Search results for "nerve"

showing 10 items of 1683 documents

SETD7 mediates spinal microgliosis and neuropathic pain in a rat model of peripheral nerve injury

2019

Abstract Gene transcription regulation is critical for the development of spinal microgliosis and neuropathic pain after peripheral nerve injury. Using a model of chronic constriction injury (CCI) of the sciatic nerve, this study characterized the role of SET domain containing lysine methyltransferase 7 (SETD7) which monomethylates histone H3 lysine 4 (H3K4me1), a marker for active gene transcription. SETD7 protein expression in the spinal dorsal horn ipsilateral to nerve lesion was increased from one day to 14 days after CCI, concomitantly with the expression of inflammatory genes, Ccl2, Il-6 and Il-1β. The CCI-induced SETD7 expression was predominantly localized to microglia, as demonstra…

Male0301 basic medicineSpinal Cord Dorsal HornPathologymedicine.medical_specialtyImmunologyCCL2MicrogliosisRats Sprague-Dawley03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinePeripheral Nerve InjuriesGanglia SpinalmedicineAnimalsGene knockdownMicrogliaEndocrine and Autonomic Systemsbusiness.industryHistone-Lysine N-MethyltransferaseNerve injurySciatic NerveSpineRats030104 developmental biologymedicine.anatomical_structureSpinal CordHyperalgesiaNeuropathic painPeripheral nerve injuryNeuralgiaFemaleMicrogliaSciatic nervemedicine.symptombusiness030217 neurology & neurosurgeryBrain, Behavior, and Immunity
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Detachment of Chain-Forming Neuroblasts by Fyn-Mediated Control of cell–cell Adhesion in the Postnatal Brain

2018

In the rodent olfactory system, neuroblasts produced in the ventricular-subventricular zone of the postnatal brain migrate tangentially in chain-like cell aggregates toward the olfactory bulb (OB) through the rostral migratory stream (RMS). After reaching the OB, the chains are dissociated and the neuroblasts migrate individually and radially toward their final destination. The cellular and molecular mechanisms controlling cell–cell adhesion during this detachment remain unclear. Here we report that Fyn, a nonreceptor tyrosine kinase, regulates the detachment of neuroblasts from chains in the male and female mouse OB. By performing chemical screening andin vivoloss-of-function and gain-of-f…

Male0301 basic medicineanimal structuresRostral migratory streamNerve Tissue ProteinsProto-Oncogene Proteins c-fynAdherens junctionMice03 medical and health sciencesFYNNeural Stem CellsNeuroblastCell MovementCell AdhesionmedicineAnimalsCell adhesionResearch ArticlesChemistryGeneral NeurosciencefungiBrainCateninsCadherinsDAB1Granule cellOlfactory BulbOlfactory bulbCell biology030104 developmental biologymedicine.anatomical_structurenervous systemGene Knockdown Techniquesembryonic structuresFemaleThe Journal of Neuroscience
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Dark exposure affects plasticity-related molecules and interneurons throughout the visual system during adulthood

2020

Several experimental manipulations, including visual deprivation, are able to induce critical period-like plasticity in the visual cortex of adult animals. In this regard, many studies have analyzed the effects of dark exposure in adult animals, but still little is known about the role of interneurons and plasticity-related molecules on such mechanisms. In this study, we analyzed the effects of 10 days of dark exposure on the connectivity and structure of interneurons, both in the primary visual cortex and in the rest of cerebral regions implicated in the transmission of visual stimulus. We found that this environmental manipulation induces changes in the expression of synaptic molecules th…

Male0301 basic medicinegenetic structuresinterneurons ()Mice TransgenicNeural Cell Adhesion Molecule L1Stimulus (physiology)PlasticityInhibitory postsynaptic potentialsensory deprivation ()Mice03 medical and health sciences0302 clinical medicineInterneuronsextracellular matrix ()medicineAnimalsVisual Cortexvisual pathways ()Neuronal PlasticitybiologyGeneral NeurosciencePerineuronal netAge FactorsDarknessPSA-NCAM ()030104 developmental biologyVisual cortexmedicine.anatomical_structureSialic Acidsbiology.proteinNeural cell adhesion moleculeneuronal plasticity ()Nerve NetSensory DeprivationNeuroscience030217 neurology & neurosurgeryParvalbumin
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A de novo microdeletion of SEMA5A in a boy with autism spectrum disorder and intellectual disability.

