Search results for "Synapse"

showing 10 items of 243 documents

Cannabinoid CB1 Receptor Calibrates Excitatory Synaptic Balance in the Mouse Hippocampus

2015

The endocannabinoid system negatively regulates the release of various neurotransmitters in an activity-dependent manner, thereby influencing the excitability of neuronal circuits. In the hippocampus, cannabinoid type 1 (CB1) receptor is present on both GABAergic and glutamatergic axon terminals. CB1 receptor-deficient mice were previously shown to have increased hippocampal long-term potentiation (LTP). In this study, we have investigated the consequences of cell-type-specific deletion of the CB1 receptor on the induction of hippocampal LTP and on CA1 pyramidal cell morphology. Deletion of CB1 receptor in GABAergic neurons in GABA-CB1-KO mice leads to a significantly decreased hippocampal …

Long-Term PotentiationHippocampusHippocampal formationBiologyHippocampusSynaptic TransmissionMiceGlutamatergicReceptor Cannabinoid CB1medicineAnimalsAxonMice KnockoutNeuronal Plasticitymusculoskeletal neural and ocular physiologyGeneral NeuroscienceExcitatory Postsynaptic Potentialsfood and beveragesLong-term potentiationArticlesEndocannabinoid systemMice Inbred C57BLmedicine.anatomical_structurenervous systemSynapsesSynaptic plasticityGABAergiclipids (amino acids peptides and proteins)NeuroscienceThe Journal of Neuroscience
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TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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Early-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants

2020

Mice lacking GAD1 show neonatal mortality, but the human phenotype associated with GAD1 disruption is poorly characterized. Neuray et al. describe six patients with biallelic GAD1 mutations, presenting with early-infantile onset epilepsy, neurodevelopmental delay, muscle weakness and non-CNS manifestations.

Male0301 basic medicineGlutamate decarboxylaseMalalties cerebralsNeurotransmissorsNeurodevelopmental delayEpilepsy0302 clinical medicineMESH: ChildAge of OnsetChildcleft palateGAD1AcademicSubjects/SCI01870Glutamate DecarboxylaseGlutamate receptorMuscle weakness//purl.org/becyt/ford/3.1 [https]NeurotransmittersMESH: InfantHypotoniamuscle weakneCleft palateMESH: EpilepsyChild PreschoolMuscle Hypotonia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]//purl.org/becyt/ford/3 [https]FemaleBrain diseasesAbnormalitiesmedicine.symptomMultiplemedicine.drugcleft palate; epilepsy; GAD1; muscle weakness; neurodevelopmental delayMESH: Glutamate Decarboxylasemedicine.medical_specialtyMESH: Abnormalities MultipleMESH: MutationMESH: Age of OnsetBiologyInhibitory postsynaptic potentialGAD1 cleft palate epilepsy muscle weakness neurodevelopmental delay.gamma-Aminobutyric acidGAD1neurodevelopmental delay03 medical and health sciencesExcitatory synapseInternal medicinemedicineHumansAbnormalities MultiplePreschoolAllelesMESH: Neurodevelopmental Disordersmuscle weaknessMESH: HumansEpilepsyMESH: Muscle HypotoniaMESH: AllelesMESH: Child PreschoolInfantmedicine.diseaseMESH: MaleEpilèpsiaEditor's Choice030104 developmental biologyEndocrinologyNeurodevelopmental DisordersMutationepilepsyAcademicSubjects/MED00310Neurology (clinical)Cleft palate; Epilepsy; GAD1; Muscle weakness; Neurodevelopmental delay; Abnormalities Multiple; Age of Onset; Alleles; Child; Child Preschool; Epilepsy; Female; Glutamate Decarboxylase; Humans; Infant; Male; Muscle Hypotonia; Mutation; Neurodevelopmental DisordersMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology030217 neurology & neurosurgeryReports
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Sub-chronic variable stress induces sex-specific effects on glutamatergic synapses in the nucleus accumbens

2017

Men and women manifest different symptoms of depression and under current diagnostic criteria, depression is twice as prevalent in woman. However, little is known of the mechanisms contributing to these important sex differences. Sub-chronic variable stress (SCVS), a rodent model of depression, induces depression-like behaviors in female mice only, modeling clinical evidence of higher susceptibility to mood disorders in women. Accumulating evidence indicates that altered neuroplasticity of excitatory synapses in the nucleus accumbens (NAc) is a key pathophysiological feature of susceptibility to social stress in males. Here we investigated the effects of SCVS on pre- and post-synaptic prote…

