Search results for " channels."

showing 10 items of 386 documents

Ca2+-activated K+ channels mediate relaxation of forearm veins in chronic renal failure

2003

In arteries, agonists such as acetylcholine release an endothelium-derived hyperpolarizing factor (EDHF) that is neither nitric oxide nor prostacyclin.To examine the responses to acetylcholine in segments of forearm veins from patients with chronic renal failure who either had never received dialysis or had undergone long-term dialysis, and to determine the contribution of nitric oxide and EDHF to endothelium-dependent relaxation in veins from patients with chronic renal failure.Isometric tension was recorded in rings of forearm vein from 34 non-dialysed patients, 27 dialysed patients and 14 multiorgan donors (controls).Relaxation in response to acetylcholine was reduced in veins of non-dia…

MaleNitroprussidemedicine.medical_specialtyPhysiologyVasodilator AgentsVasodilationIn Vitro TechniquesNitric OxideVeinsNitric oxideBiological FactorsPotassium Channels Calcium-Activatedchemistry.chemical_compoundForearmQuinoxalinesInternal medicineInternal MedicinemedicineHumansEnzyme InhibitorsVeinOxadiazolesomega-N-MethylarginineVascular diseasebusiness.industryMiddle Agedmedicine.diseaseAcetylcholinePotassium channelVasodilationForearmEndocrinologymedicine.anatomical_structurechemistrycardiovascular systemKidney Failure ChronicFemaleNitric Oxide SynthaseCardiology and Cardiovascular MedicinebusinessAcetylcholineKidney diseasemedicine.drugJournal of Hypertension
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Mechanisms underlying hyperpolarization evoked by P2Y receptor activation in mouse distal colon

2006

In murine colonic circular muscle, ATP mediates fast component of the nerve-evoked inhibitory junction potentials, via activation of P2Y receptors and opening of apamin-sensitive Ca2+-dependent K+ channels. We investigated, using microelectrode recordings, the intracellular events following P2Y-receptor activation by electrical field stimulation or by adenosine 5'-O-2-thiodiphosphate (ADPbetaS), ATP stable analogue. The fast-inhibitory junction potential amplitude was reduced by thapsigargin or ciclopiazonic acid (CPA), sarcoplasmic reticulum Ca2+-ATPase inhibitors, by ryanodine, which inhibits Ca2+ release from ryanodine-sensitive stores, and by 9-(tetrahydro-2-furanyl)-9H-purin-6-amine (S…

MaleP2Y receptormedicine.medical_specialtyThapsigarginColonMouse colonBiologyApaminSettore BIO/09 - FisiologiaEnteric inhibitory neurotransmissionAdenylyl cyclaseMicePotassium Channels Calcium-Activatedchemistry.chemical_compoundIntracellular microelectrode recordingReceptors Adrenergic alpha-1Internal medicinemedicineAnimalsCalcium-dependent potassium channelNeuronsPharmacologyModels StatisticalForskolinDose-Response Relationship DrugReceptors Purinergic P2Ryanodine receptorColforsinCalcium storeP2Y receptorHyperpolarization (biology)Inositol trisphosphate receptorElectrophysiologyMice Inbred C57BLEndocrinologychemistryBiophysicsCalciumAdenylyl CyclasesEuropean Journal of Pharmacology
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Ceramide inhibits Kv currents and contributes to TP-receptor-induced vasoconstriction in rat and human pulmonary arteries

2011

et al.

