Search results for "Drug Interaction"

showing 10 items of 246 documents

Effect of memantine and CNQX in the acquisition, expression and reinstatement of cocaine-induced conditioned place preference

2006

The present study evaluates the effect of memantine, a non-competitive N-methyl-d-aspartate (NMDA) glutamate receptor antagonist and CNQX, an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptor antagonist on the rewarding effects of cocaine in mice, using the conditioned place preference (CPP) paradigm. Cocaine-induced CPP was studied pairing this drug with different memantine or CNQX doses during either the acquisition or the expression phase of the procedure. Once CPP was established, and the preference extinguished, reinstatement was induced by a priming dose of cocaine. Both antagonists, which in themselves do not present motivational actions on the preferen…

MaleKainate receptorAMPA receptorPharmacologyExtinction PsychologicalMicechemistry.chemical_compoundCocaineDopamine Uptake InhibitorsMemantineAnimalsMedicineDrug InteractionsGlutamate receptor antagonistBiological Psychiatry6-Cyano-7-nitroquinoxaline-23-dionePharmacologyBehavior AnimalDose-Response Relationship Drugbusiness.industryGlutamate receptorMemantineConditioned place preferencenervous systemchemistryCNQXConditioning OperantNMDA receptorbusinessExcitatory Amino Acid AntagonistsReinforcement Psychologypsychological phenomena and processesmedicine.drugProgress in Neuro-Psychopharmacology and Biological Psychiatry
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The high affinity dopamine uptake inhibitor, JHW 007, blocks cocaine-induced reward, locomotor stimulation and sensitization

2009

The discovery and evaluation of high affinity dopamine transport inhibitors with low abuse liability is an important step toward the development of efficacious medications for cocaine addiction. We examined in mice the behavioural effects of (N-(n-butyl)-3Ά-[bis(4Ά-fluorophenyl)methoxy]-tropane) (JHW 007), a benztropine (BZT) analogue that blocks dopamine uptake, and assessed its potential to influence the actions of cocaine in clinically-relevant models of cocaine addiction. In the conditioned place preference (CPP) paradigm, JHW 007 exposure did not produce place conditioning within an ample dose range but effectively blocked the CPP induced by cocaine administration. Similarly, in the CP…

MaleLocomotor activityElevated plus mazemedia_common.quotation_subjectDopamine transportPharmacologyMotor ActivityAnxietyOpen fieldSensitizationMiceDopamine Uptake InhibitorsRewardCocaineDopaminemedicineAnimalsPharmacology (medical)Drug InteractionsMaze LearningBiological PsychiatrySensitizationmedia_commonPharmacologyBenztropineAnalysis of VarianceBehavior AnimalAddictionPlace preferenceBenztropineConditioned place preferencePsychiatry and Mental healthmedicine.anatomical_structureNeurologyConditioning OperantDopamine AntagonistsNeurology (clinical)PsychologyBenztropine analoguesmedicine.drug
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Phosphorylation of extracellular signal-related protein kinase is required for rapid facilitation of heat-induced currents in rat dorsal root ganglio…

2005

A subgroup of dorsal root ganglion (DRG) neurons responds to noxious heat with an influx of cations carried by specific ion channels such as the transient receptor potential channel of the vanilloid receptor type, subtype 1 (TRPV1). Application of capsaicin induces a reversible facilitation of these currents. This facilitation could be an interaction of two agonists at their common receptor or be caused by an influx of calcium ions into the cell. Calcium influx into the cell can activate protein kinases