2016

AbstractSemaphorins are a large family of secreted and membrane-associated proteins necessary for wiring of the brain. Semaphorin 5A (SEMA5A) acts as a bifunctional guidance cue, exerting both attractive and inhibitory effects on developing axons. Previous studies have suggested that SEMA5A could be a susceptibility gene for autism spectrum disorders (ASDs). We first identified a de novo translocation t(5;22)(p15.3;q11.21) in a patient with ASD and intellectual disability (ID). At the translocation breakpoint on chromosome 5, we observed a 861-kb deletion encompassing the end of the SEMA5A gene. We delineated the breakpoint by NGS and observed that no gene was disrupted on chromosome 22. We…

Male0301 basic medicinemedicine.medical_specialtyAutism Spectrum DisorderChromosomes Human Pair 22Translocation BreakpointNerve Tissue ProteinsSemaphorinsBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBioinformaticsArticleTranslocation GeneticautismeChromosome Breakpoints03 medical and health sciencesSemaphorin[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual Disabilitymental disordersIntellectual disabilityGeneticsmedicineHumans[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsChildGenetics (clinical)Genetics[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyNeurosciencesMembrane Proteinsmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderNeurons and CognitionPaternal InheritancecerveauChromosomes Human Pair 5AutismMedical geneticsChromosome DeletionmicrodélétionhumainChromosome 22[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenetic screen
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Electrocortical networks in Parkinson's disease patients with Mild Cognitive Impairment. The PaCoS study

2019

Abstract Introduction Parkinson's Disease (PD) is frequently associated with cognitive dysfunction ranging from Mild Cognitive Impairment (PD-MCI) to dementia. Few electrophysiological studies are available evaluating potential pathogenetic mechanisms linked to cognitive impairment in PD since its initial phases. The objective of the study is to analyze electrocortical networks related with cognitive decline in PD-MCI for identifying possible early electrophysiological markers of cognitive impairment in PD. Methods From the PaCoS (Parkinson's disease Cognitive impairment Study) cohort, a sample of 102 subjects including 46 PD-MCI and 56 PD with normal cognition (PD-NC) was selected based on…

Male0301 basic medicinemedicine.medical_specialtyParkinson's diseaseQuantitative EEGElectroencephalographyAudiology03 medical and health sciences0302 clinical medicinemental disordersmedicineHumansDementiaCognitive DysfunctionNeuropsychological assessmentCognitive declineTomographyAgedElectrocortical networkElectrocortical networksmedicine.diagnostic_testbusiness.industryParietal lobeMild cognitive impairmentElectroencephalographyParkinson DiseaseCognitionMiddle Agedmedicine.disease030104 developmental biologyNeurologyFrontal lobeDisease ProgressionFemaleNeurology (clinical)Nerve NetElectrocortical networks; Mild cognitive impairment; Parkinson's disease; Quantitative EEG; Neurology; Geriatrics and Gerontology; Neurology (clinical)Geriatrics and GerontologyOccipital lobebusiness030217 neurology & neurosurgeryParkinsonism & Related Disorders
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Pancreatic polypeptide stimulates mouse gastric motor activity through peripheral neural mechanisms

2016

Background Pancreatic polypeptide (PP) is supposed to be one of the major endogenous agonists of the neuropeptide Y4 receptor. Pancreatic polypeptide can influence gastrointestinal motility, acting mainly through vagal mechanisms, but whether PP acts directly on the stomach has not been explored yet. The aims of this study were to investigate the effects of PP on mouse gastric emptying, on spontaneous tone of whole stomach in vitro and to examine the mechanism of action. Methods Gastric emptying was measured by red phenol method after i.p. PP administration (1–3 nmol per mouse). Responses induced by PP (1–300 mmol L−1) on gastric endoluminal pressure were analyzed in vitro in the presence o…

