Search results for "channels"

showing 10 items of 411 documents

Multiple actions of glaucine on cyclic nucleotide phosphodiesterases, α1-adrenoceptor and benzothiazepine binding site at the calcium channel

1992

1. In the present study, the properties of glaucine (an aporphine structurally related to papaverine) were compared with those of papaverine, diltiazem, nifedipine and prazosin. The work includes functional studies on rat isolated aorta contracted with noradrenaline, caffeine or KCl, and a determination of the affinity of glaucine at calcium channel binding sites of alpha-adrenoceptors, by use of [3H]-(+)-cis-diltiazem, [3H]-nitrendipine and [3H]-prazosin binding to cerebral cortical membranes. The effects of glaucine on the different molecular forms of cyclic nucleotide phosphodiesterases (PDE) isolated from bovine aorta were also determined. 2. Contraction evoked by noradrenaline (1 micro…

MaleReceptor complexAporphinesPhosphodiesterase InhibitorsStereochemistryAorta ThoracicIn Vitro TechniquesPharmacologyBinding CompetitiveMuscle Smooth VascularNorepinephrineRadioligand Assaychemistry.chemical_compoundPrazosinmedicineAnimalsRats WistarPharmacologyPapaverineVoltage-dependent calcium channelChemistryCalcium channelDihydropyridinePhosphodiesterasePrazosinReceptors Adrenergic alphaGlaucineRats3'5'-Cyclic-AMP Phosphodiesterasescardiovascular systemCattleCalcium ChannelsResearch ArticleMuscle Contractionmedicine.drugBritish Journal of Pharmacology
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The Retinal Clock Drives the Expression ofKcnv2, a Channel Essential for Visual Function and Cone Survival

2012

PURPOSE The gene Kcnv2 codes for the voltage-gated potassium channel subunit Kv8.2, which can coassemble with Kv2.1 subfamily members to constitute functional voltage-gated potassium channels. Mutations in the Kcnv2 gene result in a retinal disorder designated "cone dystrophy with supernormal rod response (CDSRR)," revealing that Kcnv2 is essential for visual processing and cone survival. The aim of this study was to determine whether expression of Kcnv2 and Kv2.1 is under circadian regulation and may thus contribute to the clock-driven adjustment of photoreceptor function. METHODS Expression of the genes was recorded in preparations of the whole retina and microdissected retinal neurons by…

MaleRetinal Disordergenetic structuresCell SurvivalCone dystrophy with supernormal rod responseBlotting WesternBiologyReal-Time Polymerase Chain ReactionRetinaRats Sprague-Dawleychemistry.chemical_compoundShab Potassium ChannelsmedicineTranscriptional regulationAnimalsImmunoprecipitationRNA MessengerGeneVision OcularRetinaRetinalAnatomyAdaptation PhysiologicalPotassium channelCircadian RhythmRatsCell biologymedicine.anatomical_structureReal-time polymerase chain reactionGene Expression RegulationchemistryPotassium Channels Voltage-GatedRetinal Cone Photoreceptor CellsFemalesense organsInvestigative Opthalmology & Visual Science
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L-type calcium channel activity in human atrial myocytes as influenced by 5-HT.

1993

5-Hydroxytryptamine (10 mumol/l; 5-HT) exerted a positive inotropic effect associated with an increase in the Ca2+ current (ICa) in the human right atrium. For detailed analysis, L-type Ca2+ channel currents were recorded from cell-attached patches using 100 mmol/l Ba2+ as charge carrier. Ca2+ channel activity was identified, first, by burst-like inwardly directed currents and, second, by the appearance of long channel openings promoted by Bay K 8644 (1 mumol/l) upon repetitive depolarizations from -80 to 0 mV. The unitary conductance of the Ca2+ channel amounted to 25.8 pS. During superfusion with 5-HT, ensemble averaged (mean) current was enhanced by about 60%. The increase in mean curren…

MaleSerotoninchemistry.chemical_elementAction PotentialsGatingCalciumIn Vitro TechniquesMoleCyclic AMPHumansL-type calcium channelPhosphorylation5-HT receptorAgedPharmacologyMyocardiumIsoproterenolInfantDepolarizationHeartGeneral MedicineAnatomy3-Pyridinecarboxylic acid 14-dihydro-26-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl esterMiddle AgedMyocardial ContractionElectrophysiologyElectrophysiologyKineticschemistryChild PreschoolBiophysicsFemaleCalcium ChannelsIon Channel GatingCommunication channelNaunyn-Schmiedeberg's archives of pharmacology
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Changes in the expression of cation-Cl- cotransporters, NKCC1 and KCC2, during cortical malformation induced by neonatal freeze-lesion.

