Search results for "CHANNELS"

showing 10 items of 411 documents

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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Increased Hypoxic Tolerance by Chemical Inhibition of Oxidative Phosphorylation: “Chemical Preconditioning”

1997

A short ischemic episode preceding sustained ischemia is known to increase tolerance against ischemic cell death. We report early-onset long-lasting neuroprotection against in vitro hypoxia by preceding selective chemical inhibition of oxidative phosphorylation: “chemical preconditioning.” The amplitude of CA1population spikes (psap) in hippocampal slices prepared from control animals (control slices) was 31 ± 27% (mean ± SD) upon 45-min recovery from 15-min in vitro hypoxia. In slices prepared from animals treated in vivo with 20 mg/kg 3-nitropropionate (3-np) 1–24 h prior to slice preparation (preconditioned slices), psap improved to 90 ± 15% (p < 0.01). Posthypoxic oxygen free radical…

MalePotassium ChannelsFree RadicalsPopulationIschemiaNerve Tissue ProteinsBiologyPharmacologyHippocampusNeuroprotectionOxidative PhosphorylationBrain Ischemia030218 nuclear medicine & medical imagingGlibenclamide03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSlice preparationIn vivoGlyburidemedicineAnimalsEnzyme InhibitorsRats WistarHypoxia BraineducationNeuronseducation.field_of_studyAntagonistHypoxia (medical)NADNitro Compoundsmedicine.diseaseCell HypoxiaRatsSuccinate DehydrogenaseNeuroprotective AgentsNeurologyAnesthesiaNeurology (clinical)Propionatesmedicine.symptomReactive Oxygen SpeciesCardiology and Cardiovascular Medicine030217 neurology & neurosurgerymedicine.drugJournal of Cerebral Blood Flow & Metabolism
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Switching between persistent firing and depolarization block in individual rat CA1 pyramidal neurons

2018

The hippocampal formation plays a role in mnemonic tasks and epileptic discharges in vivo. In vitro, these functions and malfunctions may relate to persistent firing (PF) and depolarization block (DB), respectively. Pyramidal neurons of the CA1 field have previously been reported to engage in either PF or DB during cholinergic stimulation. However, it is unknown whether these cells constitute disparate populations of neurons. Furthermore, it is unclear which cell-specific peculiarities may mediate their diverse response properties. However, it has not been shown whether individual CA1 pyramidal neurons can switch between PF and DB states. Here, we used whole cell patch clamp in the current …

MalePotassium ChannelsPatch-Clamp Techniquesantagonists & inhibitors [TRPC Cation Channels]physiology [Electrophysiological Phenomena]Cognitive Neurosciencepharmacology [Muscarinic Agonists]metabolism [TRPC Cation Channels]drug effects [Pyramidal Cells]HippocampusStimulationMuscarinic AgonistsIn Vitro TechniquesHippocampal formation050105 experimental psychologyMembrane Potentialspharmacology [Carbachol]03 medical and health sciences0302 clinical medicineCurrent clampAnimalsRats Long-Evans0501 psychology and cognitive sciencesddc:610Patch clampCA1 Region HippocampalTRPC Cation Channelsphysiology [CA1 Region Hippocampal]Dose-Response Relationship Drugphysiology [Pyramidal Cells]ChemistryPyramidal Cells05 social sciencescytology [CA1 Region Hippocampal]drug effects [Membrane Potentials]Depolarizationmetabolism [Potassium Channels]drug effects [Electrophysiological Phenomena]Potassium channelElectrophysiological PhenomenaRatsdrug effects [CA1 Region Hippocampal]CholinergicCarbacholFemaleNeuroscience030217 neurology & neurosurgeryHippocampus
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Diminished neurogenic femoral artery vasoconstrictor response in a Zucker obese rat model: differential regulation of NOS and COX derivatives.

2014

Objective: Peripheral arterial disease is one of the macrovascular complications of type 2 diabetes mellitus. This study addresses femoral artery regulation in a prediabetic model of obese Zucker rats (OZR) by examining cross-talk between endothelial and neural factors. Methods and Results: Arterial preparations from lean (LZR) and OZR were subjected to electrical field stimulation (EFS) on basal tone. Nitric oxide synthase (NOS) and cyclooxygenase (COX) isoform expression patterns were determined by immunohistochemical labelling and Western blotting. Results indicate significantly reduced noradrenergic contractions in preparations from OZR compared with those of LZR. Functional inhibition …

MalePotassium ChannelsPhysiologylcsh:MedicineFemoral arteryCardiovascular PhysiologyBioinformaticsVascular Medicinechemistry.chemical_compoundSuperoxidesEnosMedicine and Health SciencesEndothelial dysfunctionlcsh:ScienceNeuronsDiabetisMultidisciplinarybiologyFemoral ArteryIsoenzymesVasodilationNitric oxide synthasemedicine.anatomical_structuremedicine.symptomResearch Articlemedicine.medical_specialtyEndotheliumMedicinaCardiologyEndothelial NOSCardiovascular PharmacologyNitric oxidemedicine.arteryInternal medicinemedicineAnimalsObesityVascular DiseasesPharmacologybusiness.industrylcsh:RBiology and Life Sciencesmedicine.diseasebiology.organism_classificationElectric StimulationRats ZuckerDisease Models AnimalEndocrinologychemistryProstaglandin-Endoperoxide SynthasesVasoconstrictionbiology.proteinFisiologia humanalcsh:QEndothelium VascularNitric Oxide SynthasebusinessVasoconstrictionPLoS ONE
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Different mechanisms of the inhibition of the transient outward current in rat ventricular myocytes.

