Search results for "Neuronal"

showing 10 items of 556 documents

Ultrastructure of the Retina in Adult Neuronal Ceroid Lipofuscinosis

1998

A 33-year-old woman died of biopsy-proven adult neuronal ceroid lipofuscinosis (NCL) or Kufs’ disease marked by fingerprint and curvilinear lipopigments in neural and nonneural cell types. She had never experienced visual impairment or shown electroretinographic abnormalities. At autopsy, her retina appeared intact without degeneration at the light-microscopic level, but nerve cells in different layers were loaded with lipopigments of the granular type. This appears to be the third ultrastructural study of the retina in a patient with adult NCL, a former one showing preservation of the retina, another retinal degeneration. Thus, only further molecular genetic data will clarify the nosology …

AdultRetinal Ganglion CellsRetinal degenerationCell typePathologymedicine.medical_specialtyHistologyAutopsyDegeneration (medical)BiologyRetinaAdult neuronal ceroid lipofuscinosisFatal OutcomeNeuronal Ceroid-LipofuscinosesmedicineHumansKufs diseaseRetinaPigments BiologicalAnatomymedicine.diseaseLipidsMicroscopy Electronmedicine.anatomical_structureUltrastructureFemaleAnatomyCells Tissues Organs
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Alterations in the expression of PSA-NCAM and synaptic proteins in the dorsolateral prefrontal cortex of psychiatric disorder patients.

2012

Alterations in the structure and physiology of the prefrontal cortex (PFC) have been found in different psychiatric disorders and some of them involve inhibitory networks, especially in schizophrenia and major depression. Changes in the structure of these networks may be mediated by the polysialylated neural cell adhesion molecule (PSA-NCAM), a molecule related to neuronal structural plasticity, expressed in the PFC exclusively by interneurons. Different studies have found that PSA-NCAM expression in the hippocampus and the amygdala is altered in schizophrenia, major depression and animal models of these disorders, in parallel to changes in the expression of molecules related to inhibitory …

Adultmedicine.medical_specialtyBipolar DisorderSynaptophysinHippocampusPrefrontal CortexNeural Cell Adhesion Molecule L1NeurotransmissionHippocampusmedicineNeuropilHumansPsychiatryPrefrontal cortexAgedDepressive Disorder MajorNeuronal PlasticitybiologyGlutamate DecarboxylaseGeneral NeuroscienceMental DisordersNeural InhibitionMiddle AgedAmygdalaDorsolateral prefrontal cortexmedicine.anatomical_structurenervous systemSynaptic plasticitySynapsesVesicular Glutamate Transport Protein 1Synaptophysinbiology.proteinSchizophreniaSialic AcidsNeural cell adhesion moleculePsychologyNeuroscienceNeuroscience letters
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Semaphorin and plexin gene expression is altered in the prefrontal cortex of schizophrenia patients with and without auditory hallucinations

2015

Auditory hallucinations (AH) are clinical hallmarks of schizophrenia, however little is known about molecular genetics of these symptoms. In this study, gene expression profiling of postmortem brain samples from prefrontal cortex of schizophrenic patients without AH (SNA), patients with AH (SA) and control subjects were compared. Genome-wide expression analysis was conducted using samples of three individuals of each group and the Affymetrix GeneChip Human-Gene 1.0 ST-Array. This analysis identified the Axon Guidance pathway as one of the most differentially expressed network among SNA, SA and CNT. To confirm the transcriptome results, mRNA level quantification of seventeen genes involved i…

Adultmedicine.medical_specialtyHallucinationsSEMA4DDown-RegulationPrefrontal CortexNerve Tissue ProteinsSemaphorinsTranscriptomeMolecular geneticsInternal medicineNeuroplasticitymedicineHumansRNA MessengerPrefrontal cortexBiological PsychiatryAgedOligonucleotide Array Sequence AnalysisAged 80 and overNeuronal PlasticitybiologyGene Expression ProfilingPlexinBrainMiddle Agedmedicine.diseaseAxonsbody regionsGene expression profilingPsychiatry and Mental healthEndocrinologySchizophreniaSchizophreniabiology.proteinPsychologyCell Adhesion MoleculesNeurosciencePsychiatry Research
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Quantitative morphometric analysis of the submucous plexus in age-related control groups.