Male0301 basic medicinemedicine.medical_specialtyPhysiologyGastric emptyingMuscarinic AntagonistsBiologyEndocrine and Autonomic SystemMice03 medical and health sciencesOrgan Culture Techniques0302 clinical medicineInternal medicineMuscarinic acetylcholine receptormedicineAnimalsPancreatic polypeptidePeripheral NervesPancreatic polypeptideReceptorAntrumDose-Response Relationship DrugGastric emptyingEndocrine and Autonomic SystemsStomachGastroenterologyMotilityAcetylcholineReceptors Neuropeptide YMice Inbred C57BL030104 developmental biologyEndocrinologymedicine.anatomical_structureMechanism of actionTachykininmedicine.symptomEnteric nervous systemGastrointestinal Motility030217 neurology & neurosurgeryAcetylcholinemedicine.drug
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Faim2 contributes to neuroprotection by erythropoietin in transient brain ischemia.

2018

Delayed cell death in the penumbra region of acute ischemic stroke occurs through apoptotic mechanisms, making it amenable to therapeutic interventions. Fas/CD95 mediates apoptotic cell death in response to external stimuli. In mature neurons, Fas/CD95 signaling is modulated by Fas-apoptotic inhibitory molecule 2 (Faim2), which reduces cell death in animal models of stroke, meningitis, and Parkinson disease. Erythropoietin (EPO) has been studied as a therapeutic strategy in ischemic stroke. Erythropoietin stimulates the phosphatidylinositol-3 kinase/Akt (PI3K/Akt) pathway, which regulates Faim2 expression. Therefore, up-regulation of Faim2 may contribute to neuroprotection by EPO. Male Faim…

Male0301 basic medicinemetabolism [Apoptosis Regulatory Proteins]FAIM2 protein humanlifeguard protein mouseIschemiaNerve Tissue Proteinspathology [Ischemic Attack Transient]physiology [Neuroprotection]PharmacologyBiochemistryNeuroprotectionmetabolism [Erythropoietin]metabolism [Ischemic Attack Transient]Brain ischemiaMice03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineAnimalsHumansddc:610ErythropoietinStrokeProtein kinase BPI3K/AKT/mTOR pathwayAgedpharmacology [Erythropoietin]Mice Knockoutmetabolism [Nerve Tissue Proteins]business.industryPenumbraMembrane ProteinsMiddle Agedmedicine.diseaseNeuroprotection030104 developmental biologyIschemic Attack TransientErythropoietinphysiopathology [Ischemic Attack Transient]FemaleDose-dependency ; Erythropoietin ; Fas-apoptotic Inhibitory Molecule 2 ; Ischemia-reperfusion ; Neuroprotection ; StrokeApoptosis Regulatory Proteinsbusinessmetabolism [Membrane Proteins]030217 neurology & neurosurgerymedicine.drug
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A Natural Dietary Supplement with a Combination of Nutrients Prevents Neurodegeneration Induced by a High Fat Diet in Mice

2018

Obesity and metabolic disorders can be risk factors for the onset and development of neurodegenerative diseases. The aim of the present study was to investigate the protective effects of a natural dietary supplement (NDS), containing Curcuma longa, silymarin, guggul, chlorogenic acid and inulin, on dysmetabolism and neurodegeneration in the brains of high fat diet (HFD)-fed mice. Decrease in the expression of FACL-4, CerS-1, CerS-4, cholesterol concentration and increase in the insulin receptor expression and insulin signaling activation, were found in brains of NDS-treated HFD brains in comparison with HFD untreated-mice, suggesting that NDS is able to prevent brain lipid accumulation and …

