Search results for "agonist"

showing 10 items of 2285 documents

The role of (E)-6-chloro-3-(3-methyl-1-phenyl-1H-pyrazol-5-yl)-2-styrylquinazolin-4(3H)-one in the modulation of cannabinoidergic system. A pilot stu…

2018

Abstract Background Compounds acting on endocannabinoid system regulate different neuronal processes through the cannabinoid receptors activation. The main aim of this study was determining whether the 2-styrylquinazolin-4(3H)-one 5, a structural analogue of rimonabant, was able to counteract the behavioural signs of the activation of the endocannabinoidergic system induced by CP 55.940. Methods Behavioural assessment was carried out using the tetrad task and the novel object recognition test. The endocannabinoidergic system activation was possible by the administration of CP 55.940 and 30 min after rats were tested in the tetrad task for the evaluation of the antinociceptive-, cataleptic-,…

0301 basic medicineAgonistCannabinoid receptormedicine.drug_classmedicine.medical_treatmentPilot ProjectsPharmacologyCannabinoidergicStyrenes03 medical and health sciences0302 clinical medicineRimonabantmedicineAnimalsRats WistarLatency (engineering)PharmacologyDose-Response Relationship DrugCannabinoid CB1 receptor antagonist Quinazolinone derivate Tetrad task Declarative memoryCannabinoidsChemistryRecognition PsychologyGeneral MedicineCyclohexanolsEndocannabinoid systemSettore CHIM/08 - Chimica FarmaceuticaRats030104 developmental biologyNociceptionQuinazolinesSettore BIO/14 - FarmacologiaCannabinoidLocomotion030217 neurology & neurosurgerymedicine.drug
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Biased Agonism in Drug Discovery—Is It Too Soon to Choose a Path?

2018

A single receptor can activate multiple signaling pathways that have distinct or even opposite effects on cell function. Biased agonists stabilize receptor conformations preferentially stimulating one of these pathways, and therefore allow a more targeted modulation of cell function and treatment of disease. Dedicated development of biased agonists has led to promising drug candidates in clinical development, such as the G protein-biased µ opioid receptor agonist oliceridine. However, leveraging the theoretical potential of biased agonism for drug discovery faces several challenges. Some of these challenges are technical, such as techniques for quantitative analysis of bias and development …

0301 basic medicineAgonistCell typemedicine.drug_classDecision MakingDrug AgonismOliceridineBiologyChoice BehaviorReceptors G-Protein-Coupled03 medical and health scienceschemistry.chemical_compoundDrug DiscoverymedicineFunctional selectivityAnimalsHumansReceptorPharmacologyDrug discoveryDrug Agonism030104 developmental biologychemistryMolecular MedicineSignal transductionNeuroscienceMolecular Pharmacology
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Muscarinic type-1 receptors contribute to I-K,I-ACh in human atrial cardiomyocytes and are upregulated in patients with chronic atrial fibrillation

2018

Background: Basal and acetylcholine-gated inward-rectifier K+-currents (I-K1 and I-K,I-ACh, respectively) are altered in atrial fibrillation (AF). G(i)-protein-coupled muscarinic (M) receptors type-2 are considered the predominant receptors activating I-K,I-ACh. Although a role for G(q)-coupled non-M-2-receptor subtypes has been suggested, the precise regulation of I-K,I-ACh by multiple M-receptor subtypes in the human atrium is unknown. Here, we investigated M-1-receptor-mediated I-K,I-ACh regulation and its remodeling in chronic AF (cAF). Methods and results: M-1-receptor mRNA and protein abundance were increased in atrial cardiomyocyte fractions and atrial homogenates from cAF patients, …

0301 basic medicineAgonistEXPRESSIONmedicine.medical_specialtyCarbacholmedicine.drug_classMedizin030204 cardiovascular system & hematologyPertussis toxinSUBTYPES03 medical and health sciences0302 clinical medicineInternal medicineMuscarinic acetylcholine receptormedicinePROTEIN-KINASE-CReceptorAcetylcholine receptorK+-CURRENTACETYLCHOLINE-RECEPTORSCHANNELSCONGESTIVE-HEART-FAILUREbusiness.industryMuscarinic receptor subtypesInward-rectifier K+-channelELECTROPHYSIOLOGYPirenzepineAtrial fibrillationDEPENDENT REGULATIONPOTASSIUM CURRENTS030104 developmental biologyEndocrinologyCardiology and Cardiovascular MedicinebusinessAcetylcholinemedicine.drug
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Desensitization of cAMP Accumulation via Human β3-Adrenoceptors Expressed in Human Embryonic Kidney Cells by Full, Partial, and Biased Agonists