2002

An increased number and density of the so-called “giant ganglia” (seven or greater ganglion cells per ganglion) serve as histopathological criteria for a bowel motility disorder called intestinal neuronal dysplasia of the submucous plexus (IND B). However, because these morphological criteria have been defined based upon observations in constipated patients, the diagnostic value of previous studies is open to controversy. Moreover, no age-related reference data from unaffected controls are available. This study reports on data from unaffected controls on the variability of size and distribution of ganglia in the submucous plexus during development. Therefore, for the first time, the normal …

Adultmedicine.medical_specialtyPathologyAgingAdolescentGestational AgeBiologyPathology and Forensic MedicineAge relatedmedicineSubmucous plexusHumansChildMolecular BiologyAgedPregnancyIntestinal neuronal dysplasiaInfant NewbornGestational ageInfantAnatomical pathologyCell BiologyGeneral MedicineAnatomySubmucous PlexusMiddle Agedmedicine.diseaseGanglionmedicine.anatomical_structureChild PreschoolGestationGangliaVirchows Archiv : an international journal of pathology
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A53T-Alpha-Synuclein Overexpression Impairs Dopamine Signaling and Striatal Synaptic Plasticity in Old Mice

2010

BACKGROUND: Parkinson's disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression or the A53T missense mutation of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. METHODOLOGY/PRINCIPAL FINDINGS: Here, we used two mouse lines overexpressing human A53T-SNCA and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. To characterize the progression, we employed young adult as well as old mice. Analysis of striatal neurotransmitter content demonstrated that dopamine (DA…

AgingDopaminelcsh:MedicineMicechemistry.chemical_compoundHomer Scaffolding ProteinsReceptor Cannabinoid CB1lcsh:ScienceLong-term depressionNeurotransmitterChromatography High Pressure LiquidIn Situ Hybridization FluorescenceOligonucleotide Array Sequence AnalysisMice KnockoutNeuronal PlasticityMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionDopaminergicNeurodegenerationGenetics and Genomics/Gene ExpressionElectrophysiologyalpha-SynucleinResearch ArticleRadioimmunoprecipitation Assaymedicine.medical_specialtyNeuronal Calcium-Sensor ProteinsHOMER1Substantia nigraNeurotransmissionBiologyNeurological DisordersInternal medicinemedicineAnimalsHumansddc:610Cyclic Nucleotide Phosphodiesterases Type 7Activating Transcription Factor 2lcsh:RNeuropeptidesmedicine.diseaseMolecular biologyCorpus StriatumMice Mutant StrainsEndocrinologyGenetics and Genomics/Disease ModelschemistrySynaptic plasticitylcsh:QCarrier ProteinsPLoS ONE
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Enhancement of the FGFR1 signaling in the FGFR1-5-HT1A heteroreceptor complex in midbrain raphe 5-HT neuron systems. Relevance for neuroplasticity an…

2015

New findings show existence of FGFR1-5-HT1A heteroreceptor complexes in 5-HT nerve cells of the dorsal and median raphe nuclei of the rat midbrain and hippocampus. Synergistic receptor-receptor interactions in these receptor complexes indicated their enhancing role in hippocampal plasticity. The existence of FGFR1-5-HT1A heteroreceptor complexes also in midbrain raphe 5-HT nerve cells open up the possibility that antidepressant drugs by increasing extracellular 5-HT levels can cause an activation of the FGF-2/FGFR1 mechanism in these nerve cells as well. Therefore, the agonist modulation of the FGFR1-5-HT1A heteroreceptor complexes and their specific role is now determined in rat medullary …

AgonistSerotoninmedicine.medical_specialtymedicine.drug_classCellular differentiationBiophysicsHeteroreceptor complexBiologyHeteroreceptorBiochemistrySettore BIO/09 - FisiologiaCell LineMidbrainDorsal raphe nucleusMesencephalonInternal medicinemedicineAnimalsSerotonin 5-HT1A receptorReceptor Fibroblast Growth Factor Type 1Protein Interaction MapsPhosphorylationExtracellular Signal-Regulated MAP KinasesMolecular BiologyNeurons8-Hydroxy-2-(di-n-propylamino)tetralinNeuronal PlasticityRapheDepressionAnimalExtracellular Signal-Regulated MAP KinaseCell BiologySerotonin 5-HT1 Receptor AgonistsNeuronFibroblast growth factor receptorRatsEndocrinologymedicine.anatomical_structurenervous systemReceptor Serotonin 5-HT1AAutoreceptorRatFibroblast Growth Factor 2Serotonin 5-HT1 Receptor AgonistNeuronDimerizationNeuroscienceDepression; Dimerization; Fibroblast growth factor receptor; Heteroreceptor complex; Neuronal plasticity; Serotonin 5-HT1A receptor; 8-Hydroxy-2-(di-n-propylamino)tetralin; Animals; Cell Line; Extracellular Signal-Regulated MAP Kinases; Fibroblast Growth Factor 2; Mesencephalon; Neurons; Phosphorylation; Rats; Receptor Fibroblast Growth Factor Type 1; Receptor Serotonin 5-HT1A; Serotonin; Serotonin 5-HT1 Receptor Agonists; Neuronal Plasticity; Protein Interaction Maps
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Fibroblast Growth Factor Receptor 1– 5-Hydroxytryptamine 1A Heteroreceptor Complexes and Their Enhancement of Hippocampal Plasticity

2011

Background The hippocampus and its 5-hydroxytryptamine transmission plays an important role in depression related to its involvement in limbic circuit plasticity. Methods The analysis was made with bioluminescence resonance energy transfer, co-immunoprecipitation, in situ proximity ligation assay, binding assay, in cell western and the forced swim test. Results Using bioluminescence resonance energy transfer analysis, fibroblast growth factor receptor 1 (FGFR1)-5-hydroxytryptamine 1A (5-HT1A) receptor complexes have been demonstrated and their specificity and agonist modulation characterized. Their presence based on co-immunoprecipitation and proximity ligation assay has also been indicated…

