Search results for "Monoamine Oxidase"

showing 10 items of 47 documents

The neuronal efflux of noradrenaline: Dependency on sodium and facilitation by ouabain

1974

Rabbit hearts were isolated after pretreatment with the MAO inhibitor pargyline and with reserpine and were perfused with 200 ng/ml noradrenaline for 1 h. During the subsequent wash-out with an amine-free solution for 2 h, the neuronal efflux of noradrenaline declined mono-exponentially with a mean halftime of 42 min. Both Na+-free solution and ouabain caused facilitation of the efflux which thereafter declined in a multi-exponential fashion. The maximum facilitation was reached after 3 min of Na+-free perfusion and 25 min after introduction of ouabain. The amount of exogenous noradrenaline accumulated in the heart was only partially released when the extracellular Na+-concentration was nor…

medicine.medical_specialtyMonoamine Oxidase InhibitorsReserpineTime FactorsSodiumchemistry.chemical_elementAdrenergicOuabainNorepinephrineHeart RateInternal medicinemedicineExtracellularAnimalsOuabainNeuronsPharmacologyMyocardiumSodiumGeneral MedicineReserpinePargylineEndocrinologyPargylinechemistryRabbitsEffluxPerfusionmedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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Release of endogenous 3,4-dihydroxyphenylethylamine and its metabolites from the isolated neurointermediate lobe of the rat pituitary gland. Effects …

1986

: Isolated rat neurointermediate lobes were incubated in vitro. The release of 3,4-dihydroxyphenylethylamine (dopamine, DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and methoxyphenylethanol (MOPET) was determined by HPLC with electrochemical detection. Under resting conditions, the outflow of metabolites was 35–50 times that of DA. HVA accounted for 50%, DOPAC for 45%, and MOPET for 5% of the metabolites. Although an equivalent of 40–50% of the tissue DA content was released per hour as metabolites, the tissue DA content was not reduced after 110 min of incubation. The spontaneous outflow of DA and its metabolites was not affected by the DA uptake inhibitor GBR 12921 (1…

medicine.medical_specialtyPituitary gland3-Methoxy-4-hydroxyphenylethanolMonoamine Oxidase InhibitorsMonoamine oxidaseDopamineStimulationBiochemistryPiperazinesReuptakeCellular and Molecular Neurosciencechemistry.chemical_compoundPituitary Gland PosteriorDopamineInternal medicinemedicineAnimalsChromatography High Pressure LiquidChemistryCatabolismHomovanillic acidHomovanillic AcidPargylineElectric StimulationRatsKineticsmedicine.anatomical_structureEndocrinologyPargyline34-Dihydroxyphenylacetic AcidFemalemedicine.drugJournal of neurochemistry
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A monoamine oxidase B gene variant and short-term antidepressant treatment response.

2007

Genetic differences among patients suffering from Major Depression are likely to contribute to interindividual differences in medication treatment response. Thus, the identification of gene variants affecting drug response is needed in order to be able to predict response to psychopharmacological drugs. This study analyzed a possible association of the common A644G single nucleotide polymorphism (SNP) within intron 13 of the monoamine oxidase B (MAOB) gene with antidepressant treatment response. The study population consisted of n = 102 patients with major depression (criteria of the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition; DSM-IV) participating in a randomized do…

OncologyAdultMalemedicine.medical_specialtyMirtazapineSingle-nucleotide polymorphismMirtazapineMianserinPharmacologyDouble-Blind MethodInternal medicinemedicineHumansMonoamine OxidaseBiological PsychiatryAllelesPharmacologyPsychiatric Status Rating ScalesDepressive Disorder MajorbiologyReverse Transcriptase Polymerase Chain ReactionDNAMiddle AgedMianserinParoxetineAntidepressive AgentsIntronsParoxetineData Interpretation Statisticalbiology.proteinAntidepressantFemaleMonoamine oxidase BMonoamine oxidase APsychologyPharmacogeneticsSelective Serotonin Reuptake Inhibitorsmedicine.drugProgress in neuro-psychopharmacologybiological psychiatry
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CB1 cannabinoid receptor-mediated aggressive behavior

2013

This study examined the role of cannabinoid CB1 receptors (CB1r) in aggressive behavior. Social encounters took place in grouped and isolated mice lacking CB1r (CB1KO) and in wild-type (WT) littermates. Cognitive impulsivity was evaluated in the delayed reinforcement task (DRT). Gene expression analyses of monoaminooxidase-A (MAO-A), catechol-o-methyl-transferase (COMT), 5-hydroxytriptamine transporter (5-HTT) and 5-HT1B serotonergic receptor (5HT1Br) in the median and dorsal raphe nuclei (MnR and DR, respectively) and in the amygdala (AMY) were performed by real time-PCR. Double immunohistochemistry studies evaluated COMT and CB1r co-localization in the raphe nuclei and in the cortical (AC…