2019

β3-Adrenoceptors couple not only to cAMP formation but, at least in some cell types, also to alternative signaling pathways such as phosphorylation of extracellular signal-regulated kinase (ERK). β3-Adrenoceptor agonists are used in long-term symptomatic treatment of the overactive bladder syndrome; it is only poorly understood which signaling pathway mediates the clinical response and whether it undergoes agonist-induced desensitization. Therefore, we used human embryonic kidney cells stably transfected with human β3-adrenoceptors to compare coupling of ligands with various degrees of efficacy, including biased agonists, to cAMP formation and ERK phosphorylation, particularly regarding des…

0301 basic medicineAgonistMAPK/ERK pathwaymedicine.drug_classmedicine.medical_treatmentdesensitization03 medical and health scienceschemistry.chemical_compoundpartial agonism0302 clinical medicinecAMPIsoprenalinemedicinePharmacology (medical)β3-adrenoceptorOriginal ResearchDesensitization (medicine)PharmacologyForskolinKinaselcsh:RM1-950extracellular signal-related kinaseCell biologylcsh:Therapeutics. Pharmacology030104 developmental biologybiased agonismchemistry030220 oncology & carcinogenesisPhosphorylationSignal transductionmedicine.drugFrontiers in Pharmacology
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Effects of Chronic Dopamine D2R Agonist Treatment and Polysialic Acid Depletion on Dendritic Spine Density and Excitatory Neurotransmission in the mP…

2016

Dopamine D2 receptors (D2R) in the medial prefrontal cortex (mPFC) are key players in the etiology and therapeutics of schizophrenia. The overactivation of these receptors contributes to mPFC dysfunction. Chronic treatment with D2R agonists modifies the expression of molecules implicated in neuronal structural plasticity, synaptic function, and inhibitory neurotransmission, which are also altered in schizophrenia. These changes are dependent on the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), a plasticity-related molecule, but nothing is known about the effects of D2R and PSA-NCAM on excitatory neurotransmission and the structure of mPFC pyramidal n…

0301 basic medicineAgonistMaleDendritic spineArticle SubjectGlycoside Hydrolasesmedicine.drug_classDendritic SpinesPrefrontal CortexNeural Cell Adhesion Molecule L1NeurotransmissionInhibitory postsynaptic potentialbehavioral disciplines and activitiesSynaptic Transmissionlcsh:RC321-571Rats Sprague-Dawley03 medical and health sciences0302 clinical medicineDopamineDopamine receptor D2PhenethylaminesmedicineAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryChemistryReceptors Dopamine D2Pyramidal CellsGlutamate receptorRats030104 developmental biologyNeurologynervous systemDopamine AgonistsSialic AcidsNeural cell adhesion moleculeNeurology (clinical)Neuroscience030217 neurology & neurosurgerymedicine.drugResearch ArticleNeural plasticity
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Subchronic vortioxetine treatment -but not escitalopram- enhances pyramidal neuron activity in the rat prefrontal cortex.

2017

Abstract Vortioxetine (VOR) is a multimodal antidepressant drug. VOR is a 5-HT 3 -R, 5-HT 7 -R and 5-HT 1D -R antagonist, 5-HT 1B -R partial agonist, 5-HT 1A -R agonist, and serotonin transporter (SERT) inhibitor. VOR shows pro-cognitive activity in animal models and beneficial effects on cognitive dysfunction in major depressive patients. Here we compared the effects of 14-day treatments with VOR and escitalopram (ESC, selective serotonin reuptake inhibitor) on neuronal activity in the medial prefrontal cortex (mPFC). Ten groups of rats (5 standard, 5 depleted of 5-HT with p -chlorophenylalanine -pCPA-, used as model of cognitive impairment) were fed with control food or with two doses of …

0301 basic medicineAgonistMalegenetic structuresmedicine.drug_classSerotonin reuptake inhibitorAction PotentialsPrefrontal CortexPharmacologyCitalopramSulfidesPartial agonistPiperazines03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicinePremovement neuronal activityAnimalsRats WistarSerotonin transporterPharmacologyVortioxetinebiologyPyramidal CellsAntagonistAntidepressive AgentsRats030104 developmental biologybiology.proteinAntidepressantVortioxetinesense organsPsychologyNeuroscience030217 neurology & neurosurgerySelective Serotonin Reuptake InhibitorsNeuropharmacology
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Activation of PPARβ/δ prevents hyperglycaemia-induced impairment of Kv7 channels and cAMP-mediated relaxation in rat coronary arteries.

