Search results for "Motor neuron"

showing 10 items of 140 documents

Evidence of resistance training-induced neural adaptation in older adults

2021

The deleterious effects of aging on force production are observable from the age of 40 upwards, depending on the measure. Neural mechanisms contributing to maximum force production and rate of force development have been suggested as descending drive from supraspinal centers, spinal motoneuron excitability, and corticospinal inhibition of descending drive; all of which influence motor unit recruitment and/or firing rate. Resistance-trained Master athletes offer a good source of information regarding the inevitable effects of aging despite the countermeasure of systematic resistance-training. However, most evidence of neural adaptation is derived from longitudinal intervention studies in pre…

0301 basic medicineAgingmedicine.medical_treatmentCortical imagingBiochemistry0302 clinical medicineEndocrinologymotor unitvoimantuotto (fysiologia)motoneuroninterventionMotor NeuronsbiologyexercisekuntoliikuntaNeural adaptationinterventiotutkimusAdaptation PhysiologicalTranscranial Magnetic Stimulationmedicine.anatomical_structurehermo-lihastoimintaneuromuscularvoimaharjoittelustrengthRecruitment Neurophysiologicalmedicine.medical_specialty03 medical and health sciencesPhysical medicine and rehabilitationGood evidenceGeneticsmedicineHumansMuscle SkeletalMolecular BiologyAgedAthletesbusiness.industryElectromyographyagingResistance trainingResistance TrainingCell Biologybiology.organism_classificationMotor unitTranscranial magnetic stimulation030104 developmental biologyikääntyminenMotor unit recruitmentbusiness030217 neurology & neurosurgerylihasvoima
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Dendritic and Axonal L-Type Calcium Channels Cooperate to Enhance Motoneuron Firing Output during Drosophila Larval Locomotion

2017

Behaviorally adequate neuronal firing patterns are critically dependent on the specific types of ion channel expressed and on their subcellular localization. This study combinesin situelectrophysiology with genetic and pharmacological intervention in larvalDrosophila melanogasterof both sexes to address localization and function of L-type like calcium channels in motoneurons. We demonstrate that Dmca1D (Cav1 homolog) L-type like calcium channels localize to both the somatodendritic and the axonal compartment of larval crawling motoneurons.In situpatch-clamp recordings in genetic mosaics reveal that Dmca1D channels increase burst duration and maximum intraburst firing frequencies during craw…

0301 basic medicineBK channelSodium ChannelsSK channel03 medical and health sciences0302 clinical medicineAnimalsDrosophila ProteinsLarge-Conductance Calcium-Activated Potassium ChannelsResearch ArticlesMotor NeuronsVoltage-dependent calcium channelbiologyGeneral NeuroscienceSodium channelCalcium channelfungiExcitatory Postsynaptic PotentialsAfterhyperpolarizationDendritic CellsAxonsElectrophysiological PhenomenaElectrophysiologyStretch-activated ion channel030104 developmental biologyDrosophila melanogasternervous systemLarvaSynapsesbiology.proteinCalcium ChannelsNeuroscience030217 neurology & neurosurgeryLocomotion
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Brain histamine and behavioral neuroscience

2017

ABSTRACT NON PREVISTO DALLA PUBBLICAZIONE

0301 basic medicineCarboxy-LyasesVideo RecordingEditorial: NeuroscienceBehavioral neuroscienceSettore BIO/09 - Fisiologiabehavioral sequenceHistonesMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAnimalsHumansMedicineMotor NeuronsBehaviorBehavior Animalbusiness.industryNeurosciencesBrainhistaminePhenotype030104 developmental biologyOncologychemistryAnesthesiaBehavior; Behavioral sequence; Histamine; Neuroscience; T-pattern; OncologyT-patternbusinessNeuroscience030217 neurology & neurosurgeryHistamineTourette SyndromeNeuroscienceOncotarget
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The Drosophila Hox gene Ultrabithorax acts both in muscles and motoneurons to orchestrate formation of specific neuromuscular connections