AgonistMalemedicine.medical_specialtyCannabinoid receptorTime Factorsmedicine.drug_classmedicine.medical_treatmentPoison controlArachidonic AcidsSerotonergicCatechol O-MethyltransferaseAmygdalaCellular and Molecular NeuroscienceMiceDorsal raphe nucleusReceptor Cannabinoid CB1Internal medicinemedicineAnimalsInterpersonal RelationsMonoamine OxidasePharmacologyCannabinoid Receptor AgonistsMice KnockoutSerotonin Plasma Membrane Transport ProteinsAmygdalaSurgeryAggressionmedicine.anatomical_structureEndocrinologynervous systemGene Expression RegulationImpulsive BehaviorReceptor Serotonin 5-HT1BConditioning OperantRaphe NucleiCannabinoidRaphe nucleiPsychologyReinforcement Psychology
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Impaired cannabinoid receptor type 1 signaling interferes with stress-coping behavior in mice.

2007

Dysregulation of the endocannabinoid system is known to interfere with emotional processing of stressful events. Here, we studied the role of cannabinoid receptor type 1 (CB1) signaling in stress-coping behaviors using the forced swim test (FST) with repeated exposures. We compared effects of genetic inactivation with pharmacological blockade of CB1 receptors both in male and female mice. In addition, we investigated potential interactions of the endocannabinoid system with monoaminergic and neurotrophin systems of the brain. Naive CB1 receptor-deficient mice (CB1-/-) showed increased passive stress-coping behaviors as compared to wild-type littermates (CB1+/+) in the FST, independent of se…

Malemedicine.medical_specialtyCannabinoid receptormedicine.medical_treatmentBiologyPharmacologyHippocampusMicePiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid receptor type 1MonoaminergicAdaptation PsychologicalGeneticsmedicineAnimalsBiogenic MonoaminesRNA MessengerReceptorMonoamine OxidaseSwimmingPharmacologyBrain-derived neurotrophic factormusculoskeletal neural and ocular physiologyBrain-Derived Neurotrophic FactorDesipraminefood and beveragesEndocannabinoid systemMice Inbred C57BLMonoamine neurotransmitterEndocrinologynervous systemVesicular Glutamate Transport Protein 1Molecular MedicinePyrazoleslipids (amino acids peptides and proteins)FemaleCannabinoidRimonabantpsychological phenomena and processesStress PsychologicalSignal TransductionThe pharmacogenomics journal
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Animal Models of Stress - Current Knowledge and Potential Directions

2021

Finding new therapies and new antidepressant agents is of high clinical priority given that many cases of depressive disorder do not respond to conventional monoaminergic antidepressants such as selective serotonin reuptake inhibitors, tricyclic antidepressants, and monoamine oxidase inhibitors The authors demonstrated that electroacupuncture and fluoxetine, a second-generation antidepressant categorized as a selective serotonin reuptake inhibitor (Perez-Caballero et al , 2014), regulate the expression of key proteins in the calmodulin kinase (CAMK) signaling pathway, which are related to depression in the hippocampi of rats (Takemoto-Kimura et al , 2017;Xie et al , 2019) In a paper on “Sho…

Monoamine oxidaseCognitive NeuroscienceSerotonin reuptake inhibitorContext (language use)Pharmacologyalternative therapylcsh:RC321-571stress03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compound0302 clinical medicineorganoselenium compoundsMonoaminergicmedicineNeurotransmitterlcsh:Neurosciences. Biological psychiatry. Neuropsychiatry030304 developmental biologychemistry.chemical_classification0303 health sciencesFluoxetinebusiness.industryanimal modelsEditorialNeuropsychology and Physiological PsychologychemistryAntidepressantmajor depressionbusiness030217 neurology & neurosurgeryTricyclicmedicine.drugFrontiers in Behavioral Neuroscience
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Structure-Activity Relationship Analysis of 3-Phenylcoumarin-Based Monoamine Oxidase B Inhibitors

2018

Monoamine oxidase B (MAO-B) catalyzes deamination of monoamines such as neurotransmitters dopamine and norepinephrine. Accordingly, small-molecule MAO-B inhibitors potentially alleviate the symptoms of dopamine-linked neuropathologies such as depression or Parkinson's disease. Coumarin with a functionalized 3-phenyl ring system is a promising scaffold for building potent MAO-B inhibitors. Here, a vast set of 3-phenylcoumarin derivatives was designed using virtual combinatorial chemistry or rationally de novo and synthesized using microwave chemistry. The derivatives inhibited the MAO-B at 100 nM−1 μM. The IC50 value of the most potent derivative 1 was 56 nM. A docking-based structure-activi…

