Search results for "Neuronal"

showing 10 items of 556 documents

Nitric oxide synthase in identified olivocochlear projection neurons in rat and guinea pig.

1999

Nitric oxide (NO) is thought to be involved in the effects of amino acids at the level of cochlear hair cell afferents. Recently, the isoform of the NO-producing enzyme, neuronal NO synthase (nNOS), has been demonstrated in neuronal structures of the cochlea in rats and guinea pigs histochemically and immunohistochemically. To investigate the sources of cochlear NO, we injected Fluoro-Gold (FG) into the cochlea of rats and guinea pigs. Upon terminal uptake of the tracer and neuronal transport we observed FG in terminals at the base of inner (IHC) and outer hair cells (OHC) and in neurons of the spiral ganglion. Ganglion cells and terminals at the IHC were clearly nNOS-positive, while termin…

MaleAuditory PathwaysStilbamidinesGuinea PigsNitric Oxide Synthase Type IBiologyOlivary NucleusGuinea pigRats Sprague-Dawleyotorhinolaryngologic diseasesmedicineTrapezoid bodyAnimalsInner earCochleaNeuronal transportSpiral ganglionFluorescent DyesNeuronsImmunohistochemistrySensory SystemsCell biologyCochleaRatsmedicine.anatomical_structurenervous systemSuperior olivary complexsense organsNitric Oxide SynthaseNeuroscienceNucleusHearing research
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''Comparative Effect of Treadmill Exercise on Mature BDNF Production in Control versus Stroke Rats''

2012

Quirie, Aurore | Hervieu, Marie | Garnier, Philippe | Demougeot, Celine | Mossiat, Claude | Bertrand, Nathalie | Martin, Alain | Marie, Christine | Prigent-Tessier, Anne; International audience; ''Physical exercise constitutes an innovative strategy to treat deficits associated with stroke through the promotion of BDNF-dependent neuroplasticity. However, there is no consensus on the optimal intensity/duration of exercise. In addition, whether previous stroke changes the effect of exercise on the brain is not known. Therefore, the present study compared the effects of a clinically-relevant form of exercise on cerebral BDNF levels and localization in control versus stroke rats. For this purpo…

MaleBEHAVIORAL RECOVERYTropomyosin receptor kinase BBiochemistryHippocampus0302 clinical medicineNerve Growth FactorHippocampus (mythology)StrokeCerebral Cortex0303 health sciencesNeuronal PlasticityMultidisciplinaryMOTOR RECOVERYQRTRKBNeurochemistryStrokemedicine.anatomical_structureNeurologyOrgan SpecificityCerebral cortex[ SCCO.NEUR ] Cognitive science/NeuroscienceMedicineNeurochemicalsmedicine.symptomResearch ArticleEXPRESSIONmedicine.medical_specialtyHIPPOCAMPAL PLASTICITYCORTEXCerebrovascular DiseasesAnimal TypesScienceBlotting WesternSynaptophysinEnzyme-Linked Immunosorbent AssayPhysical exerciseCONTROLLED-TRIALLesion03 medical and health sciencesPhysical Conditioning AnimalInternal medicineNeuroplasticitymedicineAnimalsLaboratory AnimalsSports and Exercise MedicineProtein PrecursorsRats WistarBiologyIschemic Stroke030304 developmental biologyBrain-derived neurotrophic factorbusiness.industry[SCCO.NEUR]Cognitive science/NeuroscienceBrain-Derived Neurotrophic FactorTRKB''AXONAL-TRANSPORTmedicine.diseaseCorpus StriatumRatsDisease Models AnimalEndocrinology''FOCAL BRAIN ISCHEMIAnervous systemFOCAL BRAIN ISCHEMIAExercise TestPhysical therapyBlood VesselsVeterinary ScienceEndothelium Vascularbusiness030217 neurology & neurosurgerySynaptic PlasticityNeuroscienceNEUROTROPHIC FACTOR
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Olfacto-retinalis pathway in Austrolebias charrua fishes: A neuronal tracer study

2013

Abstract The olfacto-retinal centrifugal system, a constant component of the central nervous system that appears to exist in all vertebrate groups, is part of the terminal nerve (TN) complex. TN allows the integration of different sensory modalities, and its anatomic variability may have functional and evolutionary significance. We propose that the olfacto-retinal branch of TN is an important anatomical link that allows the functional interaction between olfactory and visual systems in Austrolebias . By injecting three different neuronal tracers (biocytin, horseradish peroxidase, and 1,1′-dioctadecyl-3,3,3′,3′tetramethyl-indocarbocyanine perchlorate (DiI)) in the left eye of Austrolebias ch…

