Search results for "Motor Neurons"

showing 9 items of 89 documents

Sequential acquisition of cacophony calcium currents, sodium channels and voltage-dependent potassium currents affects spike shape and dendrite growt…

2014

During metamorphosis the CNS undergoes profound changes to accommodate the switch from larval to adult behaviors. In Drosophila and other holometabolous insects, adult neurons differentiate either from respecified larval neurons, newly born neurons, or are born embryonically but remain developmentally arrested until differentiation during pupal life. This study addresses the latter in the identified Drosophila flight motoneuron 5. In situ patch-clamp recordings, intracellular dye fills and immunocytochemistry address the interplay between dendritic shape, excitability and ionic current development. During pupal life, changes in excitability and spike shape correspond to a stereotyped, progr…

Patch-Clamp Techniquesmedia_common.quotation_subjectAction Potentialschemistry.chemical_elementCell EnlargementBiologyCalciumSodium ChannelsArticleMembrane PotentialsAnimalsPatch clampMetamorphosisIon channelmedia_commonMotor NeuronsMembrane potentialMicroscopy ConfocalGeneral NeuroscienceSodium channelOptical ImagingfungiMetamorphosis BiologicalDendritesImmunohistochemistryPotassium channelCell biologyDrosophila melanogasterchemistryPotassium Channels Voltage-GatedPotassiumCalciumNeuroscienceIntracellularEuropean Journal of Neuroscience
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Neuropathologic and morphometric studies in hereditary motor and sensory neuropathy type II with neurofilament accumulation.

1986

Histological, electron microscopic and morphometric data on sural nerve, muscle, and skin biopsies of three patients affected by autosomal dominant hereditary motor and sensory neuropathy type II with neurofilament accumulation, whose neurological, cardiological and electrophysiological data have been provided in a previous paper disclosed focally enlarged myelinated axons, due to aggregation of neurofilaments in sural nerves of all 3 biopsied patients, as well as densely packed clusters of filaments in occasional non-myelinated axons without axonal enlargement, in several fibroblasts and endothelial cells in muscle and particularly in skin. This accumulation of filaments was less pronounce…

Pathologymedicine.medical_specialtyNeurofilamentNeurologyIntermediate FilamentsSural nerveDermatologyBiologylaw.invention03 medical and health sciences0302 clinical medicineSural NervelawCharcot-Marie-Tooth DiseasemedicineHumansHereditary Sensory and Autonomic NeuropathiesIntermediate filamentCytoskeletonMyelin Sheath030304 developmental biologySkinMotor Neurons0303 health sciencesGeneral NeuroscienceMusclesGeneral MedicineAnatomymedicine.diseaseAxonsPsychiatry and Mental healthElectrophysiologyMicroscopy ElectronMuscular Atrophynervous systemUltrastructureNeurology (clinical)Electron microscopeHereditary motor and sensory neuropathy030217 neurology & neurosurgeryItalian journal of neurological sciences
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BAG3 mediates chaperone-based aggresome-targeting and selective autophagy of misfolded proteins.

2010

Increasing evidence indicates the existence of selective autophagy pathways, but the manner in which substrates are recognized and targeted to the autophagy system is poorly understood. One strategy is transport of a particular substrate to the aggresome, a perinuclear compartment with high autophagic activity. In this paper, we identify a new cellular pathway that uses the specificity of heat-shock protein 70 (Hsp70) to misfolded proteins as the basis for aggresome-targeting and autophagic degradation. This pathway is regulated by the stress-induced co-chaperone Bcl-2-associated athanogene 3 (BAG3), which interacts with the microtubule-motor dynein and selectively directs Hsp70 substrates …

Protein FoldingRecombinant Fusion ProteinsDyneinGreen Fluorescent ProteinsAggrephagyMice TransgenicBAG3BiochemistryMiceJUNQ and IPODChlorocebus aethiopsGeneticsAutophagyAnimalsHumansPoint MutationHSP70 Heat-Shock ProteinsMolecular BiologyAdaptor Proteins Signal TransducingSequence DeletionInclusion BodiesMotor NeuronsbiologySuperoxide DismutaseAutophagyScientific ReportsDyneinsTransport proteinCell biologyProtein TransportAggresomeHEK293 CellsSpinal CordChaperone (protein)COS Cellsbiology.proteinApoptosis Regulatory ProteinsProteasome InhibitorsEMBO reports
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An Intercellular Flow of Glutathione Regulated by Interleukin 6 Links Astrocytes and the Liver in the Pathophysiology of Amyotrophic Lateral Sclerosis

2021

Oxidative stress has been proposed as a major mechanism of damage to motor neurons associated with the progression of amyotrophic lateral sclerosis (ALS). Astrocytes are the most numerous glial cells in the central nervous system and, under physiological conditions, protect neurons from oxidative damage. However, it is uncertain how their reactive phenotype may affect motor neurons during ALS progression. In two different ALS mouse models (SOD1G93A and FUS-R521C), we found that increased levels of proinflammatory interleukin 6 facilitate glutathione (GSH) release from the liver to blood circulation, which can reach the astrocytes and be channeled towards motor neurons as a mechanism of anti…

amyotrophic lateral sclerosisPhysiologySistema nerviós central MalaltiesClinical BiochemistryastrocytesEsclerosi múltipleNeuronesCell BiologyRM1-950liverBiochemistryamyotrophic lateral sclerosis; liver; astrocytes; motor neurons; mitochondria; glutathione; oxidative stressArticlemitochondriaoxidative stressmotor neuronsTherapeutics. PharmacologyglutathioneMolecular Biology
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NAD+ Precursors and Antioxidants for the Treatment of Amyotrophic Lateral Sclerosis