MalePatch-Clamp TechniquesPhysiologyReceptors ThromboxaneSpider Venoms030204 cardiovascular system & hematologyMuscle Smooth VascularMembrane Potentialschemistry.chemical_compound0302 clinical medicineHypoxic pulmonary vasoconstrictionVasoconstrictor AgentsProtein Kinase C0303 health sciencesAniline Compounds3. Good healthSphingomyelin Phosphodiesterasemedicine.anatomical_structurePotassium Channels Voltage-GatedCirculatory systemmedicine.symptomSphingomyelinSignal TransductionBlood vesselmedicine.medical_specialtyCeramidePhosphinesMyocytes Smooth MusclePulmonary ArteryBiologyCeramidesBenzylidene Compounds03 medical and health sciencesInternal medicinemedicineAnimalsHumansRats Wistar030304 developmental biologyCell BiologySphingolipidRatsHEK293 CellsEndocrinologychemistryVasoconstriction15-Hydroxy-11 alpha9 alpha-(epoxymethano)prosta-513-dienoic AcidVascular resistanceVascular ResistancePeptidesVasoconstrictionAmerican Journal of Physiology-Cell Physiology
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Elevation in type I interferons inhibits HCN1 and slows cortical neuronal oscillations

2014

Central nervous system (CNS) inflammation involves the generation of inducible cytokines such as interferons (IFNs) and alterations in brain activity, yet the interplay of both is not well understood. Here, we show that in vivo elevation of IFNs by viral brain infection reduced hyperpolarization-activated currents (Ih) in cortical pyramidal neurons. In rodent brain slices directly exposed to type I IFNs, the hyperpolarization-activated cyclic nucleotide (HCN)-gated channel subunit HCN1 was specifically affected. The effect required an intact type I receptor (IFNAR) signaling cascade. Consistent with Ih inhibition, IFNs hyperpolarized the resting membrane potential, shifted the resonance fre…

MalePatch-Clamp TechniquesPotassium Channelsmedicine.medical_treatmentNeocortexInbred C57BLchemistry.chemical_compoundMiceReceptorsHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsReceptors InterferonMembrane potentialCerebral CortexNeuronsBlottingElectroencephalographyImmunohistochemistryCytokinemedicine.anatomical_structureInterferon Type IInterferonCytokinesSignal transductionWesternmedicine.drugSignal TransductionCognitive NeuroscienceCentral nervous systemBlotting WesternElectrophysiological ProcessesBiologyReal-Time Polymerase Chain ReactionTransfectionCellular and Molecular NeuroscienceCyclic nucleotidemedicineAnimalsHumansComputer SimulationIon channelNeuroinflammationInterferon-betaElectrophysiological PhenomenaRatsMice Inbred C57BLHEK293 CellschemistryNerve NetNeuroscienceInterferon type I
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Heterozygous nonsense SCN5A mutation W822X explains a simultaneous sudden infant death syndrome.

2008

The sudden, unexpected, and unexplained death of both members of a set of healthy twins (simultaneous sudden infant death syndrome (SSIDS)) is defined as a case in which both infants meet the definition of sudden infant death syndrome individually. A search of the world medical literature resulted in only 42 reported cases of SSIDS. We report the case of a pair of identical, male, monozygotic twins, 138 days old, who suddenly died, meeting the full criteria of SSIDS and where a genetic screen was performed, resulting in a heterozygous nonsense SCN5A mutation (W822X) in both twins. Immunohistochemistry was performed on cardiac tissue samples utilizing polyclonal antibodies anti-Na+ CP type V…

MalePathologymedicine.medical_specialtyNav1.5 protein functionv1.5 protein functionmedia_common.quotation_subject2734Nonsense mutationNonsenseNa+ channel functionMuscle ProteinsSocio-culturaleBiology+Nav1.5 protein function; Na+ channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutation; Codon Nonsense; Diseases in Twins; Humans; Infant; Male; Muscle Proteins; NAV1.5 Voltage-Gated Sodium Channel; Sodium Channels; Sudden Infant Death; 2734Sudden deathSodium ChannelsNAV1.5 Voltage-Gated Sodium ChannelPathology and Forensic MedicinePathogenesisSCN5A gene mutationDiseases in TwinsmedicineHumansSimultaneous sudden infant death syndromeSCN5A gene mutationW822X mutationNa+ channel functionNav1.5 protein functionNaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein function CodonMolecular BiologyCellular localizationmedia_commonSimultaneous sudden infant death syndromeSettore BIO/16 - Anatomia UmanaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein functionW822X mutationInfantCell BiologyGeneral MedicineSudden infant death syndromeNonsenseTerminal deoxynucleotidyl transferaseCodon NonsenseImmunohistochemistryNa; v; 1.5 protein function; Na; +; channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutationchannel functionSudden Infant Death
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Further delineation of eye manifestations in homozygous 15q13.3 microdeletions including TRPM1: a differential diagnosis of ceroid lipofuscinosis.