2007

Focal cortical malformations comprise a heterogeneous group of disturbances in brain development, often associated with intractable epilepsy. A focal freeze-lesion of cerebral cortex in newborn rat produces a cortical malformation that resembles human polymicrogyria, clinical conditions that results from abnormal neuronal migration. The change in GABAergic functions that occurs during early brain development is induced by an alteration in Cl(-) homeostasis and plays important roles in neocortical development by modulating such events as laminar organization and synaptogenesis. We therefore investigated the relationship between pathogenesis of polymicrogyria and ontogeny of Cl(-) homeostasis…

MaleSodium-Potassium-Chloride SymportersSynaptogenesisDown-RegulationBiologyNervous System MalformationsLaminar organizationChloridesCell MovementChloride ChannelsCortex (anatomy)Parietal LobeGlial Fibrillary Acidic ProteinmedicinePolymicrogyriaAnimalsSolute Carrier Family 12 Member 2RNA MessengerRats Wistargamma-Aminobutyric AcidCerebral CortexSymportersGeneral NeuroscienceColocalizationCell DifferentiationGeneral Medicinemedicine.diseaseDenervationImmunohistochemistryMicrogyrusRatsUp-RegulationCold Temperaturemedicine.anatomical_structureNeuronal migration disorderBromodeoxyuridineCerebral cortexPhosphopyruvate HydrataseNeuroscienceBiomarkersNeuroscience research
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USH3A transcripts encode clarin-1, a four-transmembrane-domain protein with a possible role in sensory synapses.

2002

Usher syndrome type 3 (USH3) is an autosomal recessive disorder characterised by the association of post-lingual progressive hearing loss, progressive visual loss due to retinitis pigmentosa and variable presence of vestibular dysfunction. Because the previously defined transcripts do not account for all USH3 cases, we performed further analysis and revealed the presence of additional exons embedded in longer human and mouse USH3A transcripts and three novel USH3A mutations. Expression of Ush3a transcripts was localised by whole mount in situ hybridisation to cochlear hair cells and spiral ganglion cells. The full length USH3A transcript encodes clarin-1, a four-transmembrane-domain protein…

MaleUsher syndromeMolecular Sequence DataBiologyPhotoreceptor cellSynapse03 medical and health sciencesExonMice0302 clinical medicineSequence Analysis ProteinRetinitis pigmentosaHair Cells Auditoryotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansAmino Acid SequenceGenetics (clinical)Spiral ganglionIn Situ HybridizationPhylogeny030304 developmental biology0303 health sciencesGene Expression ProfilingChromosome MappingMembrane ProteinsSequence Analysis DNAmedicine.diseaseCell biologyPedigreeTransmembrane domainmedicine.anatomical_structureMutationSynapsesFemalesense organsHair cellCalcium ChannelsSequence Alignment030217 neurology & neurosurgeryEuropean journal of human genetics : EJHG
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Xenon Improves Neurologic Outcome and Reduces Secondary Injury Following Trauma in an In Vivo Model of Traumatic Brain Injury*

2014

Objectives: To determine the neuroprotective efficacy of the inert gas xenon following traumatic brain injury and to determine whether application of xenon has a clinically relevant therapeutic time window. Design: Controlled animal study. Setting: University research laboratory. Subjects: Male C57BL/6N mice (n = 196). Interventions: Seventy-five percent xenon, 50% xenon, or 30% xenon, with 25% oxygen (balance nitrogen) treatment following mechanical brain lesion by controlled cortical impact. Measurements and Main Results: Outcome following trauma was measured using 1) functional neurologic outcome score, 2) histological measurement of contusion volume, and 3) analysis of locomotor functio…

MaleXenonINTRACRANIAL-PRESSURE1110 NursingCritical Care and Intensive Care MedicineGAIT ABNORMALITIESXenonGaitIntracranial pressureintegumentary systemBrainGLYCINE SITEINTRACEREBRAL-HEMORRHAGED-ASPARTATE RECEPTORNeuroprotective AgentsTreatment OutcomeAnesthesiahead traumaneuroprotectionLife Sciences & BiomedicinePOTASSIUM CHANNELSLocomotioncirculatory and respiratory physiologyinorganic chemicalsTraumatic brain injurychemistry.chemical_elementNeuroprotection1117 Public Health and Health ServicesHead traumaCritical Care MedicineIn vivoGeneral & Internal MedicineAdministration InhalationmedicineAnimalscardiovascular diseasesIntracerebral hemorrhageScience & Technologybusiness.industry1103 Clinical Sciencesbrain injurymedicine.diseaseCONTROLLED CORTICAL IMPACTCOMPETITIVE-INHIBITIONEmergency & Critical Care MedicineMice Inbred C57BLDisease Models AnimalCOGNITIVE DEFICITSchemistryBrain InjuriesClosed head injurybusinessCLOSED-HEAD INJURYinert gasesCritical Care Medicine
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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
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Characterization of a Ryanodine Receptor inPeriplaneta Americana