2016

Hox genes are known to specify motoneuron pools in the developing vertebrate spinal cord and to control motoneuronal targeting in several species. However, the mechanisms controlling axial diversification of muscle innervation patterns are still largely unknown. We present data showing that the Drosophila Hox gene Ultrabithorax (Ubx) acts in the late embryo to establish target specificity of ventrally projecting RP motoneurons. In abdominal segments A2 to A7, RP motoneurons innervate the ventrolateral muscles VL1-4, with VL1 and VL2 being innervated in a Wnt4-dependent manner. In Ubx mutants, these motoneurons fail to make correct contacts with muscle VL1, a phenotype partially resembling t…

0301 basic medicineCell typeEmbryo Nonmammaliananimal structuresNeuromuscular JunctionGenes InsectMuscle DevelopmentNeuromuscular junctionAnimals Genetically ModifiedHox genes03 medical and health sciencesWNT4MorphogenesismedicineAnimalsDrosophila ProteinsHox geneWnt Signaling PathwayMolecular BiologyTranscription factorUltrabithoraxHomeodomain ProteinsMotor NeuronsGeneticsbiologyMusclesmusculoskeletal neural and ocular physiologyfungiGenes HomeoboxGene Expression Regulation Developmentalbiology.organism_classificationMuscle innervationSegmental patterningCell biologyMotoneuronsDrosophila melanogaster030104 developmental biologymedicine.anatomical_structurenervous system209embryonic structuresDrosophilaWnt signalling pathwayDrosophila melanogasterDrosophila ProteinTranscription FactorsResearch ArticleDevelopmental BiologyDevelopment
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Sensory neuropathy in progressive motor neuronopathy(pmn)mice is associated with defects in microtubule polymerization and axonal transport

2016

Motor neuron diseases such as amyotrophic lateral sclerosis (ALS) are now recognized as multi-system disorders also involving various non-motor neuronal cell types. The precise extent and mechanistic basis of non-motor neuron damage in human ALS and ALS animal models remain however unclear. To address this, we here studied progressive motor neuronopathy (pmn) mice carrying a missense loss-of-function mutation in tubulin binding cofactor E (TBCE). These mice manifest a particularly aggressive form of motor axon dying back and display a microtubule loss, similar to that induced by human ALS-linked TUBA4A mutations. Using whole nerve confocal imaging of pmn × thy1.2-YFP16 fluorescent reporter …

0301 basic medicineGeneral NeuroscienceMotor neuronBiologymedicine.disease3. Good healthPathology and Forensic MedicineMicrotubule polymerizationTubulin binding03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structurenervous systemDorsal root ganglionmedicineAxoplasmic transportNeurology (clinical)NeuronAxonAmyotrophic lateral sclerosisNeuroscience030217 neurology & neurosurgeryBrain Pathology
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Targeting RNA structure in SMN2 reverses spinal muscular atrophy molecular phenotypes

2018

Modification of SMN2 exon 7 (E7) splicing is a validated therapeutic strategy against spinal muscular atrophy (SMA). However, a target-based approach to identify small-molecule E7 splicing modifiers has not been attempted, which could reveal novel therapies with improved mechanistic insight. Here, we chose as a target the stem-loop RNA structure TSL2, which overlaps with the 5′ splicing site of E7. A small-molecule TSL2-binding compound, homocarbonyltopsentin (PK4C9), was identified that increases E7 splicing to therapeutic levels and rescues downstream molecular alterations in SMA cells. High-resolution NMR combined with molecular modelling revealed that PK4C9 binds to pentaloop conformati…

0301 basic medicineIndolesCOMPOUND LIBRARIESDrug Evaluation PreclinicalGeneral Physics and AstronomyBiotecnologiaAnimals Genetically ModifiedExonMolecular Targeted TherapyRegulatory Elements Transcriptionallcsh:ScienceHUMAN-DISEASE GENESBIOACTIVE SMALL MOLECULESMultidisciplinaryChemistryDrug discovery[CHIM.ORGA]Chemical Sciences/Organic chemistryQImidazolesMUTATION PATTERNExonsSMA*3. Good healthCell biologySurvival of Motor Neuron 2 ProteinPhenotypeCribratgeRNA splicingNUCLEOTIDE STRUCTUREDrosophilaMESSENGER-RNACOMPUTATIONAL TOOLSMedical screeningMYOTONIC-DYSTROPHYScienceMuscular atrophyArticleGeneral Biochemistry Genetics and Molecular BiologyGenètica molecularMuscular Atrophy Spinal03 medical and health sciencesddc:570SPLICING MODIFIERSmedicineAnimalsHumansHIV-1 TARRNA MessengerAtròfia muscularMessenger RNAAlternative splicingRNAGeneral ChemistrySpinal muscular atrophymedicine.diseaseAlternative Splicing030104 developmental biologyRNAlcsh:QRNA Splice SitesHeLa CellsNature Communications
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Apoptotic Activity of MeCP2 Is Enhanced by C-Terminal Truncating Mutations.

