Search results for "Axons"

showing 10 items of 101 documents

Botulinum Toxin A reduces neurogenic flare but has almost no effect on pain and hyperalgesia in human skin.

2003

Botulinum toxin A (BoNT/A) has been used therapeutically to treat muscular hypercontractions and sudomotor hyperactivity. There is increasing evidence that BoNT/A might also have analgesic properties, in particular in headache. In the present investigation we tested the often cited hypothesis that BoNT/A-induced analgesia can be attributed to inhibition of neuropeptide release from nociceptive nerve fibers. In 15 healthy volunteers BoNT/A (5, 10, 20 mouse units BOTOX) or saline (contralateral side) was injected intracutaneously on the volar forearm. On day zero, the day of injection, no further tests were performed. We repeatedly elicited pain, mechanical hyperalgesia and neurogenic flare b…

AdultMalemedicine.medical_specialtyNeurologyAnalgesicNeuropeptidePainStimulationNerve FibersPsychophysicsMedicineHumansBotulinum Toxins Type APain MeasurementSkinHypohidrosisNeurogenic inflammationbusiness.industryNociceptorsAxonsElectric StimulationSudomotorNociceptionNeurologyHyperalgesiaAnesthesiaHyperalgesiaFemaleNeurology (clinical)medicine.symptomNeurogenic InflammationbusinessJournal of neurology
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Changes of sensory conduction velocity and refractory periods with decreasing tissue temperature in man.

1977

Changes with temperature of maximum sensory nerve conduction velocity as well as absolute and relative refractory periods were tested in 14 human subjects. Corresponding to previously published findings maximum conduction velocity decreased with cooling following a Q10 of +1.4. The absolute and relative refractory periods were increased by cooling, the Q10 being -3.1 and -3.35 respectively. There was a tendency showing a more pronounced temperature effect at low temperatures. The Q10 and the steepness of the regressionline changed at the level of 26.9 degrees C, but were significant for the relative refractory period only.

AdultTime FactorsRefractory Period ElectrophysiologicalRefractory periodQ10Neural ConductionSensationAction PotentialsSensory systemElectromyographyNerve conduction velocityBody TemperatureNuclear magnetic resonancemedicineAnimalsHumansRefractory (planetary science)Ulnar NerveTissue temperaturemedicine.diagnostic_testChemistryAnatomyAxonsNeurologyCatsNeurology (clinical)Sensory nerve conduction velocityJournal of neurology
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Semaphorin and plexin gene expression is altered in the prefrontal cortex of schizophrenia patients with and without auditory hallucinations

2015

Auditory hallucinations (AH) are clinical hallmarks of schizophrenia, however little is known about molecular genetics of these symptoms. In this study, gene expression profiling of postmortem brain samples from prefrontal cortex of schizophrenic patients without AH (SNA), patients with AH (SA) and control subjects were compared. Genome-wide expression analysis was conducted using samples of three individuals of each group and the Affymetrix GeneChip Human-Gene 1.0 ST-Array. This analysis identified the Axon Guidance pathway as one of the most differentially expressed network among SNA, SA and CNT. To confirm the transcriptome results, mRNA level quantification of seventeen genes involved i…

Adultmedicine.medical_specialtyHallucinationsSEMA4DDown-RegulationPrefrontal CortexNerve Tissue ProteinsSemaphorinsTranscriptomeMolecular geneticsInternal medicineNeuroplasticitymedicineHumansRNA MessengerPrefrontal cortexBiological PsychiatryAgedOligonucleotide Array Sequence AnalysisAged 80 and overNeuronal PlasticitybiologyGene Expression ProfilingPlexinBrainMiddle Agedmedicine.diseaseAxonsbody regionsGene expression profilingPsychiatry and Mental healthEndocrinologySchizophreniaSchizophreniabiology.proteinPsychologyCell Adhesion MoleculesNeurosciencePsychiatry Research
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Expression of Toll-Like Receptors in the Developing Brain

2012

Toll-like receptors (TLR) are key players of the innate and adaptive immune response in vertebrates. The original protein Toll in Drosophila melanogaster regulates both host defense and morphogenesis during development. Making use of real-time PCR, in situ hybridization, and immunohistochemistry we systematically examined the expression of TLR1-9 and the intracellular adaptor molecules MyD88 and TRIF during development of the mouse brain. Expression of TLR7 and TLR9 in the brain was strongly regulated during different embryonic, postnatal, and adult stages. In contrast, expression of TLR1-6, TLR8, MyD88, and TRIF mRNA displayed no significant changes in the different phases of brain develop…