MaleBiologyRetinachemistry.chemical_compoundBiocytinNeural PathwaysmedicineAnimalsAmino AcidsPretectal areaHorseradish PeroxidaseNeuronsCerebrumLysineGeneral NeuroscienceFishesAnatomybiology.organism_classificationOlfactory BulbOlfactory bulbNeuronal tracingmedicine.anatomical_structurenervous systemchemistryTerminal nerveNucleusAustrolebiasNeuroscience
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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
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Functional Inactivation of the Genome-Wide Association Study Obesity Gene Neuronal Growth Regulator 1 in Mice Causes a Body Mass Phenotype

2012

To date, genome-wide association studies (GWAS) have identified at least 32 novel loci for obesity and body mass-related traits. However, the causal genetic variant and molecular mechanisms of specific susceptibility genes in relation to obesity are yet to be fully confirmed and characterised. Here, we examined whether the candidate gene NEGR1 encoding the neuronal growth regulator 1, also termed neurotractin or Kilon, accounts for the obesity association. To characterise the function of NEGR1 for body weight control in vivo, we generated two novel mutant mouse lines, including a constitutive NEGR1-deficient mouse line as well as an ENU-mutagenised line carrying a loss-of-function mutation …

MaleCandidate geneMutantlcsh:MedicineGenome-wide association studymedicine.disease_causeEndoplasmic ReticulumEatingGene Knockout TechniquesMice0302 clinical medicineEndocrinologylcsh:ScienceObesity; NEGR1; GWAS; body weight control2. Zero hungerGenetics0303 health sciencesMutationMultidisciplinaryNeuronal growth regulator 1GenomicsPhenotypePhenotypeMedicineFemaleFunction and Dysfunction of the Nervous SystemResearch ArticleGenotypeHypothalamusNerve Tissue ProteinsBiologyMotor ActivityDiet High-FatCell Line03 medical and health sciencesGenetic MutationGenome Analysis ToolsmedicineGeneticsGenome-Wide Association StudiesCell AdhesionNeuritesAnimalsHumansObesityGene SilencingGeneBiologyAlleles030304 developmental biologyNutritionlcsh:RBody WeightMembrane ProteinsHuman GeneticsNeuroendocrinologyBody HeightMetabolic DisordersGenetics of DiseaseLean body masslcsh:QEnergy Metabolism030217 neurology & neurosurgeryGenome-Wide Association StudyPLoS ONE
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Protective activation of the endocannabinoid system during ischemia in dopamine neurons

2006

Endocannabinoids act as neuroprotective molecules promptly released in response to pathological stimuli. Hence, they may represent one component of protection and/or repair mechanisms mobilized by dopamine (DA) neurons under ischemia. Here, we show that the endocannabinoid 2-arachidonoyl-glycerol (2-AG) plays a key role in protecting DA neurons from ischemia-induced altered spontaneous activity both in vitro and in vivo. Accordingly, neuroprotection can be elicited through moderate cannabinoid receptor type-1 (CB1) activation. Conversely, blockade of endocannabinoid actions through CB1 receptor antagonism worsens the outcome of transient ischemia on DA neuronal activity. These findings indi…

MaleCannabinoid receptorDopaminePharmacologyBrain IschemiaMidbrainRats Sprague-DawleyMicePiperidinesReceptor Cannabinoid CB1IschemiaPremovement neuronal activityReceptorMice KnockoutNeuronsmusculoskeletal neural and ocular physiologyEndocannabinoid systemCB1NeuroprotectionElectrophysiologyNeurologylipids (amino acids peptides and proteins)Rimonabantpsychological phenomena and processesmedicine.drugSignal TransductionMorpholinesIschemiaArachidonic AcidsBiologyIn Vitro TechniquesNaphthalenesNeuroprotectionAmidohydrolasesGlycerideslcsh:RC321-571DopamineCannabinoid Receptor ModulatorsmedicineAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryEndocannabinoidVentral Tegmental Areamedicine.diseaseBlockadeBenzoxazinesRatsnervous systemPyrazolesNeuroscienceEndocannabinoidsNeurobiology of Disease
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Aberrant arrested in maturation neuromuscular junctions in centronuclear myopathy

1994

Unusual ultrastructural changes of the nerve terminals have been found in an infant born with severe, fatal XLR form of centronuclear myopathy. Aberrant neuromuscular junctions in myotubes decorated by N-CAM were observed. The junction changes were manifested by simplification of postsynaptic membrane and paucity of secondary synaptic clefts. These resembles fetal neuromuscular junctions. The findings suggest that the expression of N-CAM by arrested myotubes may be promoted by abnormal nerve-muscle cell interactions, induced by motor endplate immaturity.