2016

Methyl-CpG binding protein 2 (MeCP2) is a widely abundant, multifunctional protein most highly expressed in post-mitotic neurons. Mutations causing Rett syndrome and related neurodevelopmental disorders have been identified along the entire MECP2 locus, but symptoms vary depending on mutation type and location. C-terminal mutations are prevalent, but little is known about the function of the MeCP2 C-terminus. We employ the genetic efficiency of Drosophila to provide evidence that expression of p.Arg294* (more commonly identified as R294X), a human MECP2 E2 mutant allele causing truncation of the C-terminal domains, promotes apoptosis of identified neurons in vivo. We confirm this novel find…

0301 basic medicineMethyl-CpG-Binding Protein 2lcsh:MedicineApoptosisBiochemistryPhosphoserine0302 clinical medicineAnimal CellsDrosophila ProteinsPost-Translational ModificationPhosphorylationlcsh:ScienceNeuronsMotor NeuronsGeneticsMultidisciplinaryCell DeathbiologyDrosophila MelanogasterAnimal ModelsInsectsFOXG1Cell ProcessesCaspasesPhosphorylationDrosophilaBiological CulturesCellular TypesDrosophila melanogasterResearch ArticleGene isoformcongenital hereditary and neonatal diseases and abnormalitiesArthropodaProtein domainMouse ModelsMotor ActivityResearch and Analysis MethodsTransfectionModels BiologicalMECP203 medical and health sciencesModel OrganismsProtein Domainsmental disordersAnimalsHumansMolecular Biology TechniquesImmunohistochemistry TechniquesMolecular BiologyTranscription factorBinding proteinlcsh:ROrganismsBiology and Life SciencesProteinsCell BiologyCell Culturesbiology.organism_classificationInvertebratesHistochemistry and Cytochemistry TechniquesHEK293 Cells030104 developmental biologyCellular NeuroscienceMutationImmunologic TechniquesMutant Proteinslcsh:Q030217 neurology & neurosurgeryNeuroscienceTranscription FactorsPLoS ONE
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Drosophila SMN2minigene reporter model identifies moxifloxacin as a candidate therapy for SMA

2018

Spinal muscular atrophy is a rare and fatal neuromuscular disorder caused by the loss of alpha motor neurons. The affected individuals have mutated the ubiquitously expressed SMN1 gene resulting in the loss or reduction in the survival motor neuron (SMN) protein levels. However, an almost identical paralog exists in humans: SMN2. Pharmacological activation of SMN2 exon 7 inclusion by small molecules or modified antisense oligonucleotides is a valid approach to treat SMA. Here we describe an in vivo SMN2 minigene reporter system in Drosophila motor neurons that serves as a cost-effective, feasible, and stringent primary screening model for identifying chemicals capable of crossing the conser…

0301 basic medicineMoxifloxacinDrug Evaluation PreclinicalSMN1BiologyBiochemistryAnimals Genetically ModifiedMuscular Atrophy Spinal03 medical and health sciencesExon0302 clinical medicineGenes ReporterGeneticsmedicineAnimalsHumansMolecular BiologyExonsSpinal muscular atrophyMotor neuronSMA*medicine.diseasenervous system diseasesCell biologySurvival of Motor Neuron 2 ProteinAlternative SplicingDisease Models AnimalDrosophila melanogaster030104 developmental biologymedicine.anatomical_structureCajal bodyBlood-Brain BarrierRNA splicing030217 neurology & neurosurgeryBiotechnologyMinigeneThe FASEB Journal
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Protein misfolding, amyotrophic lateral sclerosis and guanabenz: Protocol for a phase II RCT with futility design (ProMISe trial)

