Search results for "PsyArXiv|Neuroscience|Behavioral Neuroscience"

showing 10 items of 8055 documents

Brain histamine and behavioral neuroscience

2017

ABSTRACT NON PREVISTO DALLA PUBBLICAZIONE

0301 basic medicineCarboxy-LyasesVideo RecordingEditorial: NeuroscienceBehavioral neuroscienceSettore BIO/09 - Fisiologiabehavioral sequenceHistonesMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAnimalsHumansMedicineMotor NeuronsBehaviorBehavior Animalbusiness.industryNeurosciencesBrainhistaminePhenotype030104 developmental biologyOncologychemistryAnesthesiaBehavior; Behavioral sequence; Histamine; Neuroscience; T-pattern; OncologyT-patternbusinessNeuroscience030217 neurology & neurosurgeryHistamineTourette SyndromeNeuroscienceOncotarget
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Daunorubicin reduces MBNL1 titration by expanded CUG repeat RNA and rescues cardiac dysfunctions in a Drosophila model of myotonic dystrophy

2018

International audience; Myotonic dystrophy (DM) is a dominantly inherited neuromuscular disorder caused by expression of mutant DMPK transcripts containing expanded CUG repeats. Pathogenic RNA sequesters the muscleblind-like (MBNL) proteins, causing alterations of RNA metabolism. Cardiac dysfunction represents the second most common cause of death in DM1 patients. However, the contribution of MBNL titration in DM1 cardiac dysfunction is unclear. We overexpressed Muscleblind (Mbl), Drosophila MBNL orthologue, in cardiomyocytes of DM1 model flies and observed a rescue of heart dysfunctions, which are characteristic of these model flies and resemble cardiac defects observed in patients. We als…

0301 basic medicineCardiac function curvecongenital hereditary and neonatal diseases and abnormalitiesDaunorubicin[SDV]Life Sciences [q-bio]Neuroscience (miscellaneous)Medicine (miscellaneous)BiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmunology and Microbiology (miscellaneous)medicineMBNL1Daunorubicin HydrochlorideRNAmedicine.diseaseTrinucleotide repeat disorder3. Good healthCell biology[SDV] Life Sciences [q-bio]030104 developmental biologychemistryTrinucleotide repeat expansion030217 neurology & neurosurgerymedicine.drug
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Gene therapy for chondral and osteochondral regeneration: is the future now?

2017

Gene therapy might represent a promising strategy for chondral and osteochondral defects repair by balancing the management of temporary joint mechanical incompetence with altered metabolic and inflammatory homeostasis. This review analysed preclinical and clinical studies on gene therapy for the repair of articular cartilage defects performed over the last 10 years, focussing on expression vectors (non-viral and viral), type of genes delivered and gene therapy procedures (direct or indirect). Plasmids (non-viral expression vectors) and adenovirus (viral vectors) were the most employed vectors in preclinical studies. Genes delivered encoded mainly for growth factors, followed by transcripti…

0301 basic medicineCartilage ArticularExpression vectorPathologymedicine.medical_specialtyCell signalingCartilage repair; Expression vectors; Gene therapy procedures; Osteoarthritis; Regenerative medicine; Molecular Medicine; Molecular Biology; Pharmacology; Cellular and Molecular Neuroscience; Cell BiologyBone RegenerationInflammatory arthritisGenetic enhancementGene therapy procedureOsteoarthritisViral vector03 medical and health sciencesCellular and Molecular NeuroscienceCartilage repairChondrocytesInterferonSettore BIO/13 - Biologia ApplicataOsteoarthritismedicineAnimalsHumansRegenerationMolecular BiologyPharmacologyExpression vectorbusiness.industryRegeneration (biology)Cell BiologyGenetic Therapymedicine.disease030104 developmental biologyRegenerative medicineCancer researchMolecular MedicineOsteoarthritibusinessmedicine.drugCellular and molecular life sciences : CMLS
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The Sensory Neocortex and Associative Memory

2016

Most behaviors in mammals are directly or indirectly guided by prior experience and therefore depend on the ability of our brains to form memories. The ability to form an association between an initially possibly neutral sensory stimulus and its behavioral relevance is essential for our ability to navigate in a changing environment. The formation of a memory is a complex process involving many areas of the brain. In this chapter we review classic and recent work that has shed light on the specific contribution of sensory cortical areas to the formation of associative memories. We discuss synaptic and circuit mechanisms that mediate plastic adaptations of functional properties in individual …