2014

The 15q13.3 heterozygous microdeletion is a fairly common microdeletion syndrome with marked clinical variability and incomplete penetrance. The average size of the deletion, which comprises six genes including CHRNA7, is 1.5 Mb. CHRNA7 has been identified as the gene responsible for the neurological phenotype in this microdeletion syndrome. Only seven patients with a homozygous microdeletion that includes at least CHRNA7, and is inherited from both parents have been described in the literature. The aim of this study was to further describe the distinctive eye manifestations from the analysis in the three French patients diagnosed with the classical 1.5 Mb homozygous microdeletion. Patients…

MalePathologymedicine.medical_specialtygenetic structuresalpha7 Nicotinic Acetylcholine ReceptorEncephalopathyTRPM Cation ChannelsChromosome DisordersBiologyBlindnessEyePupilNeuronal Ceroid-LipofuscinosesNight BlindnessSeizuresIntellectual DisabilityRetinal DystrophiesGeneticsmedicineElectroretinographyMyopiaHumansEye AbnormalitiesChildGenetics (clinical)TRPM1Genetic Association StudiesCongenital stationary night blindnessGeneticsChromosomes Human Pair 15DystrophyEye Diseases HereditaryGenetic Diseases X-LinkedOptic NerveMicrodeletion syndromemedicine.diseasePenetranceChild PreschoolFemalesense organsDifferential diagnosisChromosome DeletionAmerican journal of medical genetics. Part A
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Transient Receptor Potential Channel Polymorphisms Are Associated with the Somatosensory Function in Neuropathic Pain Patients

2011

Transient receptor potential channels are important mediators of thermal and mechanical stimuli and play an important role in neuropathic pain. The contribution of hereditary variants in the genes of transient receptor potential channels to neuropathic pain is unknown. We investigated the frequency of transient receptor potential ankyrin 1, transient receptor potential melastin 8 and transient receptor potential vanilloid 1 single nucleotide polymorphisms and their impact on somatosensory abnormalities in neuropathic pain patients. Within the German Research Network on Neuropathic Pain (Deutscher Forscbungsverbund Neuropathischer Schmerz) 371 neuropathic pain patients were phenotypically ch…

MalePharmacologyTransient receptor potential channelTransient Receptor Potential ChannelsAnesthesiologyMolecular Cell BiologyMembrane Receptor SignalingMultidisciplinaryQRMiddle AgedNeurologyHyperalgesiaNeuropathic painMedicineFemaleSensory Perceptionmedicine.symptomResearch ArticleSignal TransductionAdultAnkyrinsGenotypeScienceMedizinische Fakultät -ohne weitere Spezifikation-Receptor potential610TRPV Cation ChannelsSensory systemSingle-nucleotide polymorphism-Polymorphism Single NucleotidemedicineGeneticsHumansPain ManagementGenetic Predisposition to Diseaseddc:610BiologyGenetic Association StudiesAgedHypoalgesiaPolymorphism GeneticPopulation Biologybusiness.industryHuman Geneticsmedicine.diseaseNeuralgiaGenetic PolymorphismNeuralgiabusinessPopulation GeneticsNeuroscience
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A binary genetic approach to characterize TRPM5 cells in mice

2015

International audience; Transient receptor potential channel subfamily M member 5 (TRPM5) is an important downstream signaling component in a subset of taste receptor cells making it a potential target for taste modulation. Interestingly, TRPM5 has been detected in extra-oral tissues; however, the function of extra-gustatory TRPM5-expressing cells is less well understood. To facilitate visualization and manipulation of TRPM5-expressing cells in mice, we generated a Cre knock-in TRPM5 allele by homologous recombination. We then used the novel TRPM5-IRES-Cre mouse strain to report TRPM5 expression by activating a tau GFP transgene. To confirm faithful coexpression of tau GFP and TRPM5 we gene…

