Search results for "Drug Interaction"

showing 10 items of 246 documents

Effect of adolescent exposure to MDMA and cocaine on acquisition and reinstatement of morphine-induce CPP

2007

It is well known that an elevated percentage of ecstasy users also consume cocaine. Recently, it has been reported that a high frequency of heroin smokers first consumed heroin under the effects of ecstasy with the hope of reducing the stimulant effects of the latter drug. The aim of the present study was to evaluate the effect of exposure to MDMA and cocaine during adolescence on morphine-induced conditioned place preference (CPP) and reinstatement in adulthood. In the first experiment, adolescent mice were exposed to six injections of MDMA and three weeks later their response to the reinforcing properties of 40 mg/kg of morphine was evaluated using the CPP paradigm. All the treatment grou…

MaleNarcoticsN-Methyl-34-methylenedioxyamphetaminemedicine.medical_treatmentEcstasyPharmacologyExtinction PsychologicalHeroinMiceCocaineDopamine Uptake InhibitorsmedicineAnimalsDrug InteractionsBiological PsychiatryPharmacologyAnalysis of VarianceGateway drugAdrenergic Uptake InhibitorsBehavior AnimalDose-Response Relationship DrugMorphineMDMAExtinction (psychology)Conditioned place preferenceStimulantAnimals NewbornMorphineConditioning OperantPsychologyReinforcement Psychologypsychological phenomena and processesmedicine.drugProgress in Neuro-Psychopharmacology and Biological Psychiatry
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Memantine presents different effects from MK-801 in motivational and physical signs of morphine withdrawal

2003

Adaptive changes in neural systems due to chronic opiate exposure are related to the neural plasticity phenomenon, NMDA receptors being implicated in these processes, e.g. tolerance, dependence or withdrawal. In this work, we investigated the effect of two non-competitive NMDA antagonists, memantine and MK-801, in motivational (Conditioned Place Aversion paradigm, CPA) and physical aspects of morphine withdrawal. After the induction of morphine dependence, animals in which the CPA was studied, received memantine (5 and 10 mg/kg) or MK-801 (0.3-0.006 mg/kg) either during the acquisition (conditioning) or expression (test) phase of this procedure. Both drugs were capable of inhibiting conditi…

MaleNarcoticsTime FactorsNarcotic AntagonistsMotor ActivityPharmacologyMiceBehavioral NeuroscienceMemantineConditioning PsychologicalNeuroplasticitymedicineAnimalsDrug InteractionsBehavior AnimalDose-Response Relationship DrugMorphineNaloxoneKindlingMemantineSubstance Withdrawal SyndromeBlockadeMorphineNMDA receptorConditioningDizocilpine MaleateOpiatePsychologyExcitatory Amino Acid AntagonistsMorphine Dependencemedicine.drugBehavioural Brain Research
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GHB differentially affects morphine actions on motor activity and social behaviours in male mice

2003

There are several reports suggesting that gamma-hydroxybutyric acid (GHB) influences the endogenous opioid system. The present study aimed to investigate the effects of GHB on motor and social activities and to examine its influence on morphine's actions on these behaviours. In a first experiment, several doses of GHB were studied but only the highest (200 and 400 mg/kg) produced a decrease in spontaneous motor activity measured in an actimeter cage. When hyperactivity induced by injecting 50 mg/kg of morphine was evaluated, all the GHB doses efficiently counteracted this morphine action. Using the paradigm of isolation-induced aggression, administration of 200 mg/kg of GHB significantly de…

MaleNarcoticsmedicine.drug_classClinical BiochemistryMale miceMotor ActivityPharmacologyToxicologyBiochemistryMiceBehavioral NeuroscienceOpioid receptormedicineAnimalsDrug InteractionsMotor activitySocial BehaviorBiological PsychiatryEndogenous opioidPharmacologyMorphineAggressionBiological activityAggressionOpioidExploratory BehaviorMorphinemedicine.symptomSodium OxybatePsychologyAnesthetics Intravenousmedicine.drugPharmacology Biochemistry and Behavior
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Critical role of nitric oxide on nicotine-induced hyperactivation of dopaminergic nigrostriatal system: electrophysiological and neurochemical eviden…

2010

Nicotine, the main psychoactive ingredient in tobacco, stimulates dopamine (DA) function, increasing DA neuronal activity and DA release. DA is involved in both motor control and in the rewarding and reinforcing effects of nicotine; however, the complete understanding of its molecular mechanisms is yet to be attained. Substantial evidence indicates that the reinforcing properties of drugs of abuse, including nicotine, can be affected by the nitric oxide (NO) system, which may act by modulating central dopaminergic function. In this study, using single cell recordings in vivo coupled with microiontophoresis and microdialysis in freely moving animals, the role of NO signaling on the hyperacti…

