-A and endothelin-B receptor desensitization correlates with differential receptor phosphorylation.

1998

In the rat cardiovascular system endothelin-1 (ET-1) elicits prolonged physiologic responses mediated by the ET A receptor, whereas the effects mediated by the ET B receptor are transient. The molecular mechanisms for the subtype-specific responses are not yet clear. However, post-translational modifications such as phosphorylation and palmitoylation may play an important role. In Sf9 cells overexpressing the human ET A and ET B receptors, both subtypes are palmitoylated. However, only the ET B but not the ET A receptor is phosphorylated in a ligand-dependent manner. Because phosphorylation is believed to play an important role in ligand-dependent receptor inactivation, we analyzed whether …

Endothelin Receptor Antagonistsmedicine.medical_specialtyTropomyosin receptor kinase BCHO CellsBiologyEstrogen-related receptor alphaInternal medicineCricetinaemedicineEnzyme-linked receptorAnimalsHumansCloning MolecularPhosphorylationReceptorProtease-activated receptor 2Insulin-like growth factor 1 receptorPharmacologyReceptors EndothelinInterleukin-13 receptorReceptor Endothelin AReceptor Endothelin BCell biologyRatsInterleukin 10KineticsEndocrinologyCardiology and Cardiovascular MedicineSignal TransductionJournal of cardiovascular pharmacology
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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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The expression mechanism of the residual LTP in the CA1 region of BDNF k.o. mice is insensitive to NO synthase inhibition

2011

Abstract BDNF and nitric oxide signaling both contribute to long-term potentiation (LTP) at glutamatergic synapses, but to date, few studies analyzed the interaction of both signaling cascades in the same synaptic pathway. Here we addressed the question whether the residual LTP in the CA1 region of hippocampal slices from heterozygous BDNF knockout mice (BDNF +/− ) is dependent on nitric oxide (NO) signaling. Extracellular recording of synaptic field potentials elicited by presynaptic Schaffer collateral stimulation was performed in the CA1 region of hippocampal slices of 4- to 6-week-old mice, and LTP was induced by a theta burst stimulation protocol. Application of the nitric oxide inhibi…

Long-Term PotentiationBiophysicsTropomyosin receptor kinase BIn Vitro TechniquesBiologyNitric oxideMicechemistry.chemical_compoundmedicineAnimalsEnzyme InhibitorsCA1 Region HippocampalMolecular BiologyMice KnockoutBrain-derived neurotrophic factorBrain-Derived Neurotrophic Factormusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic PotentialsLong-term potentiationElectric StimulationCell biologyMice Inbred C57BLNG-Nitroarginine Methyl EsterSynaptic fatiguemedicine.anatomical_structureAnimals Newbornnervous systemchemistrySchaffer collateralSynaptic plasticityRetrograde signalingNeurology (clinical)Nitric Oxide SynthaseNeuroscienceDevelopmental BiologyBrain Research
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