Search results for "C3"

showing 10 items of 1295 documents

Octopamine Shifts the Behavioral Response From Indecision to Approach or Aversion in Drosophila melanogaster

2018

Animals must make constant decisions whether to respond to external sensory stimuli or not to respond. The activation of positive and/or negative reinforcers might bias the behavioral response towards approach or aversion. To analyze whether the activation of the octopaminergic neurotransmitter system can shift the decision between two identical odor sources, we active in Drosophila melanogaster different sets of octopaminergic neurons using optogenetics and analyze the choice of the flies using a binary odor trap assay. We show that the release of octopamine from a set of neurons and not acetylcholine acts as positive reinforcer for one food odor source resulting in attraction. The activat…

0301 basic medicineTβhCognitive NeuroscienceSensory systemOptogeneticsPositive Reinforcerdecision makinglcsh:RC321-57103 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compound0302 clinical medicineethanol attractionoctopaminefood odoraversionNeurotransmitterlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchbiologyOctopamine (drug)biology.organism_classificationAttraction030104 developmental biologyNeuropsychology and Physiological PsychologychemistryOdorDrosophila melanogasterNeuroscience030217 neurology & neurosurgeryNeuroscienceattractionFrontiers in Behavioral Neuroscience
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Surge of Peripheral Arginine Vasopressin in a Rat Model of Birth Asphyxia

2018

Mammalian birth is accompanied by a period of obligatory asphyxia, which consists of hypoxia (drop in blood O2 levels) and hypercapnia (elevation of blood CO2 levels). Prolonged, complicated birth can extend the asphyxic period, leading to a pathophysiological situation, and in humans, to the diagnosis of clinical birth asphyxia, the main cause of hypoxic-ischemic encephalopathy (HIE). The neuroendocrine component of birth asphyxia, in particular the increase in circulating levels of arginine vasopressin (AVP), has been extensively studied in humans. Here we show for the first time that normal rat birth is also accompanied by an AVP surge, and that the fetal AVP surge is further enhanced in…

0301 basic medicineVasopressinmedicine.medical_specialtySTRESSArgininehypothalamic-pituitary axis (HPA axis)blood gasesHYPOXIAbirth asphyxia3124 Neurology and psychiatrylcsh:RC321-571neonatal03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineCopeptinInternal medicineMedicineBRAINlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPRECURSORNEURONSperinatalOriginal ResearchRELEASEAsphyxiaFetusPARAVENTRICULAR NUCLEUSbusiness.industry3112 NeurosciencescopeptinENCEPHALOPATHYarginine vasopressin (AVP)Hypoxia (medical)base deficit030104 developmental biologyEndocrinologyHypothalamusHYPOTHALAMUSmedicine.symptombusinessHypercapnia030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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Brain Control of Plasma Cholesterol Involves Polysialic Acid Molecules in the Hypothalamus

2017

IF 3.566; International audience; The polysialic acid (PSA) is a large glycan that is added to cell-surface proteins during their post-translational maturation. In the brain, PSA modulates distances between cells and controls the plasticity of the nervous system. In the hypothalamus, PSA is involved in many aspects of energy balance including food intake, osmoregulation, circadian rhythm, and sleep. In this work, we investigated the role of hypothalamic PSA in the regulation of plasma cholesterol levels and distribution. We report that HFD consumption in mice rapidly increased plasma cholesterol, including VLDL, LDL, and HDL-cholesterol. Although plasma VLDL-cholesterol was normalized withi…

0301 basic medicineVery low-density lipoprotein[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologyurologic and male genital diseaseschemistry.chemical_compound0302 clinical medicinemaladie cardiovasculairehypothalamusOriginal Research[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism2. Zero hungerGeneral Neurosciencecholestérol[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismHypothalamus[ SDV.NEU.NB ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyAlimentation et NutritionOsmoregulationcerveaulipids (amino acids peptides and proteins)medicine.medical_specialtypolysialic acidHDLBiologylcsh:RC321-571LDL03 medical and health sciencespolysialic acid;hypothalamus;atherosclerosis;HDL;LDL;synaptic plasticityInternal medicinemedicineFood and NutritionCircadian rhythmlcsh:Neurosciences. Biological psychiatry. Neuropsychiatrysynaptic plasticityCholesterolPolysialic acidNeurosciencesathérosclérose[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiologynutritional and metabolic diseasesmedicine.disease030104 developmental biologyEndocrinologychemistryNeurons and Cognitionatherosclerosis030217 neurology & neurosurgeryDyslipidemiaHomeostasisNeuroscienceFrontiers in Neuroscience
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C3 Drives Inflammatory Skin Carcinogenesis Independently of C5

