Search results for "Axotomy"

showing 9 items of 9 documents

Response of abducens internuclear neurons to axotomy in the adult cat

2000

The highly specific projection of abducens internuclear neurons on the medial rectus motoneurons of the oculomotor nucleus constitutes an optimal model for investigating the effects of axotomy in the central nervous system. We have analyzed the morphological changes induced by this lesion on both the cell bodies and the transected axons of abducens internuclear neurons in the adult cat. Axotomy was performed by the transection of the medial longitudinal fascicle. Cell counts of Nissl-stained material and calretinin-immunostained abducens internuclear neurons revealed no cell death by 3 months postaxotomy. Ultrastructural examination of these cells at 6, 14, 24, and 90 days postaxotomy showe…

General Neurosciencemedicine.medical_treatmentAnatomyBiologyOculomotor nucleusLesionchemistry.chemical_compoundmedicine.anatomical_structurenervous systemchemistryGliosisBiocytinmedicineCalretininmedicine.symptomAxotomyAbducens nerveReinnervationThe Journal of Comparative Neurology
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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
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Wasp venom injected into the prey's brain modulates thoracic identified monoaminergic neurons.

2005

The wasp Ampulex compressa injects a cocktail of neurotoxins into the brain of its cockroach prey to induce an enduring change in the execution of locomotory behaviors. Our hypothesis is that the venom injected into the brain indirectly alters the activity of monoaminergic neurons, thus changing the levels of monoamines that tune the central synapses of locomotory circuits. The purpose of the present investigation was to establish whether the venom alters the descending control, from the brain, of octopaminergic neurons in the thorax. This question was approached by recording the activity of specific identified octopaminergic neurons after removing the input from the brain or after a wasp s…

Malemedicine.medical_treatmentWaspsVenomSensory systemWasp VenomsMotor ActivityMembrane PotentialsCellular and Molecular Neurosciencebiology.animalMonoaminergicmedicineAnimalsPeriplanetaOctopamineNeuronsCockroachbiologyGeneral NeuroscienceBrainInsect Bites and StingsAxotomyThoraxElectrophysiologyElectrophysiologyMonoamine neurotransmittermedicine.anatomical_structurenervous systemNeuronAxotomyNeuroscienceJournal of neurobiology
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Neurodegeneration in excitotoxicity, global cerebral ischemia, and target deprivation: A perspective on the contributions of apoptosis and necrosis.

1998

In the human brain and spinal cord, neurons degenerate after acute insults (e.g., stroke, cardiac arrest, trauma) and during progressive, adult-onset diseases [e.g., amyotrophic lateral sclerosis, Alzheimer's disease]. Glutamate receptor-mediated excitotoxicity has been implicated in all of these neurological conditions. Nevertheless, effective approaches to prevent or limit neuronal damage in these disorders remain elusive, primarily because of an incomplete understanding of the mechanisms of neuronal death in in vivo settings. Therefore, animal models of neurodegeneration are crucial for improving our understanding of the mechanisms of neuronal death. In this review, we evaluate experimen…

NeuronsProgrammed cell deathNecrosisCell DeathGeneral Neurosciencemedicine.medical_treatmentNeurodegenerationNeurotoxinsGlutamate receptorExcitotoxicityApoptosisAxotomyBiologymedicine.diseasemedicine.disease_causeNeuroprotectionBrain IschemiaBrain ischemiaNecrosisNerve DegenerationmedicineAnimalsmedicine.symptomAxotomyNeuroscienceBrain research bulletin
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Syntaxin13 expression is regulated by mammalian target of rapamycin (mTOR) in injured neurons to promote axon regeneration.

2014

Injured peripheral neurons successfully activate intrinsic signaling pathways to enable axon regeneration. We have previously shown that dorsal root ganglia (DRG) neurons activate the mammalian target of rapamycin (mTOR) pathway following injury and that this activity enhances their axon growth capacity. mTOR plays a critical role in protein synthesis, but the mTOR-dependent proteins enhancing the regenerative capacity of DRG neurons remain unknown. To identify proteins whose expression is regulated by injury in an mTOR-dependent manner, we analyzed the protein composition of DRGs from mice in which we genetically activated mTOR and from mice with or without a prior nerve injury. Quantitati…

ProteomicsAxon; Proteomics; Regeneration; SNARE Proteins; mTORSNARE Proteinmedicine.medical_treatmentInbred C57BLRegenerative MedicineBiochemistryMedical and Health SciencesMiceNeurobiologyGanglia SpinalAxonCells CulturedMice KnockoutGene knockdownCulturedQa-SNARE ProteinsTOR Serine-Threonine KinasesAxotomyBiological SciencesSciatic NerveCell biologymedicine.anatomical_structureNeurologicalmTORFemaleAxotomySignal transductionmedicine.symptomSNARE ProteinsBiochemistry & Molecular BiologyPhysical Injury - Accidents and Adverse EffectsSpinalSensory Receptor CellsCellsKnockout1.1 Normal biological development and functioningBiologyAxonUnderpinning researchmedicineAnimalsRegenerationMolecular BiologyPI3K/AKT/mTOR pathwayRegeneration (biology)NeurosciencesProteomicCell BiologyNerve injuryAxonsNerve RegenerationMice Inbred C57BLnervous systemChemical SciencesAxoplasmic transportGanglia
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Metabolomic changes in the rat retina after optic nerve crush.

