Search results for "Synaptic Potentials"

showing 10 items of 41 documents

Cannabinoid CB1 receptors regulate neuronal TNF-α effects in experimental autoimmune encephalomyelitis.

2011

Abstract Cannabinoid CB1 receptors (CB1Rs) regulate the neurodegenerative damage of experimental autoimmune encephalomyelitis (EAE) and of multiple sclerosis (MS). The mechanism by which CB1R stimulation exerts protective effects is still unclear. Here we show that pharmacological activation of CB1Rs dampens the tumor necrosis factor α (TNFα)-mediated potentiation of striatal spontaneous glutamate-mediated excitatory postsynaptic currents (EPSCs), which is believed to cogently contribute to the inflammation-induced neurodegenerative damage observed in EAE mice. Furthermore, mice lacking CB1Rs showed a more severe clinical course and, in parallel, exacerbated alterations of sEPSC duration af…

Cannabinoid receptorEncephalomyelitis Autoimmune ExperimentalPolyunsaturated Alkamidesmedicine.medical_treatmentImmunologyExcitotoxicityGlutamic AcidArachidonic AcidsPharmacologyBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateReceptors Tumor Necrosis FactorAmidohydrolasesEtanerceptBehavioral Neurosciencechemistry.chemical_compoundMiceReceptor Cannabinoid CB1Fatty acid amide hydrolaseCannabinoid Receptor ModulatorsmedicineAnimalsDronabinolReceptors AMPA6-Cyano-7-nitroquinoxaline-23-dioneMice KnockoutNeuronsEndocrine and Autonomic SystemsTumor Necrosis Factor-alphaNeurodegenerationExperimental autoimmune encephalomyelitisExcitatory Postsynaptic PotentialsAnandamidemedicine.diseaseEndocannabinoid systemCorpus StriatumMice Inbred C57BLchemistryImmunoglobulin GImmunologyNerve DegenerationSettore MED/26 - NeurologiaFemaleCannabinoidDizocilpine MaleateEndocannabinoidsBrain, behavior, and immunity
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Altered morphological and electrophysiological properties of Cajal-Retzius cells in cerebral cortex of embryonic Presenilin-1 knockout mice

2004

Mutations of Presenilin-1 are the major cause of familial Alzheimer's disease. Presenilin-1 knockout (PS1-/-) mice develop severe cortical dysplasia related to human type 2 lissencephaly. This overmigration syndrome has been attributed to the premature loss of Cajal-Retzius cells (CRcs), pioneer neurons required for the termination of radial neuronal migration. To elucidate the potential cellular mechanisms responsible for this premature neuronal loss, we investigated the morphological and electrophysiological properties of visually identified CRcs of wild-type (WT) and PS1-/- mouse brains at embryonic day 16.5. The density of CRcs was substantially reduced in the cerebral cortex of PS1-/-.…

Cell Adhesion Molecules NeuronalNerve Tissue ProteinsBiologyBicucullineMembrane PotentialsGABA AntagonistsMicemental disordersExcitatory Amino Acid AgonistsPresenilin-1medicineAnimalsneoplasms6-Cyano-7-nitroquinoxaline-23-dioneCerebral CortexMice KnockoutNeuronsMembrane potentialExtracellular Matrix ProteinsGABAA receptorStem CellsGeneral NeuroscienceSerine EndopeptidasesExcitatory Postsynaptic PotentialsMembrane ProteinsCortical dysplasiaBicucullineEmbryo Mammalianmedicine.diseaseImmunohistochemistryElectric Stimulationdigestive system diseasesnervous system diseasesCell biologyReelin ProteinElectrophysiologymedicine.anatomical_structure2-Amino-5-phosphonovaleratenervous systemCerebral cortexKnockout mouseExcitatory postsynaptic potentialExcitatory Amino Acid AntagonistsNeurosciencemedicine.drugEuropean Journal of Neuroscience
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Nrg1 haploinsufficiency alters inhibitory cortical circuits