2021

Nonmelanoma skin cancer such as cutaneous squamous cell carcinoma (cSCC) is the most common form of cancer and can occur as a consequence of DNA damage to the epithelium by UVR or chemical carcinogens. There is growing evidence that the complement system is involved in cancer immune surveillance; however, its role in cSCC remains unclear. Here, we show that complement genes are expressed in tissue from patients with cSCC, and C3 activation fragments are present in cSCC biopsies, indicating complement activation. Using a range of complement-deficient mice in a two-stage mouse model of chemically-induced cSCC, where a subclinical dose of 7,12-dimethylbenz[a]anthracene causes oncogenic mutatio…

0301 basic medicineWT wild typeSkin NeoplasmsComplement receptorComplement Membrane Attack Complexmedicine.disease_causeBiochemistrychemistry.chemical_compoundMice0302 clinical medicineCR complement receptorComplement ActivationSkinMice KnockoutcSCC cutaneous squamous cell carcinomaComplement C5Complement C3Receptors Complement030220 oncology & carcinogenesisCarcinoma Squamous CellDisease ProgressionTumor BiologyOriginal ArticleMAC membrane attack complexSignal TransductionHPV16 human papillomavirus type 16910-Dimethyl-12-benzanthraceneTPA 12-O-tetradecanoylphorbol-13-acetateMice TransgenicDermatologySettore MED/08 - Anatomia Patologica03 medical and health sciencesmedicineAnimalsHumansC3Molecular BiologyReceptor Anaphylatoxin C5aDMBA 712-dimethylbenz[a]anthracenebusiness.industry712-Dimethylbenz[a]anthraceneCancerCell BiologyNeoplasms Experimentalmedicine.diseaseComplement systemDisease Models Animal030104 developmental biologychemistryTumor progressionCancer researchCarcinogensTumor EscapeSkin cancerbusinessCarcinogenesisComplement membrane attack complexSkin carcinogenesis.EC epithelial cell
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Hypothesis: Etiologic and Molecular Mechanistic Leads for Sporadic Neurodegenerative Diseases Based on Experience With Western Pacific ALS/PDC

2019

Seventy years of research on Western Pacific amyotrophic lateral sclerosis and Parkinsonism-dementia Complex (ALS/PDC) have provided invaluable data on the etiology, molecular pathogenesis and latency of this disappearing, largely environmental neurodegenerative disease. ALS/PDC is linked to genotoxic chemicals (notably methylazoxymethanol, MAM) derived from seed of the cycad plant (Cycas spp.) that were used as a traditional food and/or medicine in all three disease-affected Western Pacific populations. MAM, nitrosamines and hydrazines generate methyl free radicals that damage DNA (in the form of O6-methylguanine lesions) that can induce mutations in cycling cells and degenerative changes …

0301 basic medicineamyotrophic lateral sclerosisDNA damageDiseaseBiologylcsh:RC346-429Environmental - originProgressive supranuclear palsy03 medical and health sciences0302 clinical medicineHypothesis and TheorymedicinenitrosaminesAmyotrophic lateral sclerosislcsh:Neurology. Diseases of the nervous systemhydrazinesprogressive supranuclear palsymedicine.diseaseatypical parkinsonism030104 developmental biologyBrain degenerationNeurologyImmunologyEtiologycycad methylazoxymethanol and L-BMAADNA damageNeurology (clinical)Alzheimer's diseaseAlzheimer disease030217 neurology & neurosurgeryFrontiers in Neurology
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Hypocellularity in the murine model for Down Syndrome Ts65Dn is not affected by adult neurogenesis

2016

Down syndrome (DS) is caused by the presence of an extra copy of the chromosome 21 and it is the most common aneuploidy producing intellectual disability. Neural mechanisms underlying this alteration may include defects in the formation of neuronal networks, information processing and brain plasticity. The murine model for DS, Ts65Dn, presents reduced adult neurogenesis. This reduction has been suggested to underlie the hypocellularity of the hippocampus as well as the deficit in olfactory learning in the Ts65Dn mice. Similar alterations have also been observed in individuals with DS. To determine whether the impairment in adult neurogenesis is, in fact, responsible for the hypocellularity …

0301 basic medicineanimal diseasesHippocampusSubventricular zoneBiotecnologiaHippocampusSubgranular zonelcsh:RC321-57103 medical and health sciences0302 clinical medicinedoublecortinNeuroplasticitymental disordersmedicineBrdUlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchbiologyGeneral NeuroscienceNeurogenesisOlfactory BulbOlfactory bulbDoublecortinCell biologyadult neurogenesisTs65Dn mice030104 developmental biologymedicine.anatomical_structureHypocellularityPsicobiologianervous systembiology.proteinDown SyndromeKi67Neuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Neuroscience
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MicroRNAs Dysregulation and Metabolism in Multiple System Atrophy.

2019

Multiple system atrophy (MSA) is an adult onset, fatal disease, characterized by an accumulation of alpha-synuclein (α-syn) in oligodendroglial cells. MicroRNAs (miRNAs) are small non-coding RNAs involved in post-translational regulation and several biological processes. Disruption of miRNA-related pathways in the central nervous system (CNS) plays an important role in the pathogenesis of neurodegenerative diseases, including MSA. While the exact mechanisms underlying miRNAs in the pathogenesis of MSA remain unclear, it is known that miRNAs can repress the translation of messenger RNAs (mRNAs) that regulate the following pathogenesis associated with MSA: autophagy, neuroinflammation, α-syn …

0301 basic medicineautophagyalpha-synucleinCentral nervous systemmultiple system atrophyReviewBiologylcsh:RC321-571neuroinflammationPathogenesis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAtrophystomatognathic systemmicroRNAmental disordersmedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeuroinflammationAlpha-synucleinmicroRNAGeneral NeuroscienceAutophagyTranslation (biology)medicine.diseaseCell biologynervous system diseases030104 developmental biologymedicine.anatomical_structurechemistrynervous system030217 neurology & neurosurgeryNeuroscienceFrontiers in neuroscience
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Extrinsic and intrinsic mechanisms of axon regeneration: the need for spinal cord injury treatment strategies to address both

2016

Spinal cord injury (SCI) causes disturbances in motor and sensory functions leading to paralysis, the severity of which depends on the spinal level of the injury. Traumatic lesions of spinal cord axon projection tracts are untreatable in human patients, although numerous research groups worldwide are studying putative treatment strategies. Both extrinsic factors in the environment of the axons as well as intrinsic factors in the neurons themselves play important roles in the regeneration process (Chew et al., 2012). The peripheral nervous system (PNS) provides a good example where the extrinsic and intrinsic factors play optimally together to allow regeneration. Schwann cells dedifferentiat…

0301 basic medicinebusiness.industryRegeneration (biology)Central nervous systemInhibitory postsynaptic potentialmedicine.diseaseSpinal cordlcsh:RC346-42903 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structurenervous systemDevelopmental NeurosciencePeripheral nervous systemPerspectivemedicineAxonbusinessGrowth coneSpinal cord injuryNeurosciencelcsh:Neurology. Diseases of the nervous system030217 neurology & neurosurgeryNeural Regeneration Research
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Alexander Disease Mutations Produce Cells with Coexpression of Glial Fibrillary Acidic Protein and NG2 in Neurosphere Cultures and Inhibit Differenti…

2017

Background Alexander disease (AxD) is a rare disease caused by mutations in the gene encoding glial fibrillary acidic protein (GFAP). The disease is characterized by presence of GFAP aggregates in the cytoplasm of astrocytes and loss of myelin. Objectives Determine the effect of AxD-related mutations on adult neurogenesis. Methods We transfected different types of mutant GFAP into neurospheres using the nucleofection technique. Results We find that mutations may cause coexpression of GFAP and NG2 in neurosphere cultures, which would inhibit the differentiation of precursors into oligodendrocytes and thus explain the myelin loss occurring in the disease. Transfection produces cells that diff…

0301 basic medicinecaspase-3Cathepsin Dmacromolecular substancesHSP27lcsh:RC346-429oligodendrocyte precursors03 medical and health sciencesMyelin0302 clinical medicineAlexander diseaseNG2Neurosphereneurospheresmedicinecathepsinlcsh:Neurology. Diseases of the nervous systemOriginal ResearchGlial fibrillary acidic proteinbiologyNeurogenesisNestinGFAP stainmedicine.diseaseMolecular biologyAlexander disease030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyglial fibrillary acidic proteinbiology.proteinNeurology (clinical)030217 neurology & neurosurgeryNeuroscienceFrontiers in Neurology
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Disruption of otoferlin alters the mode of exocytosis at the mouse inner hair cell ribbon synapse

2019

Sound encoding relies on Ca2+-mediated exocytosis at the ribbon synapse between cochlear inner hair cells (IHCs) and type I spiral ganglion neurons (SGNs). Otoferlin, a multi-C-2 domain protein, is proposed to regulate Ca2+-triggered exocytosis at this synapse, but the precise mechanisms of otoferlin function remain to be elucidated. Here, performing whole-cell voltage-clamp recordings of excitatory postsynaptic currents (EPSCs) from SGNs in otoferlin mutant mice, we investigated the impact of Otof disruption at individual synapses with single release event resolution. Otof deletion decreased the spontaneous release rate and abolished the stimulus-secretion coupling. This was evident from f…

0301 basic medicinecochleaRibbon synapsehair cellExocytosislcsh:RC321-571Synapse03 medical and health sciencesCellular and Molecular Neuroscienceotoferlin0302 clinical medicinemedicineOTOFauditoryMolecular Biologylcsh:Neurosciences. Biological psychiatry. NeuropsychiatrySpiral ganglionOriginal Researchribbon synapsecalciumChemistryDepolarizationCell biology030104 developmental biologymedicine.anatomical_structureEPSCExcitatory postsynaptic potentialHair cellspiral ganglion neuron030217 neurology & neurosurgeryNeuroscience
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