Search results for "Neuronal"

showing 10 items of 556 documents

Anterograde tracing of retinal afferents to the tree shrew hypothalamus and raphe

2000

The anterograde neuronal transport of Cholera toxin B subunit (CTB) was used in this study to label the termination of retinal afferents in the hypothalamus of the tree shrew Tupaia belangeri. Upon pressure-injection of the substance into the vitreous body of one eye, a major projection of the retinohypothalamic tract (RHT) was found to the hypothalamic suprachiasmatic nuclei (SCN). Although the innervation pattern was bilateral, the ipsilateral SCN received a somewhat stronger projection. Labeling was also found in the supraoptic nucleus and its perinuclear zone, respectively, mainly ipsilaterally as well as in the bilateral para- and periventricular hypothalamic regions without lateral pr…

MaleCholera ToxinHypothalamusBiologySynaptic TransmissionRetinaSupraoptic nucleusAnimalsNeurons AfferentMolecular BiologyNeuronal transportRapheSuprachiasmatic nucleusGeneral NeuroscienceTupaiidaeGeniculate BodiesAnatomyAnterograde tracingHypothalamusRaphe NucleiFemaleSuprachiasmatic NucleusNeurology (clinical)Raphe nucleiSupraoptic NucleusNeuroscienceRetinohypothalamic tractDevelopmental BiologyBrain Research
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BDNF contributes to the facilitation of hippocampal synaptic plasticity and learning enabled by environmental enrichment

2014

Sensory, motor, and cognitive stimuli, resulting from interactions with the environment, play a key role in optimizing and modifying the neuronal circuitry required for normal brain function. An experimental animal model for this phenomenon comprises environmental enrichment (EE) in rodents. EE causes profound changes in neuronal and signaling levels of excitation and plasticity throughout the entire central nervous system and the hippocampus is particularly affected. The mechanisms underlying these changes are not yet fully understood. As brain-derived neurotrophic factor (BDNF) supports hippocampal long-term potentiation (LTP), we explored whether it participates in the facilitation of sy…

MaleCognitive NeuroscienceCentral nervous systemHippocampusMice TransgenicStimulationEnvironmentHippocampal formationHippocampusMiceNeurotrophic factorsmedicineAnimalsLearningEnvironmental enrichmentNeuronal PlasticityBehavior AnimalBrain-Derived Neurotrophic FactorRecognition PsychologyLong-term potentiationMice Inbred C57BLmedicine.anatomical_structurenervous systemSynaptic plasticityFemalePsychologyNeuroscienceHippocampus
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Dysregulated Expression of Neuregulin-1 by Cortical Pyramidal Neurons Disrupts Synaptic Plasticity

2014

Summary Neuregulin-1 ( NRG1 ) gene variants are associated with increased genetic risk for schizophrenia. It is unclear whether risk haplotypes cause elevated or decreased expression of NRG1 in the brains of schizophrenia patients, given that both findings have been reported from autopsy studies. To study NRG1 functions in vivo, we generated mouse mutants with reduced and elevated NRG1 levels and analyzed the impact on cortical functions. Loss of NRG1 from cortical projection neurons resulted in increased inhibitory neurotransmission, reduced synaptic plasticity, and hypoactivity. Neuronal overexpression of cysteine-rich domain (CRD)-NRG1, the major brain isoform, caused unbalanced excitato…

MaleDendritic SpinesNeuregulin-1Nonsynaptic plasticityGene ExpressionMice TransgenicNeurotransmissionInhibitory postsynaptic potentialSynaptic TransmissionGeneral Biochemistry Genetics and Molecular BiologyCell MovementInterneuronsConditioning Psychologicalmental disordersAnimalsNeuregulin 1lcsh:QH301-705.5CA1 Region HippocampalNeuronal PlasticitybiologyPyramidal CellsAnatomyFearCortex (botany)Synaptic fatiguelcsh:Biology (General)Synaptic plasticitybiology.proteinExcitatory postsynaptic potentialFemaleNerve NetNeuroscience
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Hampered long-term depression and thin spine loss in the nucleus accumbens of ethanol-dependent rats.