Agonistmedicine.medical_specialtyReceptor complexmedicine.drug_classProximity ligation assayBiologyHippocampal formationTransfectionHeteroreceptorSettore BIO/09 - FisiologiaHippocampusRats Sprague-DawleyGrowth factor receptorInternal medicineFluorescence Resonance Energy TransfermedicineAnimalsHumansImmunoprecipitationReceptor Fibroblast Growth Factor Type 1Enzyme InhibitorsRNA Small InterferingCells CulturedBiological PsychiatryNeurons8-Hydroxy-2-(di-n-propylamino)tetralinNeuronal PlasticityDose-Response Relationship DrugFibroblast growth factor receptor 1Computational BiologyAllosteric modulation depression fibroblast growth factor receptor heteroreceptor neuronal plasticity serotonin receptorsRatsSerotonin Receptor AgonistsCell biologyEndocrinologyAnimals NewbornFibroblast growth factor receptorReceptor Serotonin 5-HT1AFibroblast Growth Factor 2PeptidesSignal TransductionBiological Psychiatry
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Selective erasure of a fear memory

2009

International audience; Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased cyclic adenosine monophosphate response element-binding protein (CREB) are preferentially activated by fear memory expression, which suggests that they are selectively recruited into the memory trace. We used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning b…

AmnesiaApoptosisMice TransgenicCREBAmygdalaMice03 medical and health sciences0302 clinical medicineMemoryConditioning PsychologicalmedicineAnimalsMemory disorderCyclic AMP Response Element-Binding ProteinNeuronal memory allocation030304 developmental biologyMemory consolidation0303 health sciencesMultidisciplinarybiologyCREBMemoriaFearmedicine.diseaseAmygdalamedicine.anatomical_structurenervous systemMental Recallbiology.proteinMemory traceMemory consolidation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]AmnesiaNeuronPavlovian conditioningmedicine.symptomNeuroscience030217 neurology & neurosurgeryScience
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Design and synthesis of new trehalose-conjugated pentapeptides as inhibitors of Aβ(1-42) fibrillogenesis and toxicity

2009

Aggregation of the amyloid A? peptide and its accumulation into insoluble deposits (plaques) are believed to be the main cause of neuronal dysfunction associated with Alzheimer's disease (AD); small molecules that can interfere with the A? amyloid fibril formation are therefore of interest for a potential therapeutic strategy. Three new trehalose-conjugated peptides of the well known ?-sheet breaker peptide iA?5p,were synthesized. The disaccharide was covalently attached to different sites of the LPFFD peptide chain, i.e. at the N-terminus, C-terminus or at the Asp side chain. CD spectroscopy in different solvents was used to assess changes in the peptide conformation of these compounds. Th…

AmyloidCell SurvivalPeptideMicroscopy Atomic ForceBiochemistryMass Spectrometrychemistry.chemical_compoundbeta-sheet breaker peptideStructural BiologySFMmental disordersDrug DiscoveryAnimalsbeta-sheet breaker peptidesMolecular BiologyCells CulturedChromatography High Pressure LiquidtrehaloseCerebral CortexPharmacologychemistry.chemical_classificationthioflavin Tbeta-amyloidOrganic ChemistryP3 peptideFibrillogenesisGeneral MedicineTrehaloseSmall moleculeGlycopeptideNeuronal culturesRatsPeptide Conformationneuronal cultureBiochemistrychemistryMolecular MedicineAmyloid-betaPeptidesJournal of Peptide Science
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Embryonic neural cell adhesion molecules on human natural killer cells

1989

The neural cell adhesion molecules (NCAM) are surface glycoproteins that were first described in brain tissue. NCAM mediate adhesion in a variety of cell-cell interactions. In the present study we show that the so-called "embryonic" NCAM, i.e., the highly polysialylated forms of these proteins, are expressed on natural killer cells and some CD3+ cells in man. Homotypic binding of NCAM, believed to be of importance for cell-cell adhesion in neural tissues, appears not to be essential for NK cell-mediated killing. Yet, NCAM might be involved in NK cell migration, homing or related functions.

Antigens Differentiation T-LymphocyteCD3 ComplexCell Adhesion Molecules NeuronalT-LymphocytesCD3Blotting WesternImmunologyReceptors Antigen T-CellChromatography AffinityNatural killer cellCell–cell interactionmedicineHumansImmunology and AllergybiologyCell adhesion moleculeAntibodies MonoclonalCell migrationFlow CytometryPrecipitin TestsMolecular biologyEmbryonic stem cellCell biologyKiller Cells Naturalmedicine.anatomical_structurenervous systembiology.proteinNeural cell adhesion moleculeHoming (hematopoietic)European Journal of Immunology
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