2013

Purpose To identify metabolic pathways and metabolites affected by optic nerve crush that can act as predictors of the disease or therapeutic targets. Methods The left optic nerve of adult rats was intraorbitally crushed and retinas were dissected 24 hours or 14 days after the lesion (n = 10 per group). Metabolic profiling analysis was carried out by Metabolon, Inc. A total of 195 metabolites were unambiguously detected. Data were normalized and the regulated metabolites were identified after comparing the different conditions. Metabolite concentration changes were analyzed using single and multivariate statistical analysis to detect discriminatory metabolites. Functional clustering and met…

Retinal Ganglion CellsNerve CrushMetaboliteProtein Array AnalysisApoptosisPharmacologymedicine.disease_causeGas Chromatography-Mass SpectrometryRetinaLesionRats Sprague-Dawleychemistry.chemical_compoundMetabolomicsTandem Mass SpectrometrymedicineAnimalsMetabolomicsAmino AcidsChemistryLipid metabolismAxotomyOptic NerveLipid MetabolismAxonsRatsMetabolic pathwayOxidative StressOptic nerveCarbohydrate MetabolismFemaleMetabolonmedicine.symptomOxidative stressChromatography LiquidSignal TransductionInvestigative ophthalmologyvisual science
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The role of mitochondrial transition pore, and its modulation, in traumatic brain injury and delayed neurodegeneration after TBI

2009

Following severe traumatic brain injury (TBI), a complex interplay of pathomechanism, such as exitotoxicity, oxidative stress, inflammatory events, and mitochondrial dysfunction occurs. This leads to a cascade of neuronal and axonal pathologies, which ultimately lead to axonal failure, neuronal energy metabolic failure, and neuronal death, which in turn determine patient outcome. For mild and moderate TBI, the pathomechanism is similar but much less frequent and ischemic cell death is unusual, except with mass lesions. Involvement of mitochondria in acute post-traumatic neurodegeneration has been extensively studied during the last decade, and there are a number of investigations implicatin…

Time FactorsTraumatic brain injurymedicine.medical_treatmentMitochondrionMitochondrial Membrane Transport ProteinsNeuroprotectionBrain Ischemiachemistry.chemical_compoundDevelopmental NeuroscienceCyclosporin aAnimalsHumansMedicineMitochondrial Permeability Transition Porebusiness.industryMPTPNeurodegenerationmedicine.diseasenervous system diseasesnervous systemNeurologyMitochondrial permeability transition porechemistryBrain InjuriesReperfusion InjuryAcute DiseaseChronic DiseaseNerve DegenerationAxotomybusinessNeuroscience
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The influence of nimodipine on chromatolysis of motoneurons following axotomy with and without reinnervation: A quantitative image analysis

1996

Using a recently developed image analysis method to quantify the time course of chromatolysis in injured motorneurons we tested the effect of the calcium entry blocker nimodipine (1000 ppm in food pellets) on regenerating and degenerating motoneurons. Following facial-facial, hypoglossal-hypoglossal anastomosis with complete regeneration and following facial and hypoglossal nerve resection which causes a partial neuronal degeneration and postoperative survival times of 4 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. Monitoring alterations of the Ni…

business.industryGeneral Neurosciencemedicine.medical_treatmentFacial nervesymbols.namesakemedicine.anatomical_structurenervous systemAnesthesiaChromatolysismedicineNissl bodysymbolsBrainstemAxotomybusinessNimodipineHypoglossal nervemedicine.drugReinnervationNeuroscience Research Communications
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Cortical gene expression in spinal cord injury and repair: insight into the functional complexity of the neural regeneration program

2011

Traumatic spinal cord injury (SCI) results in the formation of a fibrous scar acting as a growth barrier for regenerating axons at the lesion site. We have previously shown (Klapka et al., 2005) that transient suppression of the inhibitory lesion scar in rat spinal cord leads to long distance axon regeneration, retrograde rescue of axotomized cortical motoneurons, and improvement of locomotor function. Here we applied a systemic approach to investigate for the first time specific and dynamic alterations in the cortical gene expression profile following both thoracic SCI and regeneration-promoting anti-scarring treatment (AST). In order to monitor cortical gene expression we carried out micr…

corticospinal tractmedicine.medical_treatmentlesion scarlcsh:RC321-571Cellular and Molecular Neuroscienceanti-scarring treatmentmedicineAxonlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrysensorimotor cortexMolecular BiologySpinal cord injurySpinal Cord RegenerationOriginal Researchbusiness.industryRegeneration (biology)axonal regenerationmedicine.diseaseSpinal cordspinal cord injuryaxotomymedicine.anatomical_structureCorticospinal tractAxotomybusinessmicroarrayNeural developmentNeuroscienceNeuroscienceFrontiers in Molecular Neuroscience
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