Search results for "lcsh:RC321-571"

showing 10 items of 504 documents

Novel Insights of Effects of Pregabalin on Neural Mechanisms of Intracortical Disinhibition in Physiopathology of Fibromyalgia: An Explanatory, Rando…

2018

Submitted by DSpace Unilasalle (dspace@unilasalle.edu.br) on 2021-09-14T16:51:25Z No. of bitstreams: 1 adeitos.etal.pdf: 2278622 bytes, checksum: dd96bf75fdbab601238c2831da009c73 (MD5) Made available in DSpace on 2021-09-14T16:51:25Z (GMT). No. of bitstreams: 1 adeitos.etal.pdf: 2278622 bytes, checksum: dd96bf75fdbab601238c2831da009c73 (MD5) Previous issue date: 2018 Background: The fibromyalgia (FM) physiopathology involves an intracortical excitability/inhibition imbalance as measured by transcranial magnetic stimulation measures (TMS). TMS measures provide an index that can help to understand how the basal neuronal plasticity state (i.e., levels of the serum neurotrophins brain-derived n…

0301 basic medicineFibromyalgiashort intracortical inhibitionmedicine.medical_treatmentPregabalincortical silent periodPlaceboS100Blcsh:RC321-57103 medical and health sciencesBehavioral Neuroscience0302 clinical medicineFibromyalgiaNeuroplasticityMedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryBiological PsychiatryPregabalinaCortical silent periodbusiness.industryFator neurotrófico derivado do encéfaloFibromialgiaProteínas S100medicine.diseaseClinical TrialCrossover studyTranscranial magnetic stimulationPsychiatry and Mental healthBDNF030104 developmental biologyNeuropsychology and Physiological PsychologyNeurologyShort intracortical inhibitionDisinhibitionAnesthesiafibromyalgiaSilent periodmedicine.symptombusiness030217 neurology & neurosurgeryNeurosciencemedicine.drugFrontiers in Human Neuroscience
researchProduct

Taurine as an Essential Neuromodulator during Perinatal Cortical Development

2017

A variety of experimental studies demonstrated that neurotransmitters are an important factor for the development of the central nervous system, affecting neurodevelopmental events like neurogenesis, neuronal migration, programmed cell death, and differentiation. While the role of the classical neurotransmitters glutamate and gamma-aminobutyric acid (GABA) on neuronal development is well established, the aminosulfonic acid taurine has also been considered as possible neuromodulator during early neuronal development. The purpose of the present review article is to summarize the properties of taurine as neuromodulator in detail, focusing on the direct involvement of taurine on various neurode…

0301 basic medicineGABA receptorsTaurineCentral nervous systemReviewBiologymigrationlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineCajal–Retzius cellsmedicinePremovement neuronal activityGlycine receptorlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNeocortexGABAA receptorglycine receptorsNeurogenesisGlutamate receptorrodent030104 developmental biologymedicine.anatomical_structurechemistrynervous systemsubplatecerebral cortexNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
researchProduct

Improvements to Healthspan Through Environmental Enrichment and Lifestyle Interventions: Where Are We Now?

2020

Environmental enrichment (EE) is an experimental paradigm that is used to explore how a complex, stimulating environment can impact overall health. In laboratory animal experiments, EE housing conditions typically include larger-than-standard cages, abundant bedding, running wheels, mazes, toys, and shelters which are rearranged regularly to further increase stimulation. EE has been shown to improve multiple aspects of health, including but not limited to metabolism, learning and cognition, anxiety and depression, and immunocompetence. Recent advances in lifespan have led some researchers to consider aging as a risk factor for disease. As such, there is a pressing need to understand the pro…

0301 basic medicineGerontologymedia_common.quotation_subjectContext (language use)ReviewDiseasehealthspanlcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineQuality (business)hypothalamuslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrymedia_commonEnvironmental enrichmentHPA axisGeneral NeuroscienceLongevityCognitionMedical research030104 developmental biologyBDNFhealthy agingenvironmental enrichmentAnxietymedicine.symptomPsychologylifespan030217 neurology & neurosurgeryNeuroscienceFrontiers in Neuroscience
researchProduct