2017

IntroductionRecent studies suggest that endoplasmic reticulum stress may play a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS) through an altered regulation of the proteostasis, the cellular pathway-balancing protein synthesis and degradation. A key mechanism is thought to be the dephosphorylation of eIF2α, a factor involved in the initiation of protein translation. Guanabenz is an alpha-2-adrenergic receptor agonist safely used in past to treat mild hypertension and is now an orphan drug. A pharmacological action recently discovered is its ability to modulate the synthesis of proteins by the activation of translational factors preventing misfolded protein accumula…

0301 basic medicineOncologyPathologyamyotrophic lateral sclerosisamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; adrenergic alpha-2 receptor agonist s; age of onset; amyotrophic lateral sclerosis; disease progression; double-blind method; endoplasmic reticulum stress; guanabenz; humans; italy; medical futility; neuroprotective agents; proteostasis deficienciesamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Medicine (all)randomized clinical trial guanabenzHelsinki declaration0302 clinical medicineProtocolAdrenergic alpha-2 Receptor Agonists1506Amyotrophic lateral sclerosisAge of OnsetGuanabenzMedicine (all)amyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein responseNeurodegenerationamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response;amyotrophic lateral sclerosis; guanabenz; motor neurone disease; neuromuscular disease; randomized clinical trial; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis DeficienciesGeneral Medicineunfolded protein responseEndoplasmic Reticulum StressRiluzoleNeuroprotective AgentsNeurologyTolerabilityItalyDisease Progression1713GuanabenzMedical Futilitymedicine.drugmedicine.medical_specialtyamyotrophic lateral sclerosis; motor neurone disease; neuromuscular disease; randomized clinical trial guanabenz; unfolded protein response; Adrenergic alpha-2 Receptor Agonists; Age of Onset; Amyotrophic Lateral Sclerosis; Disease Progression; Double-Blind Method; Endoplasmic Reticulum Stress; Guanabenz; Humans; Italy; Medical Futility; Neuroprotective Agents; Proteostasis Deficiencies; Medicine (all)Neuroprotection03 medical and health sciencesmotor neurone diseaseDouble-Blind MethodInternal medicinemedicineHumansProteostasis Deficienciesbusiness.industryAmbientaleneuromuscular diseaserandomized clinical trialmedicine.diseaseClinical trial030104 developmental biologybusiness030217 neurology & neurosurgery
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A longitudinal DTI and histological study of the spinal cord reveals early pathological alterations in G93A-SOD1 mouse model of amyotrophic lateral s…

2017

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective motor neuron degeneration in the motor cortex, brainstem and spinal cord. It is generally accepted that ALS is caused by death of motor neurons, however the exact temporal cascade of degenerative processes is not yet completely known. To identify the early pathological changes in spinal cord of G93A-SOD1 AIS mice we performed a comprehensive longitudinal analysis employing diffusion-tensor magnetic resonance imaging alongside histology and electron microscopy, in parallel with peripheral nerve histology. We showed the gradient of degeneration appearance in spinal cord white and gray matter, startin…

0301 basic medicinePathologyNeurologyTime FactorsMotor neuron diseasesSensory Receptor CellMice0302 clinical medicineImage Processing Computer-AssistedAxonAmyotrophic lateral sclerosisGray MatterAnthracenesWhite MatterMitochondriamedicine.anatomical_structureDiffusion Tensor ImagingNeurologySpinal CordG93A-SOD1 miceBrainstemHumanMotor cortexmedicine.medical_specialtyAxon degenerationTime FactorSensory Receptor CellsSOD1Mice TransgenicWhite matter03 medical and health sciencesMagnetic resonance imagingDevelopmental NeuroscienceMicroscopy Electron TransmissionmedicineElectron microscopyAnimalsHumansMotor neuron diseaseAmyotrophic lateral sclerosiAnimalbusiness.industrySuperoxide DismutaseAmyotrophic Lateral SclerosisSpinal cordmedicine.diseaseAmyotrophic lateral sclerosisMice Inbred C57BLDisease Models Animal030104 developmental biologyAnthracenebusinessNeuroscience030217 neurology & neurosurgeryExperimental neurology
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