1994

The mechanism of drug-induced inhibition of the transient outward current, Ito, has been investigated in rat ventricular myocytes using the whole cell patch clamp technique. Ito was activated by 300 ms depolarizing voltage clamp steps in 10 mV increments from −50 mV up to +40 mV. At +40 mV, Ito peaked after about 3 ms, and the time course of inactivation was appropriately described by two time constants, τfast = 17 ms and τslow = 203 ms. Verapamil, quinidine sulfate and nifedipine preferentially depressed Ito at the end of the 300 ms depolarizing voltage clamp step; the inactivation of Ito was accelerated by all drugs, whereas peak Ito was less affected. The time course of drug action at +4…

MalePotassium ChannelsVoltage clampHeart VentriclesPharmacologydigestive systemMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundQuinidine SulfateNifedipinemedicineAnimalsVentricular FunctionPatch clampCells CulturedPharmacologyMembrane potentialCardiac transient outward potassium currentMyocardiumHeartGeneral MedicineTetraethylammonium chlorideRatsElectrophysiologychemistryBiophysicsVerapamilmedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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Two distinct phenotypes, hemiplegic migraine and episodic Ataxia type 2, caused by a novel common CACNA1A variant

2020

Abstract Background To investigate the genetic and environmental factors responsible for phenotype variability in a family carrying a novel CACNA1A missense mutation. Mutations in the CACNA1A gene were identified as responsible for at least three autosomal dominant disorders: FHM1 (Familial Hemiplegic Migraine), EA2 (Episodic Ataxia type 2), and SCA6 (Spinocerebellar Ataxia type 6). Overlapping clinical features within individuals of some families sharing the same CACNA1A mutation are not infrequent. Conversely, reports with distinct phenotypes within the same family associated with a common CACNA1A mutation are very rare. Case presentation A clinical, molecular, neuroradiological, neuropsy…

MaleProbandmedicine.medical_specialtyNeurologyMigraine with AuraFamilial hemiplegic migraine type 1Mutation MissenseneuropsychologyCase Reportmedicine.disease_causeNystagmus Pathologiclcsh:RC346-42903 medical and health sciences0302 clinical medicinemedicineHumansSpinocerebellar ataxia type 6Missense mutationFamilyChildFamilial hemiplegic migrainelcsh:Neurology. Diseases of the nervous system030304 developmental biologyEpisodic ataxiaGenetics0303 health sciencesMutationbusiness.industryCACNA1A geneEpisodic ataxia type2Cognitive affective syndromeGeneral Medicinemedicine.diseasePhenotypePhenotypeAtaxiaCalcium ChannelsNeurology (clinical)businessCognitive affective syndrome neuropsychology.030217 neurology & neurosurgeryBMC Neurology
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Selective action of two aporphines at alpha 1-adrenoceptors and potential-operated Ca2+ channels.

1993

Abstract Contractions evoked by noradrenaline (1 μM) or a depolarizing solution of 60 mM KCI were concentration dependently depressed by the aporphine alkaloids (S)-boldine and (R)-apomorphine in rataorta. Both drugs had a greater inhibitory potency on the contraction elicited by noradrenaline. Dose-response curves for noradrenaline were shifted to the right in presence of (S)-boldine. (R)-Apomorphine acted by a complex mechanism at α 1 -adrenoceptors and its inhibitory effects was irreversible. The conformational features of these alkaloids may explain their different behaviour at α 1 -adrenoceptors. In Ca 2+ -free solution, the alkaloids inhibited the contraction evoked by noradrenaline b…

MaleReceptor complexAporphinesApomorphineStereochemistryPhosphodiesterase InhibitorsMolecular ConformationIn Vitro TechniquesMuscle Smooth VascularPotassium Chloridechemistry.chemical_compoundNorepinephrineRadioligand AssaymedicinePrazosinBoldineAnimalsAporphineRats WistarEvoked PotentialsPharmacologyMembranesAlkaloidDihydropyridinePhosphodiesteraseReceptors Adrenergic alphaRatsAntitussive AgentsMechanism of actionchemistryCattleCalcium Channelsmedicine.symptommedicine.drugMuscle ContractionEuropean journal of pharmacology
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