AgingGene Expressionlcsh:MedicineMiceMolecular Cell BiologyMorphogenesislcsh:ScienceReceptorImmune ResponseRegulation of gene expressionMultidisciplinaryNeocortexToll-Like ReceptorsBrainGene Expression Regulation DevelopmentalAcquired immune systemInnate ImmunityCell biologyInfectious Diseasesmedicine.anatomical_structureMedicineResearch ArticleImmunologyCentral nervous systemMorphogenesisIn situ hybridizationBiologyMolecular GeneticsImmune ActivationDevelopmental NeuroscienceGeneticsmedicineAnimalsHumansRNA MessengerBiologyImmunity to Infectionslcsh:RImmunityComputational BiologyImmune DefenseAxonsHEK293 CellsTRIFImmune SystemCellular NeuroscienceImmunologyClinical Immunologylcsh:QTranscriptomeDevelopmental BiologyNeurosciencePLoS ONE
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Ready, STAT, go: transcription factors on the move.

2012

In this issue of The EMBO Journal, Ben-Yaakov et al (2012) explore the contribution of transcription factors (TFs) in directly communicating information about injury between the axon and the nucleus. They show that multiple TFs bind the retrograde molecular motor dynein in injured axons. Focusing on one TF family, the authors reveal that STAT3 is locally translated and activated in injured axons, and then transported retrogradely to the nucleus to promote survival of peripheral sensory neurons.

Axons
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MHCII-independent CD4+ T cells protect injured CNS neurons via IL-4

2015

A body of experimental evidence suggests that T cells mediate neuroprotection following CNS injury; however, the antigen specificity of these T cells and how they mediate neuroprotection are unknown. Here, we have provided evidence that T cell-mediated neuroprotection after CNS injury can occur independently of major histocompatibility class II (MHCII) signaling to T cell receptors (TCRs). Using two murine models of CNS injury, we determined that damage-associated molecular mediators that originate from injured CNS tissue induce a population of neuroprotective, IL-4-producing T cells in an antigen-independent fashion. Compared with wild-type mice, IL-4-deficient animals had decreased functi…

CD4-Positive T-LymphocytesCancer ResearchMAP Kinase Signaling SystemPopulationReceptors Antigen T-CellInflammationBiologyNeuroprotectionMiceAntigenClinical investigationAnimalsMedicineExtracellular Signal-Regulated MAP KinaseseducationReceptorInterleukin 4Mice Knockouteducation.field_of_studybusiness.industryT-cell receptorHistocompatibility Antigens Class IINeurodegenerative DiseasesGeneral MedicineAxonsCell biologyBrain InjuriesMyeloid Differentiation Factor 88Immunologybiology.proteinInterleukin-4medicine.symptomFunction and Dysfunction of the Nervous SystemCorrigendumbusinessProto-Oncogene Proteins c-aktResearch ArticleNeurotrophinJournal of Clinical Investigation
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VIP-containing deep short-axon cells of the olfactory bulb innervate interneurons different from granule cells

2003

This study investigates the targets of the population of vasoactive intestinal polypeptide (VIP)-containing deep short-axon cells of the rat olfactory bulb (OB), combining single- and double-immunocytochemical approaches under light and electron microscopy. It has been assumed that deep short-axon cells innervate granule cells in the mammalian OB, but their synaptic connectivity has not been demonstrated to date. Our results indicate that, instead of the accepted scheme of the bulbar circuitry, VIP-containing deep short-axon cells are gamma-aminobutyric acid (GABA)ergic interneurons specialized in the selective innervation of other GABAergic deep short-axon cells. Their axons contact with t…

CalbindinsVasoactive intestinal peptidePopulationOlfactionBiologyCalbindinS100 Calcium Binding Protein GmedicineAnimalsNeuropeptide YRats WistarAxoneducationgamma-Aminobutyric AcidNeuronseducation.field_of_studyGeneral NeuroscienceNeuropeptide Y receptorImmunohistochemistryOlfactory BulbAxonsRatsOlfactory bulbMicroscopy ElectronParvalbuminsmedicine.anatomical_structurenervous systemCalbindin 2GABAergicFemaleNeuroscienceVasoactive Intestinal PeptideEuropean Journal of Neuroscience
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Mesenchymal stromal-cell transplants induce oligodendrocyte progenitor migration and remyelination in a chronic demyelination model.