MaleNicotineIndazolesTime FactorsDopamineMicrodialysisAction PotentialsArginineSettore BIO/09 - FisiologiaCorpus striatumRats Sprague-DawleyAnimalsDrug InteractionsNicotinic Agonistsnigrostriatal systemEnzyme InhibitorsNeuronsAnalysis of VarianceDose-Response Relationship DrugResearchNitric oxideSubstantia NigraratsNG-Nitroarginine Methyl Esternervous system34-Dihydroxyphenylacetic Aciddopamine
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Modulatory effects of nitric oxide-active drugs on the anticonvulsant activity of lamotrigine in an experimental model of partial complex epilepsy in…

2007

Abstract Background The effects induced by administering the anticonvulsant lamotrigine, the preferential inhibitor of neuronal nitric oxide synthase 7-nitroindazole and the precursor of NO synthesis L-arginine, alone or in combination, on an experimental model of partial complex seizures (maximal dentate gyrus activation) were studied in urethane anaesthetized rats. The epileptic activity of the dentate gyrus was obtained through the repetitive stimulation of the angular bundle and maximal dentate gyrus activation latency, duration and post-stimulus afterdischarge duration were evaluated. Results Either Lamotrigine (10 mg kg-1) or 7-nitroindazole (75 mg kg-1) i.p. administration had an ant…

MalePARTIAL COMPLEX EPILEPSYIndazolesArgininemedicine.medical_treatmentLamotriginePharmacologyArginineLamotrigineNitric OxideSettore BIO/09 - Fisiologialcsh:RC321-571Nitric oxideCellular and Molecular Neurosciencechemistry.chemical_compoundEpilepsy Complex PartialmedicineAnimalsDrug InteractionsEnzyme InhibitorsRats Wistarlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNitric oxide Lamotrigine epilepsy controlbiologyTriazinesExperimental modelGeneral NeuroscienceDentate gyruslcsh:QP351-495BrainElectric StimulationRatsNitric oxide synthaseDisease Models Animallcsh:Neurophysiology and neuropsychologyAnticonvulsantnervous systemchemistryDentate Gyrusbiology.proteinAnticonvulsantsNitric Oxide SynthaseResearch Articlemedicine.drugBMC Neuroscience
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Interaction of phenylbutazone with racemic phenprocoumon and its enantiomers in rats.

1979

The interaction of phenylbutazone with the enantiomers and racemic [ 3 H]phenprocoumon was studied in male inbred Wistar-Lewis rats following a single i.v. dose of the three forms of phenprocoumon and chronic oral treatment with phenylbutazone (average plasma concentration of about 60 Μg/ml). Phenylbutazone augmented the anticoagulant effect of R(+), S(−), and R, S (±) phenprocoumon to a similar extent. The free fraction of drug in the plasma of the enantiomers and racemic phenprocoumon increased in the presence of phenylbutazone. However, the rate of elimination of total drug from plasma and liver and the distribution between liver and plasma of all three forms of phenprocoumon remained ne…

MalePharmacologyPhenprocoumonElimination rate constantPhenylbutazonemedicineDistribution (pharmacology)AnimalsPharmacology (medical)Drug InteractionsGeneral Pharmacology Toxicology and PharmaceuticsVolume of distributionChemistryAnticoagulantsStereoisomerism4-HydroxycoumarinsDrug interactionRatsKineticsLiverPhenylbutazoneFree fractionPhenprocoumonProthrombinEnantiomermedicine.drugJournal of pharmacokinetics and biopharmaceutics
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Preliminary experience on safety of regorafenib after sorafenib failure in recurrent hepatocellular carcinoma after liver transplantation

2019

Regorafenib is one option for second-line treatment of hepatocellular carcinoma (HCC), improving overall survival (OS) of sorafenib-tolerant patients who develop progression. We aim to evaluate the safety and outcomes of regorafenib as second-line treatment for HCC recurrence after liver transplantation (LT). This is a retrospective, multicenter, international study including regorafenib-treated LT patients (2015-2018), with analysis of baseline characteristics and evolutionary events during sorafenib/regorafenib treatment. Twenty-eight LT patients (57 years, 7% cirrhotics, 54% performance status 1) were included. Median time from LT to regorafenib initiation was 3.9 (1.1-18.5) years; media…

MalePyridinesmedicine.medical_treatment030230 surgeryLiver transplantationchemotherapyGastroenterologychemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsImmunology and AllergyPharmacology (medical)Liver NeoplasmsMiddle AgedSorafenibPrognosisRecurrent Hepatocellular Carcinomaside effectsHepatocellular carcinomaFemalemedicine.drugSorafenibAdultmedicine.medical_specialtyCarcinoma Hepatocellularcancer/malignancy/neoplasiaclinical research/practice03 medical and health sciencesYoung AdultInternal medicineRegorafenibmedicineHumansAdverse effectAgedRetrospective StudiesTransplantationdrug interactionPerformance statusbusiness.industryPhenylurea Compoundsmedicine.diseaseDiscontinuationLiver TransplantationchemistryDrug Resistance NeoplasmNeoplasm Recurrence Localpharmacologybusinessliver transplantation/hepatologyFollow-Up Studies
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Affinity and efficacy of racemic, (+)-, and (−)-methacholine in muscarinic inhibition of [3H]-noradrenaline release