2014

Alcoholism involves long-term cognitive deficits, including memory impairment, resulting in substantial cost to society. Neuronal refinement and stabilization are hypothesized to confer resilience to poor decision making and addictive-like behaviors, such as excessive ethanol drinking and dependence. Accordingly, structural abnormalities are likely to contribute to synaptic dysfunctions that occur from suddenly ceasing the use of alcohol after chronic ingestion. Here we show that ethanol-dependent rats display a loss of dendritic spines in medium spiny neurons of the nucleus accumbens (Nacc) shell, accompanied by a reduction of tyrosine hydroxylase immunostaining and postsynaptic density 95…

MaleDendritic spineDendritic SpinesGlutamic AcidNucleus accumbensNeurotransmissionMedium spiny neuronSynaptic TransmissionNucleus AccumbensOrgan Culture TechniquesAnimalsRats WistarLong-term depressionLong-Term Synaptic Depressiondopamine synaptic plasticity Golgi glutamateMultidisciplinaryNeuronal PlasticityEthanolDopaminergic NeuronsLong-Term Synaptic DepressionCentral Nervous System DepressantsRatsAlcoholismPNAS PlusSynaptic plasticitySettore BIO/14 - FarmacologiaPsychologyNeurosciencePostsynaptic densityProceedings of the National Academy of Sciences of the United States of America
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Chronic stress induces changes in the structure of interneurons and in the expression of molecules related to neuronal structural plasticity and inhi…

2011

Chronic stress in experimental animals, one of the most accepted models of chronic anxiety and depression, induces structural remodeling of principal neurons in the amygdala and increases its excitation by reducing inhibitory tone. These changes may be mediated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a molecule related to neuronal structural plasticity and expressed by interneurons in the adult CNS, which is downregulated in the amygdala after chronic stress. We have analyzed the amygdala of adult mice after 21 days of restraint stress, studying with qRT-PCR the expression of genes related to general and inhibitory neurotransmission, and of PSA synthesizi…

MaleDendritic spineInterneuronDendritic SpinesSynaptophysinNeural Cell Adhesion Molecule L1BiologyNeurotransmissionSynaptic TransmissionAmygdalaImmobilizationMiceDevelopmental NeuroscienceInterneuronsmedicineAnimalsChronic stressNeuronal PlasticityGlutamate DecarboxylaseDendritesAmygdalaImmunohistochemistrySialyltransferasesDisease Models Animalmedicine.anatomical_structurenervous systemNeurologySialic AcidsSynaptophysinbiology.proteinNeural cell adhesion moleculeNeuroscienceStress PsychologicalBasolateral amygdalaExperimental Neurology
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Mutations in the Neuronal Vesicular SNARE VAMP2 Affect Synaptic Membrane Fusion and Impair Human Neurodevelopment

2019

VAMP2 encodes the vesicular SNARE protein VAMP2 (also called synaptobrevin-2). Together with its partners syntaxin-1A and synaptosomal-associated protein 25 (SNAP25), VAMP2 mediates fusion of synaptic vesicles to release neurotransmitters. VAMP2 is essential for vesicular exocytosis and activity-dependent neurotransmitter release. Here, we report five heterozygous de novo mutations in VAMP2 in unrelated individuals presenting with a neurodevelopmental disorder characterized by axial hypotonia (which had been present since birth), intellectual disability, and autistic features. In total, we identified two single-amino-acid deletions and three non-synonymous variants affecting conserved resid…

MaleHeterozygoteAdolescentVesicle-Associated Membrane Protein 2neuronal exocytosisynaptopathyautismsynaptobrevinMembrane FusionExocytosisR-SNARE ProteinsProtein DomainsReportIntellectual DisabilityGeneticsHumansAutistic DisorderChildGenetics (clinical)NeuronsNeurotransmitter Agentsneurodevelopmental disordersvesicle fusionBrainautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusionneuronal exocytosisLipidsMagnetic Resonance Imagingneurodevelopmental disorderautism epilepsy movement disorders neurodevelopmental disorders neuronal exocytosis SNARE synaptobrevin synaptopathy VAMP2 vesicle fusion Genetics Genetics (clinical)Phenotypeautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusion; Genetics; Genetics (clinical)VAMP2SNAREChild PreschoolMutationSynapsesMuscle Hypotoniaepilepsymovement disordersFemalesense organsmovement disorder
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Differential localization of neuronal nitric oxide synthase immunoreactivity and NADPH-diaphorase activity in the cat spinal cord.

1994

The distributions of neuronal nitric oxide synthase immunoreactivity (NOS-IR) and NADPH-diaphorase (NADPH-d) activity were compared in the cat spinal cord. NOS-IR in neurons around the central canal, in superficial laminae (I and II) of the dorsal horn, in the dorsal commissure, and in fibers in the superficial dorsal horn was observed at all levels of the spinal cord. In these regions, NOS-IR paralleled NADPH-d activity. The sympathetic autonomic nucleus in the rostral lumbar and thoracic segments exhibited prominent NOS-IR and NADPH-d activity, whereas the parasympathetic nucleus in the sacral segments did not exhibit NOS-IR or NADPH-d activity. Within the region of the sympathetic autono…

