Search results for "clase"

showing 10 items of 319 documents

Hippocampal GABAergic Synapses Possess the Molecular Machinery for Retrograde Nitric Oxide Signaling

2007

Nitric oxide (NO) plays an important role in synaptic plasticity as a retrograde messenger at glutamatergic synapses. Here we describe that, in hippocampal pyramidal cells, neuronal nitric oxide synthase (nNOS) is also associated with the postsynaptic active zones of GABAergic symmetrical synapses terminating on their somata, dendrites, and axon initial segments in both mice and rats. The NO receptor nitric oxide-sensitive guanylyl cyclase (NOsGC) is present in the brain in two functional subunit compositions: α1β1and α2β1. The β1subunit is expressed in both pyramidal cells and interneurons in the hippocampus. Using immunohistochemistry andin situhybridization methods, we describe that the …

MaleInterneuronReceptors Cytoplasmic and NuclearNitric Oxide Synthase Type IBiologyNitric OxideHippocampusSynapseMiceSoluble Guanylyl CyclasemedicineAnimalsHumansRNA MessengerRats Wistargamma-Aminobutyric AcidMice Knockoutmusculoskeletal neural and ocular physiologyGeneral NeuroscienceArticlesAxon initial segmentRatsMice Inbred C57BLmedicine.anatomical_structurenervous systemGuanylate CyclaseSynaptic plasticitySynapsesbiology.proteinRetrograde signalingGABAergicSoluble guanylyl cyclaseNeuroscienceParvalbuminSignal Transduction
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Involvement of cyclic guanosine monophosphosphate (cGMP) and cytosolic guanylate cyclase in the regulation of synaptic ribbon numbers in rat pineal g…

1992

In the rat pineal gland N-acetyltransferase (NAT) activity and synaptic ribbon (SR) numbers display a circadian rhythm. It is well-known that NAT activity is regulated by adrenergic mechanisms involving cyclic adenosine monophosphate (cAMP) as a second messenger. However, the mechanism involved in the regulation of SR numbers has not been established so far. In the present in vitro study, we have investigated the effects of 8-bromo-cyclic guanosine monophosphate (8-bromo-cGMP), a cyclic guanosine monophosphate (cGMP) analog, and stimulation of guanylate cyclase on SR numbers. Incubation with 8-bromo-cGMP increased SR numbers in a dose- and time-dependent manner. Further, stimulation of the …

MaleNitroprussidemedicine.medical_specialtyGuanosineBiologyPineal Glandchemistry.chemical_compoundPineal glandCytosolOrgan Culture TechniquesInternal medicineGuanosine monophosphatemedicineAnimalsCyclic adenosine monophosphateCyclic GMPMolecular BiologyCyclic guanosine monophosphateSynaptic ribbonGeneral NeuroscienceCircadian RhythmRatsEnzyme ActivationMicroscopy Electronmedicine.anatomical_structureEndocrinologyBucladesinechemistryGuanylate CyclaseSynapsesSecond messenger systemNeurology (clinical)Atrial Natriuretic FactorDevelopmental BiologyEndocrine glandBrain Research
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Nitric oxide as neuromodulator of sympathetic transmission in rat vas deferens.

1998

Summary Electrical field stimulation (EFS) of muscle strips in vitro elicited a tetrodotoxin (TTX)-sensitive biphasic contractile response consisting of a phasic component followed by a tonic one. The amplitude of both components of the response was impaired by Nω-nitro-L-arginine and potentiated by sodium nitroprusside. Cystamine caused a reduction in amplitude of both phasic and tonic componets of the response to EFS. Neither Nω-nitro-L-arginine, sodium nitroprusside, nor cystamine induced changes in the resting muscle tone, or in the contractile response to exogenous agonists ATP and noradrenaline (NA). The nitric oxide scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, i…

MaleNitroprussidemedicine.medical_specialtySympathetic Nervous SystemCystamineNeurotransmissionNitric OxideNitroarginineTonic (physiology)Nitric oxideCyclic N-Oxideschemistry.chemical_compoundVas DeferensCystamineInternal medicinemedicineExtracellularAnimalsEnzyme InhibitorsRats WistarPharmacologyGeneral NeuroscienceVas deferensImidazolesElectric StimulationRatsmedicine.anatomical_structureEndocrinologychemistryGuanylate CyclaseTetrodotoxinSodium nitroprussideNitric Oxide Synthasemedicine.drugMuscle ContractionJournal of autonomic pharmacology
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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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MiR-133 Modulates the β1Adrenergic Receptor Transduction Cascade.