1985

The right postganglionic sympathetic nerves of rat isolated perfused hearts (previously loaded with [3H]-noradrenaline) were stimulated electrically with 10 trains of 10 pulses at 10 Hz. The inhibition by methacholine of stimulation-evoked [3H]-noradrenaline overflow into the perfusate (determined in the presence of corticosterone, desipramine, phentolamine, and propranolol) was taken as a measure for activation of presynaptic muscarinic receptors. The evoked [3H]-noradrenaline overflow was inhibited by (+)-, racemic, and (-)-methacholine in a reversible and concentration-dependent manner. The concentration causing 50% inhibition (IC50) was 0.1, 0.26, and 65 microM, respectively, resulting …

MaleReceptor complexSympathetic Nervous SystemIntrinsic activityPhenoxybenzamineStereochemistryPhysostigminePropranololIn Vitro TechniquesPropylbenzilylcholine MustardNorepinephrineMuscarinic acetylcholine receptormedicineAnimalsMethacholine CompoundsDrug InteractionsReceptorMethacholine ChlorideNeuronsPharmacologyPhenoxybenzamineChemistryHeartRats Inbred StrainsStereoisomerismReceptors MuscarinicElectric StimulationRatsDissociation constantSynapsesMethacholineCorticosteroneResearch Articlemedicine.drugBritish Journal of Pharmacology
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A novel CXCR4 antagonist counteracts paradoxical generation of cisplatin-induced pro-metastatic niches in lung cancer.

2021

Platinum-based chemotherapy remains widely used in advanced non-small cell lung cancer (NSCLC) despite experimental evidence of its potential to induce long-term detrimental effects, including the promotion of pro-metastatic microenvironments. In this study, we investigated the interconnected pathways underlying the promotion of cisplatin-induced metastases. In tumor-free mice, cisplatin treatment resulted in an expansion in the bone marrow of CCR2+CXCR4+Ly6Chigh inflammatory monocytes (IMs) and an increase in lung levels of stromal SDF-1, the CXCR4 ligand. In experimental lung metastasis assays, cisplatin-induced IMs promoted the extravasation of tumor cells and the expansion of CD133+CXCR…

MaleReceptors CXCR4Stromal cellLung NeoplasmsSettore MED/08 - Anatomia PatologicaMonocytesMetastasisMiceCarcinoma Non-Small-Cell LungCell Line TumorDrug DiscoveryGeneticsMedicineSettore MED/05 - Patologia ClinicaAnimalsHumansDrug InteractionsAC133 AntigenNeoplasm MetastasisLung cancerMolecular BiologyPharmacologyCisplatinCXCR4 antagonistchemotherapy combination therapy inflammatory monocytes lung cancer stem cells metastasis peptide anti-CXCR4 SDF-1/CXCR4 axisbusiness.industrymedicine.diseasePrimary tumorXenograft Model Antitumor AssaysExtravasationChemokine CXCL12medicine.anatomical_structureRAW 264.7 CellsA549 CellsCancer researchNeoplastic Stem CellsMolecular MedicineBone marrowCisplatinbusinessPeptidesmedicine.drugMolecular therapy : the journal of the American Society of Gene Therapy
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Mechanism-based predictions of interactions.

1994

Abstract Exposure to more than one toxic compound is common in real life. The resulting toxic effects are often more than the simple sum of the effects of the individual compounds. It is unlikely that it will ever be possible to test all combinations. It is therefore highly desirable to improve or develop means for reasonably approximating predictions of interactions. In order to be valid and extrapolatable, these predictions are most promising if they are mechanism-based. Examples will be given for possibilities of mechanism-based predictions of interactions which exceed trivialities of simple increases by enzyme induction of enzymatic rates of a given biotransformation pathway leading to …

MaleSalmonella typhimuriumEndogenous FactorsHealth Toxicology and MutagenesisMetaboliteMechanism basedRats sprague dawleyXenobioticsRats Sprague-Dawleychemistry.chemical_compoundStilbenesBenzo(a)pyreneAnimalsIn real lifeDrug InteractionsPhosphorylationEpoxide HydrolasesMutagenicity TestsMechanism (biology)Public Health Environmental and Occupational HealthRatschemistryBiochemistryEnzyme InductionMicrosomes LiverBiochemical engineeringXenobioticMutagenicity TestResearch ArticleEnvironmental Health Perspectives
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