Male0301 basic medicinesex differenceVesicular glutamate transporter 1Nucleus accumbensMedium spiny neuronmedium spiny neuronArticleNucleus Accumbens03 medical and health sciencesGlutamatergicchemistry.chemical_compound0302 clinical medicineStress PhysiologicalstreNeuroplasticityAnimalsSocial stressSex CharacteristicsLucifer yellowNeuronal PlasticityNeuroscience (all)biologynucleus accumbenGeneral NeurosciencePost-Synaptic DensityMice Inbred C57BL030104 developmental biologychemistryplasticitySynapsesVesicular Glutamate Transport Protein 1depressionVesicular Glutamate Transport Protein 2biology.proteinExcitatory postsynaptic potentialFemaleNeuroscience030217 neurology & neurosurgeryNeuroscience
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Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism-like phenot…

2021

The key role of APP for Alzheimer pathogenesis is well established. However, perinatal lethality of germline knockout mice lacking the entire APP family has so far precluded the analysis of its physiological functions for the developing and adult brain. Here, we generated conditional APP/APLP1/APLP2 triple KO (cTKO) mice lacking the APP family in excitatory forebrain neurons from embryonic day 11.5 onwards. NexCre cTKO mice showed altered brain morphology with agenesis of the corpus callosum and disrupted hippocampal lamination. Further, NexCre cTKOs revealed reduced basal synaptic transmission and drastically reduced long-term potentiation that was associated with reduced dendritic length …

Male10017 Institute of AnatomyLong-Term PotentiationHippocampal formationSynaptic TransmissionAmyloid beta-Protein Precursor0302 clinical medicine2400 General Immunology and MicrobiologyAmyloid precursor proteinMolecular Biology of DiseaseAutism spectrum disorderMice KnockoutNeurons0303 health sciencesbiologyBehavior AnimalGeneral NeuroscienceBrain2800 General NeuroscienceLong-term potentiationArticlesPhenotype10076 Center for Integrative Human PhysiologyKnockout mouseFemalelearning and memory610 Medicine & healthGeneral Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesProsencephalon1300 General Biochemistry Genetics and Molecular Biologymental disorders1312 Molecular BiologyAnimalsLearningAPLP1Autistic DisorderSocial BehaviorMolecular BiologyAPLP2CA1 Region Hippocampal030304 developmental biologysynaptic plasticityGeneral Immunology and MicrobiologyAmyloid precursor proteinSynaptic plasticityForebrainSynapsesbiology.proteinAlzheimer570 Life sciences; biologyNeuroscience030217 neurology & neurosurgeryNeuroscienceThe EMBO journal
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Alteration of inhibitory circuits in the somatosensory cortex of Ts65Dn mice, a model for Down's syndrome.

2010

Down’s syndrome (DS), with an incidence of one in 800 live births, is the most common genetic disorder associated with mental retardation. This trisomy on chromosome 21 induces a variable phenotype in which the only common feature is the presence of mental retardation. The neural mechanisms underlying mental retardation might include defects in the formation of neuronal networks and neural plasticity. DS patients have alterations in the morphology, the density and the distribution of dendritic spines in the pyramidal neurons of the cortex. Our hypothesis is that the deficits in dendritic arborization observed in the principal neurons of DS patients and Ts65Dn mice (a model for DS that mimic…

MaleAgingDendritic spineFisiologia patològicaSynaptophysinCell CountMice TransgenicInhibitory postsynaptic potentialSomatosensory systemMiceInterneuronsCortex (anatomy)NeuroplasticityNeural PathwaysmedicineAnimalsBiological PsychiatrybiologyGlutamate DecarboxylaseCalcium-Binding ProteinsNeural InhibitionSomatosensory CortexImmunohistochemistryPsychiatry and Mental healthDisease Models Animalmedicine.anatomical_structureNeurologynervous systemSynapsesbiology.proteinSynaptophysinNeurology (clinical)CalretininDown SyndromeNeuroscienceParvalbuminJournal of neural transmission (Vienna, Austria : 1996)
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Synaptic ribbons, spheres and intermediate structures in the developing rat retina

1992

The present study was conducted to investigate the qualitative and quantitative development of synaptic bodies in retinae of Wistar rats during postnatal days 4-28. In addition, the effects of different light regimens and of eye pigmentation on SB numbers were studied. Synaptic bodies were counted and measured in the outer plexiform layer of retinal tissue fixed and processed by routine electron microscopical techniques. At postnatal days 4 and 5, retinae showed only few synaptic bodies. The main numerical development of synaptic bodies occurred between postnatal days 4 and 9, numbers remaining more or less constant thereafter. The intracellular location of synaptic ribbons changed from pre…