2021

Charcot first described amyotrophic lateral sclerosis (ALS) between 1865 and 1874 as a sporadic adult disease resulting from the idiopathic progressive degeneration of the motor neuronal system, resulting in rapid, progressive, and generalized muscle weakness and atrophy. There is no cure for ALS and no proven therapy to prevent it or reverse its course. There are two drugs specifically approved for the treatment of ALS, riluzol and edaravone, and many others have already been tested or are following clinical trials. However, at the present moment, we still cannot glimpse a true breakthrough in the treatment of this devastating disease. Nevertheless, our understanding of the pathophysiology…

amyotrophic lateral sclerosisbusiness.industryQH301-705.5NAD<sup>+</sup>Medicine (miscellaneous)Degeneration (medical)Diseasemedicine.disease_causemedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyPathophysiologychemistry.chemical_compoundAtrophyantioxidantschemistryEdaravoneMedicinemotor neuronsoxidative stressNAD+ kinaseAmyotrophic lateral sclerosisBiology (General)businessNeuroscienceOxidative stressBiomedicines
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Exciting Complexity: The Role of Motor Circuit Elements in ALS Pathophysiology

2020

Amyotrophic lateral sclerosis (ALS) is a fatal disease, characterized by the degeneration of both upper and lower motor neurons. Despite decades of research, we still to date lack a cure or disease modifying treatment, emphasizing the need for a much-improved insight into disease mechanisms and cell type vulnerability. Altered neuronal excitability is a common phenomenon reported in ALS patients, as well as in animal models of the disease, but the cellular and circuit processes involved, as well as the causal relevance of those observations to molecular alterations and final cell death, remain poorly understood. Here, we review evidence from clinical studies, cell type-specific electrophysi…

interneuronslower motor neuronsexcitabilityastrocytesAmyotrophic lateral sclerosisupper motor neuronslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrylcsh:RC321-571Frontiers in Neuroscience
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Neurodegenerative changes are prevented by Erythropoietin in the pmn model of motoneuron degeneration

2014

Motoneuron diseases are fatal neurodegenerative disorders characterized by a progressive loss of motoneurons, muscle weakness and premature death. The progressive motor neuronopathy (pmn) mutant mouse has been considered a good model for the autosomal recessive childhood form of spinal muscular atrophy (SMA). Here, we investigated the therapeutic potential of Erythropoietin (Epo) on this mutant mouse. Symptomatic or pre-symptomatic treatment with Epo significantly prolongs lifespan by 84.6% or 87.2% respectively. Epo preserves muscle strength and significantly attenuates behavioural motor deficits of mutant pmn mice. Histological and metabolic changes in the spinal cord evaluated by immunoh…

medicine.medical_specialtyMutantMotor ActivitySpinal Muscular Atrophies of ChildhoodMiceCellular and Molecular NeuroscienceWestern blotInternal medicineReceptors ErythropoietinmedicineAnimalsErythropoietinMotor NeuronsPharmacologymedicine.diagnostic_testbusiness.industryMuscle weaknessSpinal muscular atrophymedicine.diseaseSpinal cordSMA*Mice Mutant StrainsDisease Models Animalmedicine.anatomical_structureEndocrinologySpinal CordErythropoietinImmunohistochemistrymedicine.symptombusinessNeurosciencemedicine.drugNeuropharmacology
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Neurochemistry of identified motoneurons of the tensor tympani muscle in rat middle ear

2008

The objective of the present study was to identify efferent and afferent transmitters of motoneurons of the tensor tympani muscle (MoTTM) to gain more insight into the neuronal regulation of the muscle. To identify MoTTM, we injected the fluorescent neuronal tracer Fluoro-Gold (FG) into the muscle after preparation of the middle ear in adult rats. Upon terminal uptake and retrograde neuronal transport, we observed FG in neurons located lateral and ventrolateral to the motor trigeminal nucleus ipsilateral to the injection site. Immunohistochemical studies of these motoneurons showed that apparently all contained choline acetyltransferase, demonstrating their motoneuronal character. Different…

medicine.medical_specialtyStilbamidinesEar MiddleNeuropeptideSubstance PCalcitonin gene-related peptideInjections IntramuscularTensor tympani muscleCholine O-AcetyltransferaseRats Sprague-Dawleychemistry.chemical_compoundInternal medicinemedicineAnimalsNeuronal transportFluorescent DyesMotor NeuronsStaining and LabelingTyrosine hydroxylaseChemistryNeuropeptidesNeurochemistryNeuropeptide Y receptorImmunohistochemistryCholine acetyltransferaseSensory SystemsRatsEndocrinologynervous systemFemaleTensor TympaniHearing Research
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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