2014

Rationale : The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, overactivation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors in cardiomyocytes and lead to increased heart rate and cardiac contractility. However, chronic stimulation of β-adrenergic receptors leads to impaired cardiac function, and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MicroRNA-133 (miR-133) is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of messenger RNA translation/stability. …

MalePhysiologyMessengerheart failureApoptosiscardiomyocytesInbred C57BLSecond Messenger SystemsTransgenicRats Sprague-DawleyBeta-1 adrenergic receptorMiceGenes ReporterReceptorsCyclic AMPGuanine Nucleotide Exchange FactorsMyocytes CardiacAlpha-1D adrenergic receptor3' Untranslated RegionsCells CulturedCulturedbiologyChemistryadrenergic beta-1 receptor antagonists; cardiac; cyclic AMP; heart failure; microRNAs; myocytes; 3' Untranslated Regions; Adenylyl Cyclases; Animals; Apoptosis; Cells Cultured; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Disease Progression; Gene Expression Regulation; Genes Reporter; Guanine Nucleotide Exchange Factors; Male; Metoprolol; Mice; Mice Inbred C57BL; Mice Transgenic; MicroRNAs; Myocardium; Myocytes Cardiac; RNA Messenger; Rats; Rats Sprague-Dawley; Receptors Adrenergic beta-1; Recombinant Fusion Proteins; Second Messenger Systems; Physiology; Cardiology and Cardiovascular Medicine; Medicine (all)Medicine (all)Cell biologyAdrenergicadrenergic beta-1 receptor antagonistsDisease ProgressionCARDIAC HYPERTROPHYSignal transductionCardiology and Cardiovascular MedicineAdenylyl CyclasesMetoprololmedicine.medical_specialtyAdrenergic receptorcardiacCellsRecombinant Fusion ProteinsMice Transgenicbeta-1Alpha-1B adrenergic receptorInternal medicinecAMPmedicineAnimalsRNA MessengerReporterPressure overloadalpha and beta adrenoceptorsMyocytesMyocardiumBeta adrenergic receptor kinaseCyclic AMP-Dependent Protein KinasesAlpha-1A adrenergic receptorRatsMice Inbred C57BLMicroRNAsEndocrinologyGenesGene Expression Regulationbiology.proteinRNASprague-DawleyReceptors Adrenergic beta-1MicroRNAs; alpha and beta adrenoceptors; cardiomyocytes; CARDIAC HYPERTROPHY; cAMP
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Can guanine-based purines be considered modulators of intestinal motility in rodents?

2010

Adenine-based purines play a pivotal role in the control of gastrointestinal motility in rodents. Recently, guanine-based purines have been also shown to exert extracellular effects in the central nervous system raising the possibility of the existence of distinct receptors for guanine-based purines. Thus, it seems likely to speculate that also guanine-based purines may play a role in the modulation of the intestinal contractility. Spontaneous and neurally-evoked mechanical activity was recorded in vitro as changes in isometric tension in circular muscle strips from mouse distal colon. Guanosine up to 3 mM or guanine up to 1 mM failed to affect the spontaneous mechanical activity, but reduc…

MalePurine(Mouse)Time FactorsGuanineGuanineColonGuanosineIn Vitro TechniquesPharmacologyBiologyCircular muscleSettore BIO/09 - FisiologiaAdenylyl cyclaseMicechemistry.chemical_compoundAnimalsPPADSPurine metabolismCholinergic contractionPharmacologyDose-Response Relationship DrugGuanosineBiological TransportBiochemistrychemistryCholinergicGastrointestinal MotilityNucleosideMuscle Contraction
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Induction of RAGE Shedding by Activation of G Protein-Coupled Receptors

2011

The multiligand Receptor for Advanced Glycation End products (RAGE) is involved in various pathophysiological processes, including diabetic inflammatory conditions and Alzheimers disease. Full-length RAGE, a cell surface-located type I membrane protein, can proteolytically be converted by metalloproteinases ADAM10 and MMP9 into a soluble RAGE form. Moreover, administration of recombinant soluble RAGE suppresses activation of cell surface-located RAGE by trapping RAGE ligands. Therefore stimulation of RAGE shedding might have a therapeutic value regarding inflammatory diseases. We aimed to investigate whether RAGE shedding is inducible via ligand-induced activation of G protein-coupled recep…