MalePhysiologytaste papillaegene targetingBehavioral NeuroscienceMice0302 clinical medicineTaste receptor[SDV.IDA]Life Sciences [q-bio]/Food engineeringGene Knock-In TechniquesIn Situ Hybridization Fluorescence0303 health sciencestaste budsiresGene targetingrosa26ImmunohistochemistrySensory SystemsCell biologyknock inmedicine.anatomical_structuretrpm5taste receptor cellsFemaleGenotypeTransgeneCre recombinaseTRPM Cation ChannelsMice TransgenicBiologyAntibodiestgfpseptal organ of masera03 medical and health sciencesOlfactory MucosaTonguemicrovillar cellsPhysiology (medical)Gene knockinmedicineAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringTRPM5cre recombinaseAlleles030304 developmental biologyPalateMice Inbred C57BLvomeronasal organolfactory epitheliumgastrointestinal tractHomologous recombinationOlfactory epithelium030217 neurology & neurosurgery
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Sequence-based bioinformatic prediction and QUASEP identify genomic imprinting of the KCNK9 potassium channel gene in mouse and human

2007

Genomic imprinting is the epigenetic marking of gene subsets resulting in monoallelic or predominant expression of one of the two parental alleles according to their parental origin. We describe the systematic experimental verification of a prioritized 16 candidate imprinted gene set predicted by sequence-based bioinformatic analyses. We used Quantification of Allele-Specific Expression by Pyrosequencing (QUASEP) and discovered maternal-specific imprinted expression of the Kcnk9 gene as well as strain-dependent preferential expression of the Rarres1 gene in E11.5 (C57BL/6 3 Cast/Ei)F1 and informative (C57BL/6 3 Cast/ Ei) 3 C57BL/6 backcross mouse embryos. For the remaining 14 candidate impr…

MalePotassium ChannelsBiologyPolymorphism Single NucleotideGenomic ImprintingMiceChromosome 15Potassium Channels Tandem Pore DomainGeneticsAnimalsHumansEpigeneticsImprinting (psychology)AlleleMolecular BiologyGeneGenetics (clinical)GeneticsBase SequenceBrainComputational BiologySequence Analysis DNAGeneral MedicineDNA MethylationMice Inbred C57BLCpG siteDNA methylationCpG IslandsFemaleGenomic imprintingHuman Molecular Genetics
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Components of after-hyperpolarization in magnocellular neurones of the rat supraoptic nucleusin vitro

1998

1. The pharmacological sensitivity of hyperpolarizing components of spike train after-potentials was examined in sixty-one magnocellular neurones of the rat supraoptic nucleus using intracellular recording techniques in a brain slice preparation. 2. In 26 % of all neurones a slow after-hyperpolarization (AHP) was observed in addition to a fast AHP. In 31 % of all neurones a depolarizing after-potential (DAP) was observed. 3. The fast AHP was blocked by apamin whereas the slow AHP was blocked by charybdotoxin (ChTX). The DAP was enhanced by ChTX or a DAP was unmasked if not present during the control period. 4. Low concentrations of TEA (0.15-1.5 mM) induced effects on the slow AHP and the D…

MalePotassium ChannelsCharybdotoxinPhysiologySpike trainAction PotentialsApaminSupraoptic nucleusRats Sprague-DawleySK channelchemistry.chemical_compoundSlice preparationAnimalsNeuronsKv1.3 Potassium ChannelVoltage-gated ion channelChemistryMargatoxinTetraethylammoniumOriginal ArticlesIberiotoxinImmunohistochemistryRatsElectrophysiologyApaminPotassium Channels Voltage-GatedBiophysicsSupraoptic NucleusNeuroscienceThe Journal of Physiology
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