MaleAgingLightgenetic structuresOuter plexiform layerRat retinaBiologyRetinaDevelopmental NeurosciencemedicineAnimalsRats WistarphotoperiodismSynaptic ribbonRetinaAnatomyDarknessEye pigmentationRatsMicroscopy Electronmedicine.anatomical_structureAnimals NewbornSynapsesDarknessBiophysicsFemalesense organsIntracellularDevelopmental BiologyInternational Journal of Developmental Neuroscience
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The response to isoproterenol of synaptic ribbon numbers in the rat pineal gland changes during postnatal development

1995

Abstract In the mammalian pineal gland synaptic ribbons (SRs) are dynamic organelles of pinealocytes undergoing a day/night rhythm, with small numbers during daytime and significantly higher numbers at night, similar to the formation of the pineal hormone melatonin. Whereas the day/night rhythm of melatonin synthesis is adrenergically regulated, data on the adrenergic regulation of SR numbers in the rat pineal gland are at variance. While some authors have demonstrated that isoproterenol (ISO) stimulates SR numbers, others could not find any effect. To clarify the issue, we carried out identical experiments in two age groups. It was found that in male Sprague-Dawley rats, administration of …

MaleAgonistendocrine systemmedicine.medical_specialtymedicine.drug_classBiologyPineal GlandPinealocyteRats Sprague-DawleyMelatoninPineal glandInternal medicineIsoprenalinemedicineAnimalsMelatoninSynaptic ribbonGeneral NeuroscienceIsoproterenolRatsMicroscopy ElectronEndocrinologymedicine.anatomical_structureEpinephrineSynapsesmedicine.drugEndocrine glandNeuroscience Letters
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The K63 deubiquitinase CYLD modulates autism-like behaviors and hippocampal plasticity by regulating autophagy and mTOR signaling.

2021

Nondegradative ubiquitin chains attached to specific targets via Lysine 63 (K63) residues have emerged to play a fundamental role in synaptic function. The K63-specific deubiquitinase CYLD has been widely studied in immune cells and lately also in neurons. To better understand if CYLD plays a role in brain and synapse homeostasis, we analyzed the behavioral profile of CYLD-deficient mice. We found that the loss of CYLD results in major autism-like phenotypes including impaired social communication, increased repetitive behavior, and cognitive dysfunction. Furthermore, the absence of CYLD leads to a reduction in hippocampal network excitability, long-term potentiation, and pyramidal neuron s…

MaleAutism Spectrum DisorderNerve Tissue ProteinsHippocampal formationHippocampusDeubiquitinating enzymeSynapseMiceUbiquitinAutophagyAnimalsAutistic DisorderMechanistic target of rapamycinPI3K/AKT/mTOR pathwayNeuronsMultidisciplinarybiologyUbiquitinLysineTOR Serine-Threonine KinasesAutophagyMicrofilament ProteinsUbiquitinationLong-term potentiationBiological SciencesDeubiquitinating Enzyme CYLDMice Inbred C57BLSynapsesbiology.proteinFemaleNeuroscienceSignal TransductionProceedings of the National Academy of Sciences of the United States of America
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Effects of Presynaptic Mutations on a Postsynaptic Cacna1s Calcium Channel Colocalized with mGluR6 at Mouse Photoreceptor Ribbon Synapses

2008

Purpose Photoreceptor ribbon synapses translate light-dependent changes of membrane potential into graded transmitter release via L-type voltage-dependent calcium channel (VDCC) activity. Functional abnormalities (e.g., a reduced electroretinogram b-wave), arising from mutations of presynaptic proteins, such as Bassoon and the VDCCalpha1 subunit Cacna1f, have been shown to altered transmitter release. L-type VDCCalpha1 subtype expression in wild-type and mutant mice was examined, to investigate the underlying pathologic mechanism. Methods Two antisera against Cacna1f, and a Cacna1f mouse mutant (Cacna1fDeltaEx14-17) were generated. Immunocytochemistry for L-type VDCCalpha1 subunits and addi…

MaleCalcium Channels L-TypeBlotting WesternPresynaptic TerminalsRibbon synapseBiologyReceptors Metabotropic GlutamateSynaptic TransmissionEpitopesMicePostsynaptic potentialAnimalsCalcium SignalingActive zoneFluorescent Antibody Technique IndirectMicroscopy ImmunoelectronSequence DeletionMembrane potentialSheepVoltage-dependent calcium channelReverse Transcriptase Polymerase Chain ReactionCalcium channelMetabotropic glutamate receptor 6ColocalizationAnatomyBlotting NorthernMice Mutant StrainsPeptide FragmentsCell biologyMice Inbred C57BLFemaleCalcium ChannelsRabbitssense organsPhotoreceptor Cells VertebrateInvestigative Opthalmology & Visual Science
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