2013

Demyelinating disorders such as leukodystrophies and multiple sclerosis are neurodegenerative diseases characterized by the progressive loss of myelin that may lead toward a chronic demyelination of the brain’s white matter, impairing normal axonal conduction velocity and ultimately causing neurodegeneration. Current treatments modifying the pathological mechanisms are capable of ameliorating the disease; however, frequently, these therapies are not sufficient to repress the progressive demyelination into a chronic condition and permanent loss of function. To this end, we analyzed the effect that bone marrow-derived mesenchymal stromal cell (BM-MSC) grafts exert in a chronically demyelinate…

Cancer ResearchPathologymedicine.medical_specialtyNeurogenesisImmunologyNeural ConductionBiologyMesenchymal Stem Cell TransplantationModels Biologicaltrophic releaseCuprizoneMiceCellular and Molecular NeuroscienceMyelinNerve FibersCell MovementmedicineSubependymal zoneAnimalsNerve Growth FactorsStem Cell NicheProgenitor cellRemyelinationMyelin Sheathdemyelinating mouse modelMultiple sclerosisMesenchymal stem cellCell DifferentiationMesenchymal Stem CellsCell Biologymedicine.diseaseAxonsOligodendrocyteTransplantationDisease Models AnimalOligodendrogliaremyelinationmedicine.anatomical_structureChronic DiseaseDentate GyrusImmunologyoligodendrocyte activationOriginal Articlemesenchymal stromal cellsGenèticaDemyelinating Diseases
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Ion conductance changes associated with spike adaptation in the rapidly adapting stretch receptor of the crayfish.

1975

The time course of the repetitive impulse discharges has been investigated for two high intensities of maintained depolarizing currents, 30 nA and 50 nA, for which the receptor adaptation was complete within 70 msec. The changes in sodium and potassium conductance associated with the decline in spike activity have been analyzed at different instances of time by interrupting in successive experiments the various action potentials in the pulse trains either at the early phase by holding the potential at about -60 mV and recording the inward current (upstroke-gNa) or by evaluating the delayed outward current flowing as the result of a depolarizing voltage pulse which at the end of the action p…

Cell Membrane PermeabilityTime FactorsPhysiologySodiumClinical BiochemistryNeural Conductionchemistry.chemical_elementAction PotentialsBiological Transport ActiveAstacoideaStimulus (physiology)IonPhysiology (medical)AnimalsMembrane potentialSodiumConductanceDepolarizationCrayfishAdaptation PhysiologicalAxonsElectric StimulationchemistryBiophysicsPotassiumMechanoreceptorsStretch receptorPflugers Archiv : European journal of physiology
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Oligodendroglial p130Cas Is a Target of Fyn Kinase Involved in Process Formation, Cell Migration and Survival

2014

Oligodendrocytes are the myelinating glial cells of the central nervous system. In the course of brain development, oligodendrocyte precursor cells migrate, scan the environment and differentiate into mature oligodendrocytes with multiple cellular processes which recognize and ensheath neuronal axons. During differentiation, oligodendrocytes undergo dramatic morphological changes requiring cytoskeletal rearrangements which need to be tightly regulated. The non-receptor tyrosine kinase Fyn plays a central role in oligodendrocyte differentiation and myelination. In order to improve our understanding of the role of oligodendroglial Fyn kinase, we have identified Fyn targets in these cells. Pur…

Cell Survival610 Medizinlcsh:MedicineProto-Oncogene Proteins c-fynSignaling PathwaysMiceCell Movement610 Medical sciencesMolecular Cell BiologyAnimalsPhosphorylationlcsh:ScienceBiologyCells CulturedNeuronslcsh:RCell DifferentiationMolecular DevelopmentSignalingAxonsOligodendrogliaCrk-Associated Substrate ProteinCellular Neurosciencelcsh:QCellular TypesMolecular NeuroscienceResearch ArticleDevelopmental BiologyNeurosciencePLoS ONE
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