Search results for " channels."

showing 10 items of 386 documents

A novel KCNQ3 mutation in familial epilepsy with focal seizures and intellectual disability

2015

Mutations in the KCNQ2 gene encoding for voltage-gated potassium channel subunits have been found in patients affected with early onset epilepsies with wide phenotypic heterogeneity, ranging from benign familial neonatal seizures (BFNS) to epileptic encephalopathy with cognitive impairment, drug resistance, and characteristic electroencephalography (EEG) and neuroradiologic features. By contrast, only few KCNQ3 mutations have been rarely described, mostly in patients with typical BFNS. We report clinical, genetic, and functional data from a family in which early onset epilepsy and neurocognitive deficits segregated with a novel mutation in KCNQ3 (c.989G>T; p.R330L). Electrophysiological stu…

MaleGenotype-phenotype correlationmedicine.medical_specialtyNeurologyBenign familial neonatal seizuresMutantGenotype-phenotype correlationsmedicine.disease_causeMutagenesiKCNQ3 Potassium ChannelEpilepsyKCNQBenign Familial Neonatal Seizures KCNQ cognitive impairment voltage-gated potassium channels epilepsy mutagenesis genotype-phenotype correlationsSeizuresSettore M-PSI/08 - Psicologia ClinicaIntellectual DisabilityIntellectual disabilitymedicineHumansKCNQ2 Potassium ChannelVoltage-gated potassium channelBenign familial neonatal seizuresGenetic Predisposition to DiseaseGenetic TestingChildGenetic testingGeneticsMutationEpilepsymedicine.diagnostic_testGenetic heterogeneitybusiness.industryMedicine (all)Benign familial neonatal seizures; Cognitive impairment; Epilepsy; Genotype-phenotype correlations; KCNQ; Mutagenesis; Voltage-gated potassium channels; Child; Female; Genetic Testing; Humans; Intellectual Disability; KCNQ2 Potassium Channel; KCNQ3 Potassium Channel; Male; Mutation; Pedigree; Seizures; Genetic Predisposition to Disease; Neurology (clinical); Neurology; Medicine (all)Benign familial neonatal seizuremedicine.diseaseSeizureSettore MED/39 - Neuropsichiatria InfantilePedigreeCognitive impairmentNeurologyMutagenesisMutationFemaleNeurology (clinical)businessVoltage-gated potassium channelsHuman
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Expression of p11 and Heteromeric TASK Channels in Rat Carotid Body Glomus Cells and Nerve Growth Factor–differentiated PC12 Cells

2020

Psychological stress activates the hypothalamus, augments the sympathetic nervous output, and elevates blood pressure via excitation of the ventral medullary cardiovascular regions. However, anatomical and functional connectivity from the hypothalamus to the ventral medullary cardiovascular regions has not been fully elucidated. We investigated this issue by tract-tracing and functional imaging in rats. Retrograde tracing revealed the rostral ventrolateral medulla was innervated by neurons in the ipsilateral dorsomedial hypothalamus (DMH). Anterograde tracing showed DMH neurons projected to the ventral medullary cardiovascular regions with axon terminals in contiguity with tyrosine hydroxyl…

MaleHistologyNerve Tissue ProteinsProximity ligation assayPC12 Cells03 medical and health sciencesPotassium Channels Tandem Pore Domain0302 clinical medicineGlomus cellmedicineAnimalsHomomericRats WistarAnnexin A2030304 developmental biologyCarotid Body0303 health sciencesChemistryEndoplasmic reticulumS100 ProteinsfungiArticlesImmunohistochemistryRatsCell biologymedicine.anatomical_structureNerve growth factorCytoplasmCarotid bodyAnatomySignal transduction030217 neurology & neurosurgeryJournal of Histochemistry & Cytochemistry
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Acetylsalicylic acid reduces heat responses in rat nociceptive primary sensory neurons – evidence for a new mechanism of action

2002

Acetylsalicylic acid (ASA) is thought to exert its peripheral analgesic effects via inhibition of cyclooxygenase. We now studied the effects of ASA on heat responses in primary nociceptive neurons by whole-cell patch-clamp and calcium microfluorimetry experiments. Heat-evoked inward currents in acutely dissociated rat dorsal root ganglion neurons were significantly reduced by ASA in a dose-dependent and reversible manner (IC(50) 375 nM, Hill slope -2.2, maximum effect 55%). Heat-evoked calcium transients (measured with FURA-2) were reversibly reduced by 53+/-14% (P0.05) by co-application of 1 microM ASA. The low IC(50) value, the rapid occurrence, and the reversibility of the observed effec…

MaleHot TemperaturePatch-Clamp TechniquesPainchemistry.chemical_elementCalciumPharmacologyIon ChannelsMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundDorsal root ganglionGanglia SpinalmedicineAnimalsCyclooxygenase InhibitorsThermosensingCalcium SignalingNeurons AfferentPatch clampCells CulturedAspirinDose-Response Relationship DrugGeneral NeuroscienceNociceptorsMicrofluorimetryElectric StimulationSensory neuronRatsmedicine.anatomical_structurechemistryMechanism of actionBiochemistryCapsaicinNociceptorCalciumCapsaicinmedicine.symptomSignal TransductionNeuroscience Letters
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Changes in cytosolic calcium in response to noxious heat and their relationship to vanilloid receptors in rat dorsal root ganglion neurons.