MaleHistologyPathology and Forensic MedicineNitric oxidechemistry.chemical_compoundLumbarDorsal root ganglionGanglia SpinalmedicineAnimalsNeuronsNADPH-diaphorase activityChemistryNADPH DehydrogenaseCell BiologyAnatomyCommissureSpinal cordImmunohistochemistrymedicine.anatomical_structureSpinal NervesSpinal CordCatsFemaleAmino Acid OxidoreductasesNitric Oxide SynthaseNucleusNeuronal Nitric Oxide SynthaseCell and tissue research
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In vitro anticholinergic drugs affect CD8+ peripheral blood T-cells apoptosis in COPD

2011

Novel pharmacological strategies are aimed at the resolution of systemic inflammation in COPD potentiating peripheral blood T-cell (PBT-cell) apoptosis. Although muscarinic acetylcholine receptors (mAChRs) M(3) and choline-acetyltransferase (ChAT) participate in the airway inflammation of COPD, their role in PBT-cell apoptosis remains unexplained. We evaluated in PBT-cells from COPD patients, smoker (S) and control (C) subjects: (1) apoptosis (by annexin V binding), (2) mAChR M(3) and ChAT expression, acetylcholine (ACh)-binding; (3) choline levels in serum and PBT-cells extracts. We tested the effects of Tiotropium (Spiriva(®)) and hemicholinium-3 (HCh-3) on apoptosis, NFκB pathway, caspas…

MaleImmunologyScopolamine DerivativesApoptosisCD8-Positive T-LymphocytesPharmacologySystemic inflammationCholinergic AntagonistsCholineCholine O-AcetyltransferasePulmonary Disease Chronic ObstructiveAnnexinMuscarinic acetylcholine receptormedicineHumansImmunology and AllergyLymphocyte CountTiotropium BromideCaspaseAgedReceptor Muscarinic M3Caspase 8COPDbiologyCaspase 3Systemic inflammation Non-neuronal components of cholinergic system Caspases NF B pathwaybusiness.industryNF-kappa BHematologyTiotropium bromideMiddle Agedmedicine.diseaserespiratory tract diseasesEnzyme ActivationApoptosisbiology.proteinFemalemedicine.symptombusinessAcetylcholineProtein BindingSignal Transductionmedicine.drugImmunobiology
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Bruce/apollon promotes hippocampal neuron survival and is downregulated by kainic acid

2005

Prolonged or excess stimulation of excitatory amino acid receptors leads to seizures and the induction of excitotoxic nerve cell injury. Kainic acid acting on glutamate receptors produces degeneration of vulnerable neurons in parts of the hippocampus and amygdala, but the exact mechanisms are not fully understood. We have here investigated whether the anti-apoptotic protein Bruce is involved in kainic acid-induced neurodegeneration. In the rat hippocampus and cortex, Bruce was exclusively expressed by neurons. The levels of Bruce were rapidly downregulated by kainic acid in hippocampal neurons as shown both in vivo and in cell culture. Caspase-3 was activated in neurons exhibiting low level…

MaleKainic acidCell SurvivalBiophysicsExcitotoxicityBruce/apollon Hippocampus Kainic acid Excitotoxicity Neuronal death Caspase-3 Cytochrome cDown-RegulationHippocampusStimulationBiologyHippocampal formationmedicine.disease_causeHippocampusBiochemistrychemistry.chemical_compoundDownregulation and upregulationmedicineAnimalsRats WistarMolecular BiologyCells CulturedNeuronsKainic AcidDose-Response Relationship DrugNeurodegenerationGlutamate receptorCell Biologymedicine.diseaseRatsCell biologynervous systemchemistryBiochemistryUbiquitin-Conjugating Enzymeshuman activitiescirculatory and respiratory physiology
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Zinc chelation during non-lesioning overexcitation results in neuronal death in the mouse hippocampus

2003

In the hippocampus, chelatable zinc is accumulated in vesicles of glutamatergic presynaptic terminals, abounding specially in the mossy fibers, from where it is released with activity and can exert a powerful inhibitory action upon N-methyl-D-aspartate receptors. Zinc is therefore in a strategic situation to control overexcitation at the zinc-rich excitatory synapses, and consequently zinc removal during high activity might result in excitotoxic neuronal damage. We analyzed the effect of zinc chelation with sodium dietyldithiocarbamate under overexcitation conditions induced by non-lesioning doses of kainic acid in the mouse hippocampus, to get insight into the role of zinc under overexcita…

MaleKainic acidSodiumchemistry.chemical_elementAMPA receptorPharmacologyInhibitory postsynaptic potentialHippocampusMicechemistry.chemical_compoundSeizuresmedicineAnimalsPremovement neuronal activityCell damageChelating AgentsNeuronsKainic AcidCell DeathGeneral NeuroscienceGlutamate receptormedicine.diseaseZincnervous systemBiochemistrychemistryNMDA receptorDitiocarbNeuroscience
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