2021

Neuregulin 1 (NRG1) and its receptor ERBB4 are schizophrenia (SZ) risk genes that control the development of both excitatory and inhibitory cortical circuits. Most studies focused on the characterization ErbB4 deficient mice. However, ErbB4 deletion concurrently perturbs the signaling of Nrg1 and Neuregulin 3 (Nrg3), another ligand expressed in the cortex. In addition, NRG1 polymorphisms linked to SZ locate mainly in non-coding regions and they may partially reduce Nrg1 expression. Here, to study the relevance of Nrg1 partial loss-of-function in cortical circuits we characterized a recently developed haploinsufficient mouse model of Nrg1 (Nrg1tm1Lex). These mice display SZ-like behavioral d…

Cortical neuronsReceptor ErbB-4Neuregulin-1Gene ExpressionneuronsNeurosciences. Biological psychiatry. NeuropsychiatryHaploinsufficiencyBiologyInhibitory postsynaptic potentialHippocampusMagnetic&nbspMiceInterneuronsNeuregulin 3mental disordersMagnetic resonance spectroscopyAnimalsRNA MessengerneurotransmissionNeuregulin 1GABAergic Neuronsgamma-Aminobutyric AcidInhibitory&nbspCerebral CortexNrg1resonance spectroscopyNeural InhibitionMagnetic Resonance ImagingCortex (botany)Inhibitory neurotransmissionParvalbuminsNeurologyInhibitory Postsynaptic PotentialsCalbindin 2Vesicular Glutamate Transport Protein 1biology.proteinExcitatory postsynaptic potentialSchizophreniaCalretininHaploinsufficiencyCortical&nbspNeuroscienceParvalbuminRC321-571Neurobiology of Disease
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Sox2-Mediated Conversion of NG2 Glia into Induced Neurons in the Injured Adult Cerebral Cortex

2014

Summary The adult cerebral cortex lacks the capacity to replace degenerated neurons following traumatic injury. Conversion of nonneuronal cells into induced neurons has been proposed as an innovative strategy toward brain repair. Here, we show that retrovirus-mediated expression of the transcription factors Sox2 and Ascl1, but strikingly also Sox2 alone, can induce the conversion of genetically fate-mapped NG2 glia into induced doublecortin (DCX)+ neurons in the adult mouse cerebral cortex following stab wound injury in vivo. In contrast, lentiviral expression of Sox2 in the unlesioned cortex failed to convert oligodendroglial and astroglial cells into DCX+ cells. Neurons induced following …

Doublecortin ProteinGene ExpressionBiochemistryArticleMiceSOX2Cortex (anatomy)Basic Helix-Loop-Helix Transcription FactorsGeneticsmedicineAnimalslcsh:QH301-705.5Cell ProliferationCerebral CortexNeuronslcsh:R5-920biologySOXB1 Transcription FactorsCell BiologyAnatomySynaptic PotentialsCellular ReprogrammingDoublecortinASCL1medicine.anatomical_structurelcsh:Biology (General)nervous systemCerebral cortexCell Transdifferentiationbiology.proteinNeurogliaNeuNlcsh:Medicine (General)NeurogliaReprogrammingNeuroscienceDevelopmental BiologyStem Cell Reports
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Pre- and postsynaptic type-1 cannabinoid receptors control the alterations of glutamate transmission in experimental autoimmune encephalomyelitis

2013

Type-1 cannabinoid receptors (CB1R) are important regulators of the neurodegenerative damage in multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis (EAE). In GABAergic striatal neurons, CB1R stimulation exerts protective effects by limiting inflammation-induced potentiation of glutamate-mediated spontaneous excitatory postsynaptic currents (sEPSCs). Here we show that CB1R located on GABAergic or on glutamatergic neurons are differentially involved in the pre- and postsynaptic alterations of sEPSCs caused by EAE in the striatum. After induction of EAE, mice selectively lacking CB1R on GABAergic neurons (GABA-CB1R-KO) showed exacerbated alterations of sEPSC duration in GA…