0301 basic medicineCategorical perceptionNeocortexSensory systemContent-addressable memoryAuditory cortex03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureSynaptic plasticitymedicineAssociation (psychology)PsychologyNeuroscience030217 neurology & neurosurgeryAssociative property
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Autism Related Neuroligin-4 Knockout Impairs Intracortical Processing but not Sensory Inputs in Mouse Barrel Cortex

2016

Neuroligin-4 (Nlgn4) is a cell adhesion protein that regulates synapse organization and function. Mutations in human NLGN4 are among the causes of autism spectrum disorders. In mouse, Nlgn4 knockout (KO) perturbs GABAergic synaptic transmission and oscillatory activity in hippocampus, and causes social interaction deficits. The complex profile of cellular and circuit changes that are caused by Nlgn4-KO is still only partly understood. Using Nlgn4-KO mice, we found that Nlgn4-KO increases the power in the alpha frequency band of spontaneous network activity in the barrel cortex under urethane anesthesia in vivo. Nlgn4-KO did not affect single-whisker-induced local field potentials, but suppr…

0301 basic medicineCell Adhesion Molecules NeuronalCognitive NeuroscienceHippocampusNeocortexNeuroliginSensory systemIn Vitro TechniquesNeurotransmissionMice03 medical and health sciencesCellular and Molecular NeuroscienceGlutamatergic0302 clinical medicineAnimalsEvoked PotentialsSynapse organizationMice KnockoutNeuronsAfferent PathwaysNeurotransmitter AgentsChemistryBarrel cortexElectric StimulationVoltage-Sensitive Dye Imaging030104 developmental biologyAnimals NewbornVibrissaeExcitatory postsynaptic potentialNerve NetNeuroscience030217 neurology & neurosurgeryCerebral Cortex
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Toxic Tau Oligomers Modulated by Novel Curcumin Derivatives

2019

AbstractThe pathological aggregation and accumulation of tau, a microtubule-associated protein, is a common feature amongst more than 18 different neurodegenerative diseases that are collectively known as tauopathies. Recently, it has been demonstrated that the soluble and hydrophobic tau oligomers are highly toxic in vitro due to their capacity towards seeding tau misfolding, thereby propagating the tau pathology seen across different neurodegenerative diseases. Modulating the aggregation state of tau oligomers through the use of small molecules could be a useful therapeutic strategy to target their toxicity, regardless of other factors involved in their formation. In this study, we screen…

0301 basic medicineCell biologyCurcuminCell SurvivalNeurotoxinsChemical biologyBiophysicsDrug Evaluation Preclinicallcsh:Medicinetau ProteinsProtein aggregationOligomerBiochemistryArticleBiophysical Phenomena03 medical and health scienceschemistry.chemical_compoundMiceProtein Aggregates0302 clinical medicineCell Line Tumormental disordersAnimalsHumanslcsh:ScienceNeuronsMultidisciplinaryCell DeathDrug discoveryDrug discoverySettore BIO/16 - Anatomia Umanalcsh:RSettore CHIM/06 - Chimica OrganicaSmall moleculeChemical biologyIn vitro3. Good healthTau protein Curcumin030104 developmental biologychemistryCell cultureBiophysicsCurcuminAlzheimerlcsh:QProtein Multimerization030217 neurology & neurosurgeryNeuroscience
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Bioenergetic Failure in Rat Oligodendrocyte Progenitor Cells Treated with Cerebrospinal Fluid Derived from Multiple Sclerosis Patients

2017

In relapsing-remitting multiple sclerosis (RRMS) subtype, the patient's brain itself is capable of repairing the damage, remyelinating the axon and recovering the neurological function. Cerebrospinal fluid (CSF) is in close proximity with brain parenchyma and contains a host of proteins and other molecules, which influence the cellular physiology, that may balance damage and repair of neurons and glial cells. The purpose of this study was to determine the pathophysiological mechanisms underpinning myelin repair in distinct clinical forms of MS and neuromyelitis optica (NMO) patients by studying the effect of diseased CSF on glucose metabolism and ATP synthesis. A cellular model with primary…

0301 basic medicineCell physiologyglucose metabolismneuromyelitis opticaTransferrin receptorBiologymultiple sclerosiscerebrospinal fluidlcsh:RC321-571myelin repair03 medical and health sciencesCellular and Molecular NeuroscienceMyelin0302 clinical medicineCerebrospinal fluidGene expressionmedicineAxonlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchMultiple sclerosisoligodendrocyte progenitor cellsmedicine.disease3. Good health030104 developmental biologymedicine.anatomical_structureHypoxanthine-guanine phosphoribosyltransferaseImmunologyCancer researchgene expression030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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The Guanine-Based Purinergic System: The Tale of An Orphan Neuromodulation.