2016

PPARβ/δ activation protects against endothelial dysfunction in diabetic models. Elevated glucose is known to impair cAMP-induced relaxation and Kv channel function in coronary arteries (CA). Herein, we aimed to analyse the possible protective effects of the PPARβ/δ agonist GW0742 on the hyperglycaemic-induced impairment of cAMP-induced relaxation and Kv channel function in rat CA. As compared with low glucose (LG), incubation under high glucose (HG) conditions attenuated the relaxation induced by the adenylate cyclase activator forskolin in CA and this was prevented by GW0742. The protective effect of GW0742 was supressed by a PPARβ/δ antagonist. In myocytes isolated from CA under LG, forsk…

0301 basic medicineAgonistMalemedicine.medical_specialtymedicine.drug_classPDK4Protein Serine-Threonine Kinasesmedicine.disease_causeGW0742Diabetes Mellitus Experimental03 medical and health scienceschemistry.chemical_compoundInternal medicinemedicineCyclic AMPAnimalsHumansPPAR deltaRats WistarPPAR-betaForskolinAntagonistPyruvate Dehydrogenase Acetyl-Transferring KinaseGeneral MedicineHyperpolarization (biology)Coronary VesselsPotassium channelRatsVasodilationThiazoles030104 developmental biologyEndocrinologychemistryHyperglycemiaKCNQ1 Potassium ChannelReactive Oxygen SpeciesOxidative stressClinical science (London, England : 1979)
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Heat shock protein (Hsp) regulation by muscarinic acetylcholine receptor (mAChR) activation in the rat hippocampus.

2018

The cholinergic system plays a crucial role in modulating in the central nervous system physiological responses such as neurogenesis, neuronal differentiation, synaptic plasticity, and neuroprotection. In a recent study, we showed that Oxotremorine-M, a non-selective muscarinic acetylcholine receptor agonist, is able to transactivate the fibroblast growth factor receptor and to produce a significant increase in the hippocampal primary neurite outgrowth. In the present study we aimed to explore in the rat hippocampus the possible effect of acute or chronic treatment with Oxotremorine-M on some heat shock proteins (Hsp60, Hsp70, Hsp90) and on activation of related transcription factor heat sh…

0301 basic medicineAgonistMalemedicine.medical_specialtymedicine.drug_classPhysiologyClinical BiochemistryNeuronal OutgrowthScopolamineheat shock proteinHsp90NeuroprotectionHippocampusHsp7003 medical and health sciencesmuscarinic receptor0302 clinical medicineHeat Shock Transcription FactorsHeat shock proteinInternal medicineMuscarinic acetylcholine receptormedicineOxotremorineAnimalsRats WistarHSF1Heat-Shock ProteinsNeuronsNeuronal PlasticityChemistryOxotremorineNeurodegenerative DiseasesCell BiologyReceptors Fibroblast Growth FactorReceptors MuscarinicHsp70Rats030104 developmental biologyEndocrinologyheat shock factor 1HSP60030217 neurology & neurosurgerymedicine.drugSignal TransductionJournal of cellular physiology
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A Computational Assay of Estrogen Receptor α Antagonists Reveals the Key Common Structural Traits of Drugs Effectively Fighting Refractory Breast Can…

2017

AbstractSomatic mutations of the Estrogen Receptor α (ERα) occur with an up to 40% incidence in ER sensitive breast cancer (BC) patients undergoing prolonged endocrine treatments. These polymorphisms are implicated in acquired resistance, disease relapse, and increased mortality rates, hence representing a current major clinical challenge. Here, multi-microseconds (12.5 µs) molecular dynamics simulations revealed that recurrent ERα polymorphisms (i. e. L536Q, Y537S, Y537N, D538G) (mERα) are constitutively active in their apo form and that they prompt the selection of an agonist (active)-like conformation even upon antagonists binding. Interestingly, our simulations rationalize, for the firs…

0301 basic medicineAgonistModels MolecularBreast cancerComputational chemistryMolecular dynamicsSomatic cellmedicine.drug_classlcsh:MedicineEstrogen receptorBreast Neoplasms-Molecular Dynamics SimulationPolymorphism Single NucleotideArticleProtein Structure SecondaryEstrogen Receptor Antagonists03 medical and health sciences0302 clinical medicineBreast cancermedicineEndocrine systemHumanslcsh:ScienceMultidisciplinarybusiness.industrylcsh:REstrogen Receptor alphamedicine.diseaseEstrogen Receptor Antagonist030104 developmental biologySelective estrogen receptor modulator030220 oncology & carcinogenesisCancer researchlcsh:QFemaleEstrogen Receptor AntagonistsbusinessEstrogen receptor alphaBreast NeoplasmHuman
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Do β3-adrenoceptor agonists cause urinary bladder smooth muscle relaxation by inhibiting acetylcholine release?

2017

The mechanisms leading to improvement of overactive bladder syndrome upon treatment with a β3-adrenoceptor agonist remain controversial. New research points to a role of inhibition of neuronal acetylcholine release. Whether this occurs by a direct effect on prejunctional β3-adrenoceptors or indirectly by formation of adenosine and activation of A1 adenosine receptors is being discussed.

0301 basic medicineAgonistSmooth muscle relaxationmedicine.medical_specialtyUrinary bladderPhysiologymedicine.drug_classbusiness.industryOveractive bladder syndromeAdenosine receptorAdenosine03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureEndocrinologyInternal medicinemedicineβ3 adrenoceptorbusiness030217 neurology & neurosurgeryAcetylcholinemedicine.drugAmerican Journal of Physiology-Renal Physiology
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