MaleCell Adhesion Molecules NeuronalCellNeuromuscular JunctionElectromyographyBiologyMicrotubulesMotor EndplateNeuromuscular junctionMotor EndplateMicrotubulemedicineHumansCentronuclear myopathyMotor NeuronsFetusTissue Embeddingmedicine.diagnostic_testElectromyographyMyogenesisMusclesInfantNeuromuscular Diseasesmedicine.diseaseCell biologyMicroscopy Electronmedicine.anatomical_structureNeurologySynapsesNeurology (clinical)NeuroscienceJournal of the Neurological Sciences
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Early life stress stimulates hippocampal reelin gene expression in a sex-specific manner: Evidence for corticosterone-mediated action

2010

Early life stress predisposes to the development of psychiatric disorders. In this context the hippocampal formation is of particular interest, because it is affected by stress on the structural and cognitive level. Since little is known how early life stress is translated on the molecular level, we mimicked early life stress in mouse models and analyzed the expression of the glycoprotein Reelin, a master molecule for development and differentiation of the hippocampus. From postnatal day 1 (P1) to P14, mouse pups were subjected to one of the following treatments: nonhandling (NH), handling (H), maternal separation (MS), and early deprivation (ED) followed by immediate (P15) or delayed (P70)…

MaleCell Adhesion Molecules NeuronalCognitive NeuroscienceGene ExpressionCell CountNerve Tissue ProteinsContext (language use)Hippocampal formationHippocampusMiceCajal–Retzius cellchemistry.chemical_compoundSex FactorsCorticosteronemedicineAnimalsRNA MessengerReelinBrain-derived neurotrophic factorExtracellular Matrix ProteinsMaternal deprivationbiologyMaternal DeprivationSerine EndopeptidasesDAB1Reelin Proteinmedicine.anatomical_structurenervous systemchemistrybiology.proteinFemaleCorticosteroneNeuroscienceStress PsychologicalHippocampus
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Glia talk back.

2014

This study shows that the activity of neurons can trigger shedding of a protein, NG2, from the surface of oligodendrocyte precursor cells; this protein in turn modulates synaptic transmission, revealing a two-way conversation between neurons and glia.

MaleCell signalingNeural NetworksQH301-705.5AMPA receptorBiologyNeurotransmissionResearch and Analysis MethodsMechanical Treatment of SpecimensGeneral Biochemistry Genetics and Molecular BiologyBehavioral NeuroscienceNeurotransmitter receptormedicineBiological neural networkPremovement neuronal activityAnimalsBiology (General)AntigensNeuronsGeneral Immunology and MicrobiologyGeneral NeuroscienceMembrane ProteinsBiology and Life SciencesLong-term potentiationADAM ProteinsOligodendrogliamedicine.anatomical_structureElectroporationnervous systemSpecimen DisruptionSpecimen Preparation and TreatmentCellular NeuroscienceImmunologyProteoglycansNeuronAmyloid Precursor Protein SecretasesMolecular NeuroscienceGeneral Agricultural and Biological SciencesNeuroscienceResearch ArticleNeurosciencePLoS biology
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Morphological studies on CLN2

2001

Electron microscopic, fluorescence microscopic, and immunohistochemical studies earlier performed on archivalcerebral tissue from Max Bielchowsky's original three patients revealed curvilinear bodies rich in subunit C of mitochondrial ATP synthase (SCMAS). Recent progress in the elucidation of CLN2, i.e. identification of the defective lysosomal enzyme tripeptidyl-peptidase I (TPP-I) and mutations in the CLN2 gene have further corroborated earlier data. Immunohistochemically the absence of the TPP-I protein could be confirmed in the archival tissues using pathological controls. Unlike biochemistry, immunohistochemistry enables examination of these archival tissues elucidating the causative …

MaleCell typePathologymedicine.medical_specialtyProtein subunitEncephalopathyBiologymedicine.disease_causeAminopeptidasesNeuronal Ceroid-LipofuscinosesChloroquineEndopeptidasesmedicineHumansChildDipeptidyl-Peptidases and Tripeptidyl-PeptidasesMyopathyGeneMutationTripeptidyl-Peptidase 1BrainGeneral MedicineMitochondrial Proton-Translocating ATPasesmedicine.diseaseImmunohistochemistryProton-Translocating ATPasesMutationPediatrics Perinatology and Child HealthImmunohistochemistryFemaleNeurology (clinical)Serine Proteasesmedicine.symptomPeptide Hydrolasesmedicine.drugEuropean Journal of Paediatric Neurology
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