Search results for "motor neurons"

showing 10 items of 89 documents

Computation of inverse functions in a model of cerebellar and reflex pathways allows to control a mobile mechanical segment.

2003

Abstract The command and control of limb movements by the cerebellar and reflex pathways are modeled by means of a circuit whose structure is deduced from functional constraints. One constraint is that fast limb movements must be accurate although they cannot be continuously controlled in closed loop by use of sensory signals. Thus, the pathways which process the motor orders must contain approximate inverse functions of the bio-mechanical functions of the limb and of the muscles. This can be achieved by means of parallel feedback loops, whose pattern turns out to be comparable to the anatomy of the cerebellar pathways. They contain neural networks able to anticipate the motor consequences …

CerebellumEfferentMovementModels NeurologicalSensory systemOlivary NucleusCerebellar CortexArtificial IntelligenceCerebellumNeural PathwaysReflexmedicineSet (psychology)Muscle SkeletalRed NucleusMotor NeuronsNeuronsArtificial neural networkGeneral NeuroscienceSupervised learningExtremitiesBiomechanical Phenomenamedicine.anatomical_structureMemory Short-TermCerebellar NucleiCerebellar cortexReflexNeural Networks ComputerPsychologyNeuroscienceAlgorithmsMuscle ContractionNeuroscience
researchProduct

Separation of presynaptic Cav2 and Cav1 channel function in synaptic vesicle exo- and endocytosis by the membrane anchored Ca2+ pump PMCA

2021

Significance Synaptic vesicle (SV) release from presynaptic terminals requires nanometer precise control of action potential (AP)–triggered calcium influx through voltage-gated calcium channels (VGCCs). SV recycling also depends on calcium signals, though in different spatiotemporal domains. Mechanisms for separate control of SV release and recycling by AP-triggered calcium influx remain elusive. Here, we demonstrate largely independent regulation of release and recycling by two different populations of VGCCs (Cav2, Cav1), identify Cav1 as one of potentially multiple calcium entry routes for endocytosis regulation, and show functional separation of simultaneous calcium signals in the nanome…

Drosophila ; Dmca1D ; cacophony ; PMCA ; synapse0301 basic medicine570ATPasecacophonyPresynaptic TerminalsAction PotentialsEndocytosisDmca1DSynaptic vesicleExocytosis03 medical and health scienceschemistry.chemical_compoundGlutamatergicPlasma Membrane Calcium-Transporting ATPases0302 clinical medicinePMCAsynapsemedicineAnimalsDrosophila ProteinsAxonNeurotransmitterProbabilityMotor NeuronsMultidisciplinaryVoltage-dependent calcium channelbiologyCell Membrane424500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie::570 Biowissenschaften; BiologieBiological SciencesEndocytosisCell biologyElectrophysiology030104 developmental biologymedicine.anatomical_structureDrosophila melanogasterchemistryReceptors Glutamatebiology.proteinDrosophilaCalciumCalcium ChannelsSynaptic Vesicles030217 neurology & neurosurgeryNeuroscienceProceedings of the National Academy of Sciences of the United States of America
researchProduct

Neuromuscular junction disassembly and muscle fatigue in mice lacking neurotrophin-4

2001

Neurotrophin-4 (NT-4) is produced by slow muscle fibers in an activity-dependent manner and promotes growth and remodeling of adult motorneuron innervation. However, both muscle fibers and motor neurons express NT-4 receptors, suggesting bidirectional NT-4 signaling at the neuromuscular junction. Mice lacking NT-4 displayed enlarged and fragmented neuromuscular junctions with disassembled postsynaptic acetylcholine receptor (AChR) clusters, reduced AChR binding, and acetylcholinesterase activity. Electromyographic responses, posttetanic potentiation, and action potential amplitude were also significantly reduced in muscle fibers from NT-4 knock-out mice. Slow-twitch soleus muscles from thes…

End-plate potentialNeuromuscular JunctionElectromyographyBiologyNeuromuscular junctionCellular and Molecular NeuroscienceMicePostsynaptic potentialmedicineAnimalsReceptors CholinergicNerve Growth FactorsMuscle SkeletalMolecular BiologyAcetylcholine receptorMice KnockoutMotor Neuronsmedicine.diagnostic_testMuscle fatigueElectromyographyAge FactorsLong-term potentiationneuromuscular junction; neurotrophin-4; synaptic transmissionCell Biologymedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle FatigueAcetylcholinesteraseTetanic stimulationNeuroscienceMuscle Contraction
researchProduct

Dendrites are dispensable for basic motoneuron function but essential for fine tuning of behavior.