2001

Heat transduction mechanisms in primary nociceptive afferents have been suggested to involve a vanilloid receptor channel with high calcium permeability. To characterize the changes in free cytosolic calcium evoked by noxious heat stimuli (< or =51 degrees C, 10s), we performed microfluorometric measurements in acutely dissociated small dorsal root ganglion neurons (< or =32.5 microm) of adult rats using the dye FURA-2. Only neurons that responded with a reversible increase in intracellular calcium to high potassium were evaluated. Heat-induced calcium transients (exceeding mean + 3S.D. of the temperature dependence of the dye) were found in 66 of 105 neurons. These transients increased non…

MaleHot Temperaturemedicine.drug_classReceptors Drugchemistry.chemical_elementPainCalcium channel blockerCalciumCalcium in biologyRats Sprague-Dawleychemistry.chemical_compoundCytosolGanglia SpinalmedicineAnimalsThermosensingCalcium SignalingNeurons AfferentCells CulturedFluorescent DyesCalcium metabolismVoltage-dependent calcium channelGeneral NeuroscienceMyocardiumT-type calcium channelNociceptorsRatschemistryBiochemistryCapsaicinBiophysicsPotassiumCalciumFemaleCalcium ChannelsCapsaicinCapsazepineFura-2Signal TransductionNeuroscience
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Novel SCNN1A gene splicing-site mutation causing autosomal recessive pseudohypoaldosteronism type 1 (PHA1) in two Italian patients belonging to the s…

2021

Abstract Introduction Pseudohypoaldosteronism type 1 (PHA1) is a rare genetic disease due to the peripheral resistance to aldosterone. Its clinical spectrum includes neonatal salt loss syndrome with hyponatremia and hypochloraemia, hyperkalemia, metabolic acidosis and increased plasmatic levels of aldosterone. Two genetically distinct forms of disease, renal and systemic, have been described, showing a wide clinical expressivity. Mutations in the genes encoding for the subunits of the epithelial sodium channels (ENaC) are responsible for generalized PHA1. Patients’ presentation We hereby report on two Italian patients with generalized PHA1, coming from the same small town in the center of S…

MaleHyperkalemiaPseudohypoaldosteronismENaCCase ReportGene mutationBioinformaticsPediatricsRJ1-570chemistry.chemical_compoundConsanguinityYoung AdultNext generation sequencingmedicineHumansFamily historyEpithelial Sodium ChannelsSicilyENaC Next generation sequencing SCNN1A gene Splicing mutation Consanguinity Epithelial Sodium Channels Female Humans Infant Newborn Male Mutation Pseudohypoaldosteronism Sicily Young AdultAldosteronebusiness.industryInfant NewbornPseudohypoaldosteronismmedicine.diseasechemistrySCNN1A geneMutation (genetic algorithm)MutationFemalemedicine.symptombusinessHyponatremiaSplicing mutationAuntItalian Journal of Pediatrics
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Involvement of K+ channels in the relaxant effects of YC-1 in vascular smooth muscle

1999

This study addresses the question whether K(+) channels are involved in the vasorelaxant effects of 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl-indazole (YC-1 ). In rat aorta, guinea pig aorta, and guinea pig a. carotis, YC-1 inhibited contractions induced by phenylephrine (3 microM) more potently than those induced by K(+)(48 mM). In rat aorta, tetraethylammonium (10 mM), charybdotoxin (0.2 microM), and iberiotoxin (0.1 microM), but not glibenclamide (10 microM), attenuated the relaxant effects of YC-1. In guinea pig a. carotis, YC-1 (30 microM) induced a hyperpolarisation which was antagonised by 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ; 50 microM). In rat aorta, YC-1 (30 microM) incr…

MaleIndazolesPotassium ChannelsTime FactorsVascular smooth muscleCharybdotoxinMuscle RelaxationGuinea PigsAorta ThoracicIn Vitro TechniquesPharmacologyMuscle Smooth VascularMembrane PotentialsRats Sprague-DawleyGlibenclamidePhenylephrinechemistry.chemical_compoundmedicine.arterymedicineAnimalsDrug InteractionsPhenylephrinePharmacologyAortaTetraethylammoniumDose-Response Relationship DrugChemistryAnatomyIberiotoxinRatsVasodilationCarotid ArteriesPotassiumFemaleZaprinastmedicine.drugEuropean Journal of Pharmacology
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A de novo heterozygous mutation in KCNC2 gene implicated in severe developmental and epileptic encephalopathy

2020

Abstract An increasing number of developmental and epileptic encephalopathies have been correlated with variants of ion channel genes, and in particular of potassium channels genes, such as KCNA1, KCNA2, KCNB1, KCNQ2, KCTD7 and KCNT1. Here we report a child with an early severe developmental and epileptic encephalopathy, spastic tetraplegia, opisthotonos attacks. The whole exome sequencing showed the de novo heterozygous variant c.1411G > C (p.Val471Leu) in the KCNC2 gene. Although this is, to our knowledge, the first case of encephalopathy associated with a KCNC2 gene variant, and further confirmatory studies are needed, previous preclinical and clinical evidence seems to suggest that KCNC…