Male0301 basic medicineobesityAntioxidantmedicine.medical_treatmentAnti-Inflammatory AgentsApoptosismedicine.disease_causeSettore BIO/09 - FisiologiaAntioxidantsLipid peroxidationchemistry.chemical_compound0302 clinical medicineinsulin resistanceInsulinnatural antioxidantsNutrition and DieteticsbiologyChemistryneurodegenerationobesity; HFD mice; natural antioxidants; insulin resistance; neurodegenerationBrainfood and beveragesNeurodegenerative Diseaseslipids (amino acids peptides and proteins)Inflammation Mediatorsmedicine.symptomlcsh:Nutrition. Foods and food supplySignal Transductionmedicine.medical_specialtylcsh:TX341-641endocrinology_metabolomicsInflammationDiet High-FatNeuroprotectionArticle03 medical and health sciencesInsulin resistanceInternal medicinemedicineAnimalsHFD miceCholesterolInsulinLipid Metabolismmedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative StressInsulin receptor030104 developmental biologyEndocrinologyDietary SupplementsNerve Degenerationbiology.proteinLipid Peroxidationnatural antioxidant030217 neurology & neurosurgeryOxidative stressFood ScienceNutrients
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Backfiring of the isolated rat phrenic nerve does not collide with impulse propagation following repetitive nerve stimulation at 1-50 Hz.

1991

Acetylcholinesterase inhibition with neostigmine in the isolated rat phrenic nerve-hemidiaphragm preparation induced axonal backfiring and repetitive compound muscle action potentials following single nerve stimulation. The duration of backfiring and the repetitive compound muscle action potentials did not exceed 55 ms. With repetitive nerve stimulation at frequencies ranging from 1 to 50 Hz, backfiring was present only with the first stimulus and the amplitude of the second compound muscle action potential was maximally reduced, while the subsequent responses recovered gradually. However, the amplitudes of the concommitant antidromic nerve action potentials remained unchanged during the en…

MaleAction potentialPhysiologyChemistryRefractory periodClinical BiochemistryAction PotentialsRats Inbred StrainsNeuromuscular junctionElectric StimulationCompound muscle action potentialAntidromicRatsPhrenic NerveElectrophysiologymedicine.anatomical_structurePhysiology (medical)medicineAnimalsRepetitive nerve stimulationNeurosciencePhrenic nervePflugers Archiv : European journal of physiology
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Analysis of N-terminal-pro-brain natriuretic peptide and C-reactive protein for risk stratification in stable and unstable coronary artery disease: r…

2004

Aims N-terminal-pro-brain natriuretic peptide (Nt-proBNP) is a reliable risk predictor in acute coronary artery disease (CAD). Little is known about patients with stable angina pectoris (SAP). We aimed to investigate the prognostic impact of Nt-proBNP in a population with CAD especially focussing on patients with SAP. Methods and results We obtained baseline samples from a prospective cohort of 904 consecutive patients with CAD. Cardiovascular events were registered during followup (median 2 years; maximum 3.7 years). Baseline Nt-proBNP was significantly higher among individuals with cardiovascular events compared with those without (711.5 vs. 238.8 pg/mL; P , 0.0001). A similar association…

MaleAcute coronary syndromemedicine.medical_specialtymedicine.drug_classPopulationNerve Tissue ProteinsCoronary Artery DiseaseRisk AssessmentAngina PectorisCohort StudiesCoronary artery diseasePredictive Value of TestsRisk FactorsInternal medicineNatriuretic Peptide BrainmedicineNatriuretic peptideHumansProspective Studiescardiovascular diseasesRisk factoreducationeducation.field_of_studybiologybusiness.industryC-reactive proteinMiddle AgedPrognosismedicine.diseaseBrain natriuretic peptideSurvival AnalysisPeptide FragmentsC-Reactive ProteinEndocrinologyQuartilebiology.proteinCardiologyFemaleCardiology and Cardiovascular MedicinebusinessEuropean Heart Journal
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