2014

Dendrites are highly complex 3D structures that define neuronal morphology and connectivity and are the predominant sites for synaptic input. Defects in dendritic structure are highly consistent correlates of brain diseases. However, the precise consequences of dendritic structure defects for neuronal function and behavioral performance remain unknown. Here we probe dendritic function by using genetic tools to selectively abolish dendrites in identified Drosophila wing motoneurons without affecting other neuronal properties. We find that these motoneuron dendrites are unexpectedly dispensable for synaptic targeting, qualitatively normal neuronal activity patterns during behavior, and basic …

Flight altitudeMotor NeuronsDendritic spikeFine-tuningMultidisciplinaryMicroscopy ConfocalPatch-Clamp TechniquesbiologyBehavior AnimalMotor behaviorDendritesBiological Sciencesbiology.organism_classificationImmunohistochemistryStatistics NonparametricSynapseDrosophila melanogasterFlight AnimalPremovement neuronal activityAnimalsWings AnimalDrosophila melanogasterNeuroscienceFunction (biology)Proceedings of the National Academy of Sciences of the United States of America
researchProduct

Quantitative image analysis of the chromatolysis in rat facial and hypoglossal motoneurons following axotomy with and without reinnervation.

1996

Image analysis was used to quantify the time course of chromatolysis in regenerating and degenerating motoneurons. Following facial-facial, hypoglossal-hypoglossal nerve suture, or resection of facial and hypoglossal nerves with postoperative survival times of 4 h to 112 days, the texture of the Nissl substance of facial and hypoglossal motoneurons was analyzed on both sides of the brainstem in paraffin serial sections with a VIDASplus image analyzer. In this quantitative study of 149 Wistar rats, alterations of the Nissl substance were measured that were statistically significant but not yet visible to the human eye. Chromatolysis started significantly as early as 8 h and was not fully rev…

Hypoglossal NerveHistologyTime Factorsmedicine.medical_treatmentPathology and Forensic Medicinesymbols.namesakemedicineImage Processing Computer-AssistedAnimalsRats WistarMotor Neuronsbusiness.industryCell BiologyAnatomyFacial nerveAxonsNerve RegenerationRatsFacial Nervemedicine.anatomical_structurenervous systemNissl BodiesChromatolysisTime courseNerve DegenerationNissl bodysymbolsFemaleBrainstemAxotomybusinessHypoglossal nerveReinnervationCell and tissue research
researchProduct

The use of texture analysis to study the time course of chromatolysis

1998

Image analysis of the textural feature entropy of the Nissl substance was used to monitor the time course of chromatolysis in regenerating hypoglossal motoneurons and degenerating facial motoneurons 4-112 days after hypoglossal-facial anastomosis in rats. Changes in the Nissl substance were detected that were not obvious on the basis of subjective judgement of the light-microscopical appearance of the neurons. Chromatolysis started 4 days post operation (dpo) and was not reversed at 112 dpo in both nuclei. The increase of chromatolysis was 14-28 dpo faster in the regenerating hypoglossal neurons than in degenerating facial neurons. Maximal chromatolysis was measured at 56-70 dpo in both nuc…

Hypoglossal NerveTime FactorsEntropyBiologysymbols.namesakeImage Processing Computer-AssistedmedicineAnimalsRats WistarMotor NeuronsGeneral NeuroscienceAnastomosis SurgicalAnatomyMotor neuronFacial nerveNerve RegenerationRatsFacial Nervemedicine.anatomical_structurenervous systemNissl BodiesChromatolysisTime courseNissl bodysymbolsFemaleNeuronNeuronal cell bodyNeuroscienceHypoglossal nerveJournal of Neuroscience Methods
researchProduct

Post-translational modifications in the survival motor neuron protein

2004

Spinal muscular atrophy (SMA) is an autosomal recessive disease characterized by a progressive loss of the spinal motoneurons. The SMA-determining gene has been termed survival motor neuron (SMN) and is deleted or mutated in over 98% of patients. The encoded gene product is a protein expressed as different isoforms. In particular, we showed that the rat SMN cDNA produces two isoforms with Mr of 32 and 35 kDa, both localized in nuclear coiled bodies, but the 32 kDa form is also cytoplasmic, whereas the 35 kDa form is also microsomal. To determine the molecular relationship between these two isoforms and potential post-translational modifications, we performed transfection experiments with a …

INVOLVEMENTFORMSPRODUCTBiochemistryMiceChlorocebus aethiopsProtein IsoformsPhosphorylationCyclic AMP Response Element-Binding ProteinSMN PROTEINCells CulturedMotor NeuronsSPINAL MUSCULAR-ATROPHYRNA-Binding ProteinsSMN Complex Proteins3T3 CellsTransfectionmedicine.anatomical_structureSpinal CordCOS CellsSUBCELLULAR-LOCALIZATIONEXPRESSIONGene isoformRecombinant Fusion ProteinsBiophysicsNerve Tissue ProteinsBiologyMuscular Atrophy SpinalGene productSMN Complex ProteinsComplementary DNAmedicineAnimalsHumansMolecular BiologyCell BiologySpinal muscular atrophyMotor neuronmedicine.diseaseSurvival of Motor Neuron 1 ProteinMolecular biologyRatsnervous system diseasesMolecular WeightSEVERITYnervous systemBODIESProtein Processing Post-TranslationalDETERMINING GENEImmunostainingBiochemical and Biophysical Research Communications
researchProduct

Mutations in ATP13A2 (PARK9) are associated with an amyotrophic lateral sclerosis-like phenotype, implicating this locus in further phenotypic expans…