MaleReceptors Vasopressinendocrine system diseasesReceptor for Advanced Glycation End Productslcsh:MedicineHydroxamic Acids570 Life sciencesRAGE (receptor)Adenylyl cyclaseADAM10 ProteinMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundMolecular Cell BiologyNeurobiology of Disease and RegenerationSignaling in Cellular ProcessesMembrane Receptor SignalingReceptors Immunologiclcsh:ScienceReceptorLungCellular Stress ResponsesCalcium signalingMultidisciplinaryKinaseDipeptidesHormone Receptor SignalingCell biologyMatrix Metalloproteinase 9NeurologyReceptors OxytocinGene Knockdown Techniquescardiovascular systemMatrix Metalloproteinase 2Pituitary Adenylate Cyclase-Activating PolypeptideMedicineRNA InterferenceAdenylyl CyclasesResearch ArticleSignal Transduction570 Biowissenschaftenmedicine.medical_specialtyMAP Kinase Signaling SystemADAM17 ProteinBiologyAlzheimer DiseaseCa2+/calmodulin-dependent protein kinaseInternal medicinemedicineAnimalsHumansProtease InhibitorsCalcium Signalingcardiovascular diseasesBiologyG protein-coupled receptorlcsh:RHEK 293 cellsMembrane Proteinsnutritional and metabolic diseasesCyclic AMP-Dependent Protein KinasesADAM ProteinsG-Protein SignalingHEK293 CellsEndocrinologychemistryProteolysisDementialcsh:QAmyloid Precursor Protein SecretasesMolecular Neurosciencehuman activitiesReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type INeurosciencePLoS ONE
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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
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Effects of nitric oxide-active drugs on the discharge of subthalamic neurons: microiontophoretic evidence in the rat.

2006

The presence of nitric oxide (NO) synthase and of soluble guanylyl cyclase, the main NO-activated metabolic pathway, has been demonstrated in many cells of the subthalamic nucleus. In this study, the effects induced on the firing of 96 subthalamic neurons by microiontophoretically administering drugs modifying NO neurotransmission were explored in anaesthetized rats. Recorded neurons were classified into regularly and irregularly discharging on the basis of their firing pattern. Nω-nitro-l-arginine methyl ester (L-NAME; a NO synthase inhibitor), 3-morpholino-sydnonimin-hydrocloride (SIN-1; a NO donor), S-nitroso-glutathione (SNOG; another NO donor) and 8-Br-cGMP (a cell-permeable analogue o…

MaleTime FactorsAction PotentialsNeurotransmissionInhibitory postsynaptic potentialNitric OxideSettore BIO/09 - FisiologiaNitric oxideS-Nitrosoglutathionechemistry.chemical_compoundSubthalamic NucleusAnimalsNitric Oxide DonorsEnzyme InhibitorsRats WistarCyclic GMPNeuronsAnalysis of VarianceIontophoresisDose-Response Relationship DrugChemistryGeneral Neuroscience8-Br-cGMP L-NAME SIN-1 SNOG subthalamic nucleusIontophoresisThionucleotidesRatsEnzyme ActivationSubthalamic nucleusNG-Nitroarginine Methyl EsterMolsidomineS-NitrosoglutathioneExcitatory postsynaptic potentialSoluble guanylyl cyclaseNeuroscience
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Chronic lithium salt treatment reduces CRE/CREB-directed gene transcription and reverses its upregulation by chronic psychosocial stress in transgeni…

2007

The molecular mechanism of action of the mood stabilizer lithium is assumed to involve changes in gene expression leading to neuronal adaptation. The transcription factor CREB (cAMP-responsive element binding protein) regulates the expression of many genes and has been implicated in important brain functions and the action of psychogenic agents. We here investigated the effect of lithium on cAMP-responsive element (CRE)/CREB-mediated gene transcription in the brain, using transgenic reporter mice that express the luciferase reporter gene under the control of four copies of the rat somatostatin gene promoter CRE. Chronic (21 days) but not acute (24 h) treatment with lithium (7.5 mmol/kg) sig…

MaleTranscriptional ActivationBipolar DisorderTransgeneDown-RegulationMice TransgenicCREBDrug Administration Schedule03 medical and health sciencesGlycogen Synthase Kinase 3Mice0302 clinical medicineGSK-3Transcription (biology)Antimanic AgentsGenes ReporterGene expressionAnimalsPhosphorylationProtein kinase ACyclic AMP Response Element-Binding ProteinSocial BehaviorTranscription factor030304 developmental biologyPharmacology0303 health sciencesReporter genebiologyBehavior AnimalBrainMolecular biologyUp-RegulationPsychiatry and Mental healthDisease Models AnimalGene Expression RegulationChronic Diseasebiology.proteinLithium Compounds030217 neurology & neurosurgeryStress PsychologicalAdenylyl CyclasesSignal TransductionNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
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