0301 basic medicineentsyymitParkinson's diseaseParkinsonin tautita311101 natural scienceslääkesuunnittelumonoamine oxidase B (MAO-B)lcsh:Chemistry03 medical and health scienceschemistry.chemical_compoundstructure-activity relationship (SAR)Dopamine3-phenylcoumarinmedicineStructure–activity relationshipoksidoreduktaasitkumariinitta116ta317inhibiittoritOriginal Researchchemistry.chemical_classificationbiologyvirtual drug designta1182General ChemistryCoumarin3. Good health0104 chemical sciences010404 medicinal & biomolecular chemistryChemistry030104 developmental biologyMonoamine neurotransmitterEnzymeBiochemistrychemistrylcsh:QD1-999Docking (molecular)biology.proteinParkinson’s diseaseMonoamine oxidase BMonoamine oxidase Amedicine.drugFrontiers in Chemistry
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TheMAOA T941G polymorphism and short-term treatment response to mirtazapine and paroxetine in major depression

2006

This study investigated the possible association of the MAOA T941G gene variant with differential antidepressant response to mirtazapine and/or paroxetine in 102 patients with major depression (DSM-IV criteria) participating in a randomized double-blind controlled clinical trial. Female mirtazapine-treated patients homozygous for the T-allele had a significantly faster and better treatment response than TG/GG-patients. In males, we failed to show an association between MAOA T941G gene variant and mirtazapine response. In the paroxetine-treated group, there were no significant differences in treatment response between MAOA T941G genotype groups. Time course of response and antidepressant eff…

AdultMaleOncologymedicine.medical_specialtyTime FactorsGenotypeGenetic LinkageMirtazapineMirtazapineMianserinPolymorphism Single NucleotideCellular and Molecular NeuroscienceDouble-Blind MethodGene FrequencyInternal medicineGenotypemedicineHumansAlleleMonoamine OxidaseGenotypingGenetics (clinical)Depressive Disorder MajorSex Characteristicsbusiness.industryMiddle AgedParoxetineAntidepressive AgentsClinical trialParoxetinePsychiatry and Mental healthTreatment OutcomeEndocrinologyAntidepressantFemalebusinessReuptake inhibitormedicine.drugAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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(±)- BIGI-3h: Pentatarget-Directed Ligand combining Cholinesterase, Monoamine Oxidase, and Glycogen Synthase Kinase 3β Inhibition with Calcium Channe…

2021

Multitarget-directed ligands (MTDLs) are considered a promising therapeutic strategy to address the multifactorial nature of Alzheimer's disease (AD). Novel MTDLs have been designed as inhibitors of human acetylcholinesterases/butyrylcholinesterases, monoamine oxidase A/B, and glycogen synthase kinase 3β and as calcium channel antagonists via the Biginelli multicomponent reaction. Among these MTDLs, (±)-BIGI-3h was identified as a promising new hit compound showing in vitro balanced activities toward the aforementioned recognized AD targets. Additional in vitro studies demonstrated antioxidant effects and brain penetration, along with the ability to inhibit the aggregation of both τ protein…

cholinesterasePhysiologyMonoamine oxidaseCognitive NeuroscienceLigandPharmacologyLigandsCalcium ChannelBiochemistry03 medical and health sciences0302 clinical medicineAlzheimer DiseaseIn vivoGSK-3HumansCholinesterasesCholinesterase InhibitorBiginelli reactionAlzheimer's disease; Biginelli reaction; calcium channel; cholinesterases; GSK 3β; MAO; Calcium Channel Blockers; Calcium Channels; Cholinesterase Inhibitors; Glycogen Synthase Kinase 3 beta; Humans; Ligands; Monoamine Oxidase; Alzheimer DiseaseMonoamine OxidaseGSK3B030304 developmental biologyCholinesterase0303 health sciencesGlycogen Synthase Kinase 3 betaVoltage-dependent calcium channelbiologyChemistryCalcium channelCell BiologyGeneral MedicineAlzheimer's diseaseCalcium Channel BlockersCalcium channel GSK 3β MAOMAObiology.proteinCalcium ChannelsCholinesterase InhibitorsGSK 3βMonoamine oxidase ACalcium Channel BlockerAlzheimer’s disease030217 neurology & neurosurgeryHuman
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Brunner syndrome associated MAOA dysfunction in human dopaminergic neurons results in NMDAR hyperfunction and increased network activity

2020

AbstractBackgroundMonoamine neurotransmitter abundance affects motor control, emotion, and cognitive function and is regulated by monoamine oxidases. Amongst these, monoamine oxidase A (MAOA) catalyzes the degradation of dopamine, norepinephrine, and serotonin into their inactive metabolites. Loss-of-function mutations in the X-linked MAOA gene cause Brunner syndrome, which is characterized by various forms of impulsivity, maladaptive externalizing behavior, and mild intellectual disability. Impaired MAOA activity in individuals with Brunner syndrome results in bioamine aberration, but it is currently unknown how this affects neuronal function.MethodsWe generated human induced pluripotent s…

Brunner syndromeDopaminergicBiologymedicine.diseaseNorepinephrineMonoamine neurotransmitterDopaminebiology.proteinmedicineGRIN2BSerotoninMonoamine oxidase ANeurosciencemedicine.drug
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