Encephalomyelitis Autoimmune ExperimentalTime FactorsPostsynaptic CurrentPresynaptic TerminalsExcitotoxicityGlutamic AcidIn Vitro TechniquesBiologyMedium spiny neuronmedicine.disease_causeSynaptic TransmissionMiceCellular and Molecular NeuroscienceGlutamatergicReceptor Cannabinoid CB1Postsynaptic potentialmedicineAnimalsgamma-Aminobutyric AcidMice KnockoutNeuronsPharmacologyExperimental autoimmune encephalomyelitisGlutamate receptorExcitatory Postsynaptic Potentialsmedicine.diseaseCorpus StriatumMice Inbred C57BLnervous systemDisease ProgressionExcitatory postsynaptic potentialFemaleSettore MED/26 - NeurologiaNeuroscience
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Transporter-mediated replacement of extracellular glutamate for GABA in the developing murine neocortex

2013

During early development, cortical neurons migrate from their places of origin to their final destinations where they differentiate and establish synaptic connections. During corticogenesis, radially migrating cells move from deeper zone to the marginal zone, but they do not invade the latter. This "stop" function of the marginal zone is mediated by a number of factors, including glutamate and γ-aminobutyric acid (GABA), two main neurotransmitters in the central nervous system. In the marginal zone, GABA has been shown to be released via GABA transporters (GAT)-2/3, whereas glutamate transporters (EAATs) operate in the uptake mode. In this study, GABAergic postsynaptic currents (GPSCs) were…

GABA Plasma Membrane Transport ProteinsAmino Acid Transport System X-AGGlutamic AcidNeocortexBiologyGABAB receptorMicemedicineAnimalsGABA transporterGABAergic Neuronsgamma-Aminobutyric AcidNeocortexGeneral NeuroscienceSodiumGlutamate receptorDepolarizationSynaptic PotentialsMarginal zoneCell biologyMice Inbred C57BLmedicine.anatomical_structurebiology.proteinGABAergicGABA Uptake InhibitorsNeuroscienceIntracellularEuropean Journal of Neuroscience
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GABA transporters control GABAergic neurotransmission in the mouse subplate.

2015

The subplate is a transient layer between the cortical plate and intermediate zone in the developing cortex. Thalamo-cortical axons form temporary synapses on subplate neurons (SPns) before invading the cortical plate. Neuronal activity within the subplate is of critical importance for the development of neocortical circuits and architecture. Although both glutamatergic and GABAergic inputs on SPns were reported, short-term plasticity of GABAergic transmission has not been investigated yet. GABAergic postsynaptic currents (GPSCs) were recorded from SPns in coronal neocortical slices prepared from postnatal day 3-4 mice using whole-cell patch-clamp technique. Evoked GPSCs (eGPSCs) elicited b…

GABA Plasma Membrane Transport ProteinsGABA Plasma Membrane Transport ProteinsPatch-Clamp TechniquesGABAB receptorBiologyNeurotransmissionSynaptic Transmissiongamma-Aminobutyric acidTissue Culture TechniquesGlutamatergicSubplatemedicinePremovement neuronal activityAnimalsgamma-Aminobutyric AcidGeneral NeuroscienceSomatosensory CortexSynaptic PotentialsReceptors GABA-AElectric StimulationMice Inbred C57BLmedicine.anatomical_structureReceptors GABA-BGABAergicNeurosciencemedicine.drugCentral Nervous System AgentsNeuroscience
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Lack of APP and APLP2 in GABAergic Forebrain Neurons Impairs Synaptic Plasticity and Cognition.

2020

AbstractAmyloid-β precursor protein (APP) is central to the pathogenesis of Alzheimer’s disease, yet its physiological functions remain incompletely understood. Previous studies had indicated important synaptic functions of APP and the closely related homologue APLP2 in excitatory forebrain neurons for spine density, synaptic plasticity, and behavior. Here, we show that APP is also widely expressed in several interneuron subtypes, both in hippocampus and cortex. To address the functional role of APP in inhibitory neurons, we generated mice with a conditional APP/APLP2 double knockout (cDKO) in GABAergic forebrain neurons using DlxCre mice. These DlxCre cDKO mice exhibit cognitive deficits i…

InterneuronCognitive NeuroscienceLong-Term PotentiationSpatial LearningHippocampusAction PotentialsInhibitory postsynaptic potentialHippocampusNesting Behavior03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein PrecursorMice0302 clinical medicineCognitionProsencephalonAmyloid precursor proteinmedicineAnimalsGABAergic NeuronsCA1 Region Hippocampal030304 developmental biologySpatial MemoryMice Knockout0303 health sciencesNeuronal PlasticitybiologyPyramidal CellsExcitatory Postsynaptic PotentialsLong-term potentiationmedicine.anatomical_structurenervous systemInhibitory Postsynaptic PotentialsSynaptic plasticityForebrainExcitatory postsynaptic potentialbiology.proteinNeuroscience030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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mGluR control of interneuron output regulates feedforward tonic GABAA inhibition in the visual thalamus

2011

Metabotropic glutamate receptors (mGluRs) play a crucial role in regulation of phasic inhibition within the visual thalamus. Here we demonstrate that mGluR-dependent modulation of interneuron GABA release results in dynamic changes in extrasynaptic GABAA receptor (eGABAAR)-dependent tonic inhibition in thalamocortical (TC) neurons of the rat dorsal lateral geniculate nucleus (dLGN). Application of the group I selective mGluR agonist dihydroxyphenylglycine produces a concentration-dependent enhancement of both IPSC frequency and tonic GABAA current (IGABAtonic) that is due to activation of both mGluR1a and mGluR5 subtypes. In contrast, group II/III mGluR activation decreases both IPSC freque…

InterneuronReceptors metabotropic glutamateAction PotentialsMetabotropic glutamate receptors GABA dorsal geniculate neurons ratNeurotransmissionReceptors Metabotropic GlutamateQ1DihydroxyphenylglycineSynaptic TransmissionSettore BIO/09 - Fisiologiagamma-Aminobutyric acidArticlechemistry.chemical_compoundThalamusKidney glomerulusInterneuronsmedicineAnimalsVisual Pathwaysgamma-Aminobutyric AcidChemistryGABAA receptorGeneral Neurosciencemusculoskeletal neural and ocular physiologyNeural InhibitionReceptors GABA-ARatsElectrophysiologymedicine.anatomical_structureInhibitory Postsynaptic Potentialsnervous systemMetabotropic glutamate receptorRC0321GABAergicNeuronNeurosciencemedicine.drug
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Subventricular zone neural progenitors protect striatal neurons from glutamatergic excitotoxicity.

2012

The functional significance of adult neural stem and progenitor cells in hippocampal-dependent learning and memory has been well documented. Although adult neural stem and progenitor cells in the subventricular zone are known to migrate to, maintain and reorganize the olfactory bulb, it is less clear whether they are functionally required for other processes. Using a conditional transgenic mouse model, selective ablation of adult neural stem and progenitor cells in the subventricular zone induced a dramatic increase in morbidity and mortality of central nervous system disorders characterized by excitotoxicity-induced cell death accompanied by reactive inflammation, such as 4-aminopyridine-i…

LipopolysaccharidesPolyunsaturated AlkamidesSubventricular zoneGlutamic AcidMice TransgenicArachidonic AcidsBiologyAmidohydrolasesGlutamatergicMiceNeural Stem CellsLateral VentriclesmedicineAnimalsDronabinolProgenitor cell4-Aminopyridineneurogenesis; ischaemia; neural stem cells; excitotoxicity; endocannabinoidsGanciclovirEpilepsyStem CellsNeurogenesisExcitatory Postsynaptic PotentialsNeural stem cellCorpus StriatumNeuroepithelial cellMice Inbred C57BLStrokeneurogenesisDisease Models Animalmedicine.anatomical_structureNeuroprotective AgentsBenzamidesSettore MED/26 - NeurologiaNeurology (clinical)ischaemiaCarbamatesStem cellNeuroscienceexcitotoxicityExcitatory Amino Acid AntagonistsAdult stem cellEndocannabinoidsBrain : a journal of neurology
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