Search results for "Synaptic Transmission"

showing 10 items of 178 documents

Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model.

2021

Abstract Background Dravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. Methods A knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantificati…

MaleProteomics0301 basic medicineProteomeHippocampusEpilepsies MyoclonicHaploinsufficiencyScn1aHippocampusSynaptic TransmissionElevated Plus Maze TestEpilepsyMice0302 clinical medicineTandem Mass Spectrometry11-beta-Hydroxysteroid Dehydrogenase Type 1Genetic epilepsyCarbon-Nitrogen LigasesGene Knock-In TechniquesGliosisNeuronal PlasticityBehavior AnimalEpileptic encephalopathyImmunohistochemistryAstrogliosisNeurologyProteomeDisease ProgressionFemaleHaploinsufficiencySignal TransductionRC321-571Dopamine and cAMP-Regulated Phosphoprotein 32Neovascularization PhysiologicNeurosciences. Biological psychiatry. NeuropsychiatryBiologyNitric Oxide03 medical and health sciencesDravet syndromemedicineAnimalsHyperthermiaSocial Behaviorras-GRF1Proteomic Profilingmedicine.diseaseVascular Endothelial Growth Factor Receptor-2NAV1.1 Voltage-Gated Sodium ChannelDisease Models Animal030104 developmental biologyRotarod Performance TestSynaptic plasticityEpileptic Encephalopathy ; Genetic Epilepsy ; Mice ; Proteome ; Scn1aCalcium-Calmodulin-Dependent Protein Kinase Type 2Open Field TestNeuroscience030217 neurology & neurosurgeryChromatography Liquid
researchProduct

Lateral differences in the GABAergic system of the rat striatum.

1985

Asymmetric differences have been found in the pre- and postsynaptic activity of the GABAergic system of the left and right striata of the rat. 3H-GABA binding shows a higher dissociation constant (KD) and a higher number of sites (Bmax) in the left striatum than in the right. Moreover, 3H-diazepam binding seems to be more extensively activated by GABA in the right striatum suggesting a more sensitive postsynaptic GABAergic activity than on the left side. However, when the presynaptic marker (GAD activity) was measured, the asymmetry was in the opposite direction. The results provide further neurochemical evidence of the functional asymmetry of the rat brain.

MaleRight striatumDermatologyStriatumSynaptic TransmissionRat striatumNeurochemicalPostsynaptic potentialBrain asymmetryAnimalsgamma-Aminobutyric AcidBinding SitesDiazepamChemistryGlutamate DecarboxylaseGeneral NeuroscienceRats Inbred StrainsGeneral MedicineCorpus StriatumRatsDissociation constantPsychiatry and Mental healthnervous system4-Aminobutyrate TransaminaseGABAergicNeurology (clinical)NeuroscienceItalian journal of neurological sciences
researchProduct

Alterations in the spontaneous activity of cells in the guinea pig pineal gland and visual system produced by pineal indoles

1982

The indoles serotonin (SER), melatonin (MEL), 5-methoxytryptophol (5-MTL) and 5-hydroxytryptophol (5-HTL) were administered during daytime microelectrophoretically to 240 cells in the pineal gland of the guniea-pig. The action of SER and 5-HTL was predominantly depressant on the electrical activity, MEL and 5-MTL caused an excitation in most of the units. Although MEL and 5-MTL caused fairly similar reactions on average, they appear to act on different cells. The effects of microelectrophoretically applied MEL and 5-MTL on the spontaneous or evoked activity in the visual system (retinal ganglion cells, optic tract, lateral lateral geniculate body, superior colliculus) of the guinea-pig were…

MaleSerotoninmedicine.medical_specialtyIndolesgenetic structuresOptic tractGuinea PigsVisual systemBiologyPineal GlandSynaptic TransmissionRetinal ganglionRetinaPinealocytePineal glandInternal medicinemedicineAnimalsVisual PathwaysBiological PsychiatryMelatoninNeuronsRetinaSuperior colliculusGeniculate BodiesNeural InhibitionOptic NervePsychiatry and Mental healthmedicine.anatomical_structureEndocrinologyNeurologyHydroxytryptopholOptic nerveNeurology (clinical)psychological phenomena and processesJournal of Neural Transmission
researchProduct

The effects of nitric oxide on striatal serotoninergic transmission involve multiple targets: an in vivo microdialysis study in the awake rat

2004

Abstract The role of endogenous nitric oxide (NO) in N -methyl- d -aspartate (NMDA)-induced modulation of serotonin (5-HT) release in the striatum of freely moving rats has been studied using microdialysis technique. NMDA-induced increase in 5-HT release was significantly inhibited by selective nitric oxide synthase (nNOS) inhibitor S -methylthiocitrulline (S-Me-TC), ONOO − scavenger l -cysteine ( l -cys), and guanylate cyclase (GC) inhibitor 1 H [1,2,4]oxadiazolo[4,3- a ]quinoxalin-1-one (ODQ). These data suggest that modulation of 5-HT levels is linked to the formation of NO produced by NMDA receptor activation and that endogenously produced NO increases 5-HT concentrations both by stimul…

MaleSerotoninmedicine.medical_specialtyMicrodialysisN-MethylaspartateMicrodialysisNitric Oxide Synthase Type IPharmacologyNitric OxideSerotonergicSynaptic TransmissionNitric oxidechemistry.chemical_compoundSuperoxidesPeroxynitrous AcidInternal medicinemedicineAnimalsEnzyme InhibitorsRats WistarNeurotransmitterCyclic GMPMolecular Biologyneurotransmitters; modulators; transporters; and receptors; nitric oxide; serotonin; striatumbiologyGeneral NeuroscienceFree Radical ScavengersRatsNeostriatumNitric oxide synthasePeroxynitrous acidEndocrinologychemistryGuanylate Cyclasebiology.proteinNMDA receptorNeurology (clinical)SerotoninNitric Oxide SynthaseSignal TransductionDevelopmental Biology
researchProduct

Electrophysiological investigations on the central innervation of the rat and guinea-pig pineal gland

1984

The possible influence of central nervous structures on the electrical activity of single pineal cells was investigated in rat and guinea-pig. In the rat electrical stimulation of the hippocampal formation elicited both single cell responses with different latencies and mostly long-term excitations in single pineal cells, while stimulation of the habenular nuclei caused clear orthodromical responses with different latencies, alterations in the rate of spontaneous electrical activity and evoked discharges of "silent" units. In the guinea-pig electrical stimulation of the paraventricular nucleus influenced predominantly cells in the deeper layers of the posterior part of the pineal gland. Ele…

MaleSuperior Colliculiendocrine systemmedicine.medical_specialtyGuinea PigsCentral nervous systemBiologyHippocampusPineal GlandSynaptic TransmissionGuinea pigPineal glandDiencephalonInternal medicineNeural PathwaysmedicineAnimalsEvoked PotentialsBiological PsychiatryBrain MappingSuperior colliculusInferior ColliculiRatsPsychiatry and Mental healthElectrophysiologymedicine.anatomical_structureEndocrinologyHabenulaNeurologyHypothalamusThalamic NucleiNeurology (clinical)Paraventricular Hypothalamic NucleusJournal of Neural Transmission
researchProduct

Interaction Between Uridine and GABA-Mediated Inhibitory Transmission: Studies In Vivo and In Vitro

1985

Na+-independent [3H]gamma-aminobutyric acid (GABA) binding to membrane preparations from frontal cortex, hippocampus, and thalamus is competitively inhibited by the in vitro addition of a naturally occurring pyrimidinic compound, uridine. Moreover, the intraperitoneal injection of uridine produces a dose-related decrease in the cerebellar content of cyclic GMP and antagonizes its increase elicited by bicuculline. The pyrimidinic compound also shows an antagonism toward bicuculline-induced seizures. The relationship between the anti-convulsant actions of uridine and GABA-mediated inhibitory neurotransmission is discussed in terms of an activation of GABA receptor function by the naturally oc…

MaleSynaptic MembranesNeurotransmissionPharmacologyBicucullineInhibitory postsynaptic potentialHippocampusSynaptic Transmissiongamma-Aminobutyric acidchemistry.chemical_compoundThalamusGABA receptorSeizuresIn vivomedicineAnimalsCyclic GMPUridinegamma-Aminobutyric AcidNeurotransmitter AgentsBicucullineReceptors GABA-AUridineIn vitroFrontal LobeRatsnervous systemNeurologychemistryBiochemistryNeurology (clinical)medicine.drugEpilepsia
researchProduct

AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders.

2019

AMPA receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits encoded by GRIA1-4 genes. GluA2 has an especially important role because, following post-transcriptional editing at the Q607 site, it renders heteromultimeric AMPARs Ca2+-impermeable, with a linear relationship between current and trans-membrane voltage. Here, we report heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abnormalities including autism spectrum disorder (ASD), Rett syndrome-like features, and seizures or developmental epileptic encephalopathy (DEE). In functional expression studies, mutations lead to a dec…

Male[SDV.GEN] Life Sciences [q-bio]/GeneticsIon channels in the nervous systemCohort Studiesfluids and secretionsLoss of Function MutationReceptorsAMPAAMPA receptorlcsh:ScienceChildreproductive and urinary physiologyAMPA receptor GluA2 neurodevelopmental disorders autism spectrum disorder glutamatergic synaptic transmission GRIA2neurodevelopmental disordersDevelopmental disordersQNeurodevelopmental disordersBrainMagnetic Resonance ImagingSettore MED/26 - NEUROLOGIAGluA2Child PreschoolFemaleAdultHeterozygoteAdolescentScienceautism spectrum disorderArticleYoung Adult[SDV.MHEP.PED] Life Sciences [q-bio]/Human health and pathology/PediatricsMESH: Intellectual Disability/genetics; Neurodevelopmental Disorders/genetics; Receptors AMPA/genetics; HeterozygoteIntellectual Disabilitymental disordersAdolescent; Adult; Brain; Child; Child Preschool; Cohort Studies; Female; Heterozygote; Humans; Infant; Intellectual Disability; Loss of Function Mutation; Magnetic Resonance Imaging; Male; Neurodevelopmental Disorders; Receptors AMPA; Young AdultHumansReceptors AMPAGRIA2PreschoolIon channel in the nervous system Developmental disorders Synaptic development NG sequencing[SDV.GEN]Life Sciences [q-bio]/Genetics[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/Pediatricsglutamatergic synaptic transmission[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceInfantNG sequencingSynaptic developmentIon channel in the nervous systemNext-generation sequencinglcsh:Q
researchProduct

Nitric oxide-sensitive guanylyl cyclase inhibits acetylcholine release and excitatory motor transmission in the guinea-pig ileum

1997

Abstract This study examined the mechanism through which nitric oxide inhibits the release of acetylcholine and excitatory motor neurotransmission in the guinea-pig ileum. The selective inhibitor of nitric oxide-sensitive guanylyl cyclase, 1 H -[1,2,4]oxadiazolo[4,3- a ]quinoxalin-1-one (ODQ), concentration-dependently enhanced both basal release (−log EC 50 : 6.8) and electrically (10 Hz) -evoked release (−log EC 50 : 6.0) of [ 3 H]acetylcholine from longitudinal muscle-myenteric plexus preparations preincubated with [ 3 H]choline. The increase by ODQ of basal release appeared to be exocytotic since it was prevented by tetrodotoxin (300 nM) and absence of calcium from the superfusion mediu…

Malemedicine.medical_specialtyIndazolesGuinea PigsMyenteric PlexusNeurotransmissionNitric OxideNitroarginineSynaptic TransmissionNitric oxidechemistry.chemical_compoundIleumQuinoxalinesInternal medicinemedicineAnimalsEnzyme InhibitorsNeurotransmitterMyenteric plexusMotor NeuronsOxadiazolesbiologyGeneral NeuroscienceMuscle SmoothAcetylcholineElectric StimulationNitric oxide synthaseEndocrinologychemistryGuanylate CyclaseDepression Chemicalbiology.proteinCholinergicFemaleNitric Oxide SynthaseSoluble guanylyl cyclaseAcetylcholineMuscle Contractionmedicine.drugNeuroscience
researchProduct

Dopamine acting through D2 receptors modulates the expression of PSA-NCAM, a molecule related to neuronal structural plasticity, in the medial prefro…

2008

A "neuroplastic" hypothesis proposes that changes in neuronal structural plasticity may underlie the aetiology of depression and the action of antidepressants. The medial prefrontal cortex (mPFC) is affected by this disorder and shows an intense expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a plasticity-associated molecule, which is expressed mainly in interneurons. The monoamines serotonin, dopamine and noradrenaline are the principal targets of antidepressant action. Pharmacological manipulation of serotonin levels regulates synaptophysin and PSA-NCAM expression in the adult mPFC. However, the involvement of structural plasticity on the antidepress…

Malemedicine.medical_specialtyInterneuronDopamineSynaptophysinPrefrontal CortexNeural Cell Adhesion Molecule L1Synaptic TransmissionDopamine agonistRats Sprague-DawleyDevelopmental NeuroscienceDopamineDopamine receptor D2Internal medicinePhenethylaminesmedicineAnimalsNeuronsAnalysis of VarianceMicroscopy ConfocalNeuronal PlasticityGlutamate DecarboxylaseReceptors Dopamine D2ChemistryDopaminergicDopamine antagonistImmunohistochemistryRatsmedicine.anatomical_structureEndocrinologynervous systemNeurologyDopamine receptorDopamine AgonistsSialic AcidsDopamine AntagonistsHaloperidolNeural cell adhesion moleculeNeurosciencemedicine.drugExperimental Neurology
researchProduct

Streptozotocin diabetic mice display depressive-like behavior and alterations in the structure, neurotransmission and plasticity of medial prefrontal…

2015

Diabetes mellitus patients are at increased risk of developing depression, although the neurobiological bases of this comorbidity are not yet fully understood. These patients show CNS alterations, similar to those found in major depression, including changes in the structure and neurotransmission of excitatory neurons. However, although depressive patients and animal models also display alterations in inhibitory networks, little is known about the effects of diabetes on interneurons. Our main objective was to study the impact of diabetes on interneurons of the medial prefrontal cortex (mPFC), one of the regions most affected by major depression. For this purpose we have induced diabetes wit…

Malemedicine.medical_specialtyInterneuronGlutamate decarboxylaseGreen Fluorescent ProteinsSynaptophysinPrefrontal CortexMice TransgenicNeural Cell Adhesion Molecule L1NeurotransmissionInhibitory postsynaptic potentialSynaptic TransmissionDiabetes Mellitus ExperimentalInterneuronsInternal medicinemedicineAnimalsPrefrontal cortexDepressive DisorderNeuronal PlasticitybiologyGlutamate Decarboxylasemusculoskeletal neural and ocular physiologyGeneral NeuroscienceDendritesTail suspension testEndocrinologymedicine.anatomical_structurenervous systemExcitatory postsynaptic potentialSynaptophysinbiology.proteinSialic AcidsPsychologyNeuroscienceBrain research bulletin
researchProduct