Oxidative Stress-Induced Axon Fragmentation Is a Consequence of Reduced Axonal Transport in Hereditary Spastic Paraplegia SPAST Patient Neurons

2020

Hereditary spastic paraplegia (HSP) is a group of inherited disorders characterized by progressive spasticity and paralysis of the lower limbs. Autosomal dominant mutations in SPAST gene account for ∼40% of adult-onset patients. We have previously shown that SPAST patient cells have reduced organelle transport and are therefore more sensitive to oxidative stress. To test whether these effects are present in neuronal cells, we first generated 11 induced pluripotent stem (iPS) cell lines from fibroblasts of three healthy controls and three HSP patients with different SPAST mutations. These cells were differentiated into FOXG1-positive forebrain neurons and then evaluated for multiple aspects …

0301 basic medicineHereditary spastic paraplegiaOxidative phosphorylationSpastinmedicine.disease_causelcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASTAxonFragmentation (cell biology)hereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGeneral Neuroscienceperoxisomesaxon transportmedicine.diseaseepothilone Daxon degenerationCell biology030104 developmental biologymedicine.anatomical_structurenervous systemForebrainAxoplasmic transport030217 neurology & neurosurgeryOxidative stressFrontiers in Neuroscience
researchProduct

Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem Cells

2020

Mutations in SPG7 and SPAST are common causes of hereditary spastic paraplegia (HSP). While some SPG7 mutations cause paraplegin deficiency, other SPG7 mutations cause increased paraplegin expression. Mitochondrial function has been studied in models that are paraplegin-deficient (human, mouse, and Drosophila models with large exonic deletions, null mutations, or knockout models) but not in models of mutations that express paraplegin. Here, we evaluated mitochondrial function in olfactory neurosphere-derived cells, derived from patients with a variety of SPG7 mutations that express paraplegin and compared them to cells derived from healthy controls and HSP patients with SPAST mutations, as …

0301 basic medicineHereditary spastic paraplegiaoxidative phosphorylationOxidative phosphorylationMitochondrionmedicine.disease_causeSpastinSPG7lcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASThereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMutationparapleginParapleginGeneral NeuroscienceBrief Research Reportspastinmedicine.diseasePhenotypeCell biologymitochondria030104 developmental biology030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in Neuroscience
researchProduct

Shank3 Mice Carrying the Human Q321R Mutation Display Enhanced Self-Grooming, Abnormal Electroencephalogram Patterns, and Suppressed Neuronal Excitab…

2019

Shank3, a postsynaptic scaffolding protein involved in regulating excitatory synapse assembly and function, has been implicated in several brain disorders, including autism spectrum disorders (ASD), Phelan-McDermid syndrome, schizophrenia, intellectual disability, and mania. Here we generated and characterized a Shank3 knock-in mouse line carrying the Q321R mutation (Shank3Q321R mice) identified in a human individual with ASD that affects the ankyrin repeat region (ARR) domain of the Shank3 protein. Homozygous Shank3Q321R/Q321R mice show a selective decrease in the level of Shank3a, an ARR-containing protein variant, but not other variants. CA1 pyramidal neurons in the Shank3Q321R/Q321R hip…

0301 basic medicineHippocampusautism spectrum disorderBiologyNeurotransmissionElectroencephalographyInhibitory postsynaptic potentiallcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceExcitatory synapse assembly0302 clinical medicinePostsynaptic potentialexcitabilitymedicineself-groomingEEGMolecular Biologylcsh:Neurosciences. Biological psychiatry. Neuropsychiatrypatient mutationsOriginal Researchmedicine.diagnostic_testanxiety-like behaviorseizure susceptibilitymedicine.disease030104 developmental biologyShank3SchizophreniaExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
researchProduct

The Role of the Multifunctional BAG3 Protein in Cellular Protein Quality Control and in Disease