2019

Background Amyotrophic lateral sclerosis [1] is a genetically heterogeneous neurodegenerative disorder, characterized by late-onset degeneration of motor neurons leading to progressive limb and bulbar weakness, as well as of the respiratory muscles, which is the primary cause of disease fatality. To date, over 25 genes have been implicated as causative in ALS with C9orf72, SOD1, FUS, and TARDBP accounting for the majority of genetically positive cases. Results We identified two patients of Italian and French ancestry with a clinical diagnosis of juvenile-onset ALS who were mutation-negative in any of the known ALS causative genes. Starting with the index case, a consanguineous family of Ita…

MaleAmyotrophic lateral sclerosis ATP13A2 parkinsonismlcsh:Medicine0302 clinical medicineC9orf72Drug DiscoveryAmyotrophic lateral sclerosisIndex caseZebrafishExome sequencingMotor NeuronsGenetics0303 health sciencesDEMENTIA1184 Genetics developmental biology physiologyMiddle AgedPedigree3. Good healthProton-Translocating ATPasesPhenotypeMolecular MedicineFemaleSettore MED/26 - NeurologiaPrimary ResearchAdultlcsh:QH426-470SOD1BiologyTARDBP03 medical and health sciencesParkinsonian DisordersNeuronal Ceroid-LipofuscinosesExome SequencingGeneticsmedicineAnimalsHumansGenetic Predisposition to DiseaseMolecular Biology030304 developmental biologyGenetic heterogeneityAmyotrophic Lateral Sclerosislcsh:Rmedicine.diseaseDisease Models Animallcsh:GeneticsMutationNeuronal ceroid lipofuscinosis030217 neurology & neurosurgeryPARKINSONISM
researchProduct

Absence of an aging-related increase in fiber type grouping in athletes and non-athletes

2020

The ageing-related loss of muscle mass is thought to be partly attributable to motor neuron loss and motor unit remodelling that result in fibre type grouping. We examined fibre type grouping in 19- to 85-year-old athletes and non-athletes and evaluated to which extent any observed grouping is explained by the fibre type composition of the muscle. Since regular physical activity may stimulate reinnervation, we hypothesised that fibre groups are larger in master athletes than in age-matched non-athletes. Fibre type grouping was assessed in m. vastus lateralis biopsies from 22 young (19-27 years) and 35 healthy older (66-82 years) non-athletes, and 14 young (20-29 years), 51 middle-aged (38%6…

MaleBiopsy030204 cardiovascular system & hematologyMuskel- und KnochenstoffwechselQuadriceps Muscleudc:612.74:612.660302 clinical medicinegroupingOrthopedics and Sports MedicineFibre typeAged 80 and overMotor NeuronsDenervationbiologyFiber typestaranjemišična vlaknaMiddle Agedfibre typeMuscle Fibers Slow-Twitchmedicine.anatomical_structureMuscle Fibers Fast-TwitchreinervacijaFemaleSportsReinnervationAdultmedicine.medical_specialtyPhysical Therapy Sports Therapy and RehabilitationYoung Adult03 medical and health sciencesInternal medicinevastus lateralismedicineHumansAgeddenervationbusiness.industryAthletesaging030229 sport sciencesMotor neuronbiology.organism_classificationfiber typereinnervationMotor unitdenervacijaCross-Sectional StudiesEndocrinologyAgeingbusiness
researchProduct

Clobetasol promotes neuromuscular plasticity in mice after motoneuronal loss via sonic hedgehog signaling, immunomodulation and metabolic rebalancing

2021

AbstractMotoneuronal loss is the main feature of amyotrophic lateral sclerosis, although pathogenesis is extremely complex involving both neural and muscle cells. In order to translationally engage the sonic hedgehog pathway, which is a promising target for neural regeneration, recent studies have reported on the neuroprotective effects of clobetasol, an FDA-approved glucocorticoid, able to activate this pathway via smoothened. Herein we sought to examine functional, cellular, and metabolic effects of clobetasol in a neurotoxic mouse model of spinal motoneuronal loss. We found that clobetasol reduces muscle denervation and motor impairments in part by restoring sonic hedgehog signaling and …

MaleCancer ResearchPhysiology129 StrainBiochemistryMiceDatabases GeneticMedicineMyocyteMotor NeuronsNeuronal PlasticitySkeletalSmoothened ReceptorHedgehog signaling pathwayMuscle atrophyMitochondriaAstrogliosisNeuroprotective AgentsMusclemedicine.symptomInflammation MediatorsSignal TransductionCholera ToxinMice 129 StrainhedgehogImmunologyMotor ActivityNeuroprotectionArticleDatabasesCellular and Molecular NeurosciencesmoothenedGeneticAnimalsHumansHedgehog ProteinsMuscle SkeletalHedgehogGlucocorticoidsMuscle DenervationQH573-671Animalbusiness.industryAmyotrophic Lateral SclerosisGlial biologyCell Biologymedicine.diseaseSaporinsSpineMitochondria MuscleDisease Models AnimalclobetasolinflammationCase-Control StudiesDisease ModelsDiseases of the nervous systemCytologySmoothenedbusinessEnergy MetabolismNeuroscienceOpen Field Test
researchProduct