MaleKCNC2 geneKCTD7EncephalopathyBiologyEpilepsyGeneticsmedicineHumansExomeEEGChildGeneExomeSpastic tetraplegiaGenetics (clinical)Exome sequencingGeneticsEpilepsyKv3.2ElectroencephalographyDevelopmental and epileptic encephalopathieGeneral Medicinemedicine.diseaseKCNC2Shaw Potassium ChannelsNGSMutationEuropean Journal of Medical Genetics
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Role of Ca2+-Activated K+ Channels on Adrenergic Responses of Human Saphenous Vein

2006

Background We studied the participation of K + channels on the adrenergic responses in human saphenous veins as well as the intervention of dihydropyridine-sensitive Ca 2+ channels on modulation of adrenergic responses by K + channels blockade. Methods Saphenous vein rings were obtained from 40 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. Results Iberiotoxin (10 −7 mol/L), an inhibitor of large conductance Ca 2+ -activated K + channels, and charybdotoxin (10 −7 mol/L), an inhibitor of both large and intermediate conductance Ca 2+ -activated K + channels, enhanced the contractions elicited by elec…

MaleNifedipineCharybdotoxinAdrenergicStimulationIn Vitro TechniquesApaminMuscle Smooth VascularNorepinephrinePotassium Channels Calcium-Activatedchemistry.chemical_compoundInternal MedicinemedicineHumansSaphenous VeinChannel blockerbusiness.industryDihydropyridineMiddle AgedIberiotoxinCalcium Channel BlockersElectric StimulationchemistryVasoconstrictionMuscle TonusAnesthesiaBiophysicsFemalemedicine.symptombusinessMuscle contractionmedicine.drugAmerican Journal of Hypertension
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Nitric oxide induces muscular relaxation via cyclic GMP-dependent and -independent mechanisms in the longitudinal muscle of the mouse duodenum

2003

The aim of this study was to investigate, in mouse duodenum, the role of nitric oxide (NO) in the relaxation of longitudinal muscle evoked by nerve activation and the coupled action mechanism. Electrical field stimulation (EFS; 0.5ms, 10-s train duration, supramaximal voltage, at various frequencies) under nonadrenergic noncholinergic conditions evoked muscular relaxation occasionally followed, at the higher stimulus frequencies, by rebound contractions. Inhibition of the synthesis of NO by Nω-nitro-L-arginine methyl ester (L-NAME; 100μM) virtually abolished the evoked relaxation. The relaxation was reduced also by apamin (0.1μM) and by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1μM)…

MaleNitroprussideCancer Researchmedicine.medical_specialtyPotassium ChannelsDuodenumPhysiologyMuscle RelaxationClinical BiochemistryNonadrenergic noncholinergic relaxationStimulationStimulus (physiology)Inhibitory postsynaptic potentialApaminSettore BIO/09 - FisiologiaBiochemistryNitric oxideMicechemistry.chemical_compoundInternal medicineK+ -channelmedicineAnimalsCyclic GMPMolecular BiologyDose-Response Relationship DrugMuscle SmoothNitric oxideElectric StimulationDose–response relationshipEndocrinologychemistryTetrodotoxinSodium nitroprussideMouse duodenummedicine.drugNitric Oxide
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Mechanisms underlying the nitric oxide inhibitory effects in mouse ileal longitudinal muscle

2005

We investigated the mechanisms involved in the nitric oxide (NO)-induced inhibitory effects on longitudinal smooth muscle of mouse ileum, using organ bath technique. Exogenously applied NO, delivered as sodium nitroprusside (SNP; 0.1–100 µmol/L) induced a concentration-dependent reduction of the ileal spontaneous contractions. 1H-[1,2,4]oxadiazolol[4,3,a]quinoxalin-1-one (ODQ; 1 µmol/L), a guanilyl cyclase inhibitor, reduced the SNP-induced effects. Tetraethylammonium chloride (20 mmol/L), a non-selective K+ channel blocker, and charybdotoxin (0.1 µmol/L), blocker of large conductance Ca2+-dependent K+ channels, significantly reduced SNP-induced inhibitory effects. In contrast, apamin (0.1…

MaleNitroprussideThapsigarginCharybdotoxinPhysiologyMouse ileumIn Vitro TechniquesPharmacologyApaminSettore BIO/09 - FisiologiaPotassium channelsMicePotassium Channels Calcium-Activatedchemistry.chemical_compoundIleumPhysiology (medical)Cyclic GMP-Dependent Protein KinasesPotassium Channel BlockersmedicineAnimalsNitric Oxide DonorsChannel blockerCyclic GMPPharmacologyRyanodineRyanodine receptorCalcium storeMuscle SmoothPotassium channel blockerNitric oxideGeneral MedicineTetraethylammonium chlorideMice Inbred C57BLchemistryCalciumSodium nitroprussideMuscle ContractionSignal Transductionmedicine.drug
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