2017

In neurons, but also in all other cells the complex proteostasis network is monitored and tightly regulated by the cellular protein quality control (PQC) system. Beyond folding of newly synthesized polypeptides and their refolding upon misfolding the PQC also manages the disposal of aberrant proteins either by the ubiquitin-proteasome machinery or by the autophagic-lysosomal system. Aggregated proteins are primarily degraded by a process termed selective macroautophagy (or aggrephagy). One such recently discovered selective macroautophagy pathway is mediated by the multifunctional HSP70 co-chaperone BAG3 (BCL-2-associated athanogene 3). Under acute stress and during cellular aging, BAG3 in …

0301 basic medicineHuntingtinSOD1AggrephagyReviewBAG3lcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceUbiquitinselective macroautophagymedicineprotein quality controllcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyproteostasisbiologyBAG3NeurodegenerationAutophagymedicine.diseaseCell biology030104 developmental biologyProteostasisneurodegenerative disordersbiology.proteinNeuroscienceFrontiers in Molecular Neuroscience
researchProduct

Boosting Action Observation and Motor Imagery to Promote Plasticity and Learning

2018

Neural Plasticity, 2018

0301 basic medicineImagery PsychotherapyBoosting (machine learning)Article SubjectComputer scienceMovementMachine learningcomputer.software_genrestimulationlcsh:RC321-57103 medical and health sciences0302 clinical medicineMotor imageryHumansLearninglcsh:Neurosciences. Biological psychiatry. NeuropsychiatryComputingMilieux_MISCELLANEOUSNeuronal Plasticitybusiness.industryBraincortexEditorial030104 developmental biologyNeurologyAction observationImagination[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Neurology (clinical)Artificial intelligencebusinesscomputer030217 neurology & neurosurgery
researchProduct

Chronic Stress Modulates Interneuronal Plasticity: Effects on PSA-NCAM and Perineuronal Nets in Cortical and Extracortical Regions.

2018

Chronic stress has an important impact on the adult brain. However, most of the knowledge on its effects is focused on principal neurons and less on inhibitory neurons. Consequently, recent reports have begun to describe stress-induced alterations in the structure, connectivity and neurochemistry of interneurons. Some of these changes appear to be mediated by certain molecules particularly associated to interneurons, such as the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) and components of the perineuronal nets (PNN), specialized regions of the extracellular matrix. These plasticity-related molecules modulate interneuronal structure and connectivity, particularly of …

0301 basic medicineInterneuronPSA-NCAMhippocampusHippocampuslcsh:RC321-57103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineChronic stresslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal Researchchronic stressreticular thalamic nucleusThalamic reticular nucleusbiologyhabenulaPerineuronal netmusculoskeletal neural and ocular physiology030104 developmental biologymedicine.anatomical_structureHabenulanervous systembiology.proteinperineuronal netNeuroscience030217 neurology & neurosurgeryParvalbuminmedial prefrontal cortexbasolateral amygdalaBasolateral amygdalaNeuroscienceFrontiers in cellular neuroscience
researchProduct

MicroRNA-22 Controls Aberrant Neurogenesis and Changes in Neuronal Morphology After Status Epilepticus

2018

Prolonged seizures (status epilepticus, SE) may drive hippocampal dysfunction and epileptogenesis, at least partly, through an elevation in neurogenesis, dysregulation of migration and aberrant dendritic arborization of newly-formed neurons. MicroRNA-22 was recently found to protect against the development of epileptic foci, but the mechanisms remain incompletely understood. Here, we investigated the contribution of microRNA-22 to SE-induced aberrant adult neurogenesis. SE was induced by intraamygdala microinjection of kainic acid (KA) to model unilateral hippocampal neuropathology in mice. MicroRNA-22 expression was suppressed using specific oligonucleotide inhibitors (antagomir-22) and ne…

0301 basic medicineKainic acidDendritic spineMicroRNA-22NeurogenesisStatus epilepticusBiologyHippocampal formationEpileptogenesislcsh:RC321-571Mouse model03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryStatus epilepticusMolecular BiologyOriginal ResearchEpilepsyDentate gyrusNeurogenesisBiología y Biomedicina / BiologíaGranule cell3. Good health030104 developmental biologymedicine.anatomical_structurenervous systemchemistrymedicine.symptomNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
researchProduct