2016

Guanine-based purines (GBPs) have been recently proposed to be not only metabolic agents but also extracellular signaling molecules that regulate important functions in the central nervous system. In such way, GBPs-mediated neuroprotection, behavioral responses and neuronal plasticity have been broadly described in the literature. However, while a number of these functions (i.e., GBPs neurothophic effects) have been well-established, the molecular mechanisms behind these GBPs-dependent effects are still unknown. Furthermore, no plasma membrane receptors for GBPs have been described so far, thus GBPs are still considered orphan neuromodulators. Interestingly, an intricate and controversial f…

0301 basic medicineCell signalingAdenosineAdenosinaguanine-based purines; guanosine; neuroprotectionReviewBiologySettore BIO/09 - FisiologiaNeuroprotection03 medical and health sciences0302 clinical medicineguanine-based purinespurinergic receptorsmedicineGuanosine triphosphatasePharmacology (medical)ReceptorPharmacologyTrifosfat de guanosinasynaptic plasticityPurinergic receptorAdenosine; Guanine-based purines; Guanosine; Neuroprotection; Purinergic receptors; Synaptic plasticity; Pharmacology; Pharmacology (medical)Adenosine receptorAdenosineNeuromodulation (medicine)guanosine030104 developmental biologyBiochemistryPurinesadenosineSynaptic plasticityneuroprotectionNeurosciencePurinergic receptor030217 neurology & neurosurgeryGuanine-based purinemedicine.drugFrontiers in pharmacology
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The FOXP2-Driven Network in Developmental Disorders and Neurodegeneration

2017

The transcription repressor FOXP2 is a crucial player in nervous system evolution and development of humans and songbirds. In order to provide an additional insight into its functional role we compared target gene expression levels between human neuroblastoma cells (SH-SY5Y) stably overexpressing either human FOXP2 cDNA or its orthologues from the common chimpanzee, Rhesus monkey, and marmoset, respectively. Subsequent RNA-seq led to identification of 27 genes with differential regulation under the control of human FOXP2, which were previously reported to have FOXP2-driven and/or songbird song-related expression regulation. Importantly, RT-qPCR and Western blotting indicated differential re…

0301 basic medicineCell signalingCytoskeleton organizationspeechbrainBiologyAxonogenesislcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceHuntington's diseasemedicineGeneTranscription factorlcsh:Neurosciences. Biological psychiatry. Neuropsychiatryneuronal circuitryOriginal ResearchlanguageNeurodegenerationFOXP2medicine.diseaseschizophrenia030104 developmental biologyParkinson’s diseaseNeuroscienceAlzheimer’s diseaseNeuroscienceHuntington’s diseaseFrontiers in Cellular Neuroscience
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How repair-or-dispose decisions under stress can initiate disease progression

2020

Summary Glia, the helper cells of the brain, are essential in maintaining neural resilience across time and varying challenges: By reacting to changes in neuronal health glia carefully balance repair or disposal of injured neurons. Malfunction of these interactions is implicated in many neurodegenerative diseases. We present a reductionist model that mimics repair-or-dispose decisions to generate a hypothesis for the cause of disease onset. The model assumes four tissue states: healthy and challenged tissue, primed tissue at risk of acute damage propagation, and chronic neurodegeneration. We discuss analogies to progression stages observed in the most common neurodegenerative conditions and…

0301 basic medicineCell signalingDisease onsetBioinformaticsSystems biology02 engineering and technologyArticle03 medical and health sciencesMathematical BiosciencesTissue damageMedicineddc:610Systems NeuroscienceResilience (network)lcsh:ScienceSystems neuroscienceMultidisciplinarybusiness.industrySystems BiologyNeurodegenerationDisease progression021001 nanoscience & nanotechnologymedicine.diseaseCrosstalk (biology)030104 developmental biologylcsh:Q0210 nano-technologybusinessNeuroscienceNeuroscience
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