1997

Specific binding sites for the alkaloid ryanodine were characterized in membrane preparations from sarcoplasmatic reticulum of Periplaneta americana skeletal muscle. Binding of [3H]ryanodine was optimal at pH 8 and at CaCl2 concentration of about 300 mumol l-1. The Ca-chelating agents EGTA (100 mumol l-1) and EDTA (100 mumol l-1) abolished 95% and 90% of the [3H]ryanodine binding respectively. Preincubation with Ca2+ (100 mumol l-1) restored the ryanodine binding in presence of up to 300 mumol l-1 EGTA. Radioligand binding experiments showed one class of high affinity binding sites for ryanodine. Determination of rate constants revealed 7.05 x 10(6) l mol-1 min-1 for associating and 3.77 x …

Maleanimal structuresMuscle ProteinsBiochemistrymedicineAnimalsPeriplanetaheterocyclic compoundsBinding siteEgtazic AcidMolecular BiologyEdetic AcidbiologyRyanodineRyanodine receptorChemistryMusclesAlkaloidSodiumfungiSkeletal muscleRyanodine Receptor Calcium Release ChannelCell BiologyHydrogen-Ion Concentrationbiology.organism_classificationmedicine.anatomical_structureBiochemistryPotassiumCalciumCalmodulin-Binding ProteinsFemaleCalcium ChannelsReticulumPeriplanetaJournal of Receptors and Signal Transduction
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Differences in the nitric oxide/soluble guanylyl cyclase signalling pathway in the myocardium of neonatal and adult rats

2000

Abstract The effects of a nitric oxide-donor, S -nitroso- N -acetylpenicillamine, and a direct activator of soluble guanylyl cyclase, 3-(5′-hydroxymethyl-2′-furyl)-1-benzyl indazole (YC-1), on force of contraction ( F c ) and L-type Ca 2+ currents ( I Ca(L) ) were investigated in myocardial preparations from neonatal and adult rats. Since hearts from adult and neonatal animals contained 160 and 47 mg/100 g wet weight myoglobin, respectively, its possible interaction with both drugs was also investigated. Both S -nitroso- N -acetylpenicillamine (100 μM) and YC-1 (30 μM) were ineffective in myocardial preparations from adult rats but reduced the magnitude of I Ca(L) and F c in preparations fr…

Maleinorganic chemicalsmedicine.medical_specialtyContraction (grammar)Calcium Channels L-Typechemistry.chemical_elementCalciumNitric OxideNitric oxideRats Sprague-Dawleychemistry.chemical_compoundInternal medicinemedicineAnimalsCyclic GMPPharmacologychemistry.chemical_classificationDose-Response Relationship DrugMyoglobinMyocardiumPenicillamineAge FactorsMyocardial ContractionIn vitroRatsEndocrinologyEnzymeAnimals NewbornchemistryMyoglobinGuanylate Cyclasemedicine.symptomSoluble guanylyl cyclaseSignal TransductionMuscle contractionEuropean Journal of Pharmacology
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A1 receptors mediate adenosine inhibitory effects in mouse ileum via activation of potassium channels.

2008

Abstract Aims We investigated the effects induced by exogenous adenosine on the spontaneous contractile activity of the longitudinal muscle of a mouse ileum, the receptor subtypes activated, the involvement of enteric nerves and whether opening of K + channels was a downstream event leading to the observed effects. Main methods Mechanical responses of the mouse ileal longitudinal muscle to adenosine were examined in vitro as changes in isometric tension. Key findings Adenosine caused a concentration-dependent reduction of the spontaneous contraction amplitude of the ileal longitudinal muscle up to its complete disappearance. This effect induced was markedly reduced by an A 1 receptor antago…

Malemedicine.medical_specialtyAdenosinePotassium ChannelsAdenosine A2 Receptor AgonistsMouse ileumBlotting WesternAdenosine A3 Receptor AntagonistsAdenosine A1 Receptor AntagonistsApaminSettore BIO/09 - FisiologiaGeneral Biochemistry Genetics and Molecular BiologyAdenosine A1 receptorchemistry.chemical_compoundMiceAdenosine A3 Receptor AgonistsIleumInternal medicineNeural PathwaysmedicinePotassium Channel BlockersPurinergic P1 Receptor AgonistsAnimalsGeneral Pharmacology Toxicology and PharmaceuticsP1 purinoceptorDose-Response Relationship DrugChemistryReceptor Adenosine A1Mechanical activityMuscle SmoothGeneral MedicinePurinergic signallingIberiotoxinAdenosine A3 receptorAdenosineAdenosine receptorAdenosine A1 Receptor AgonistsAdenosine A2 Receptor AntagonistsMice Inbred C57BLEndocrinologyPurinergic P1 Receptor AntagonistsAdenosine A2B receptormedicine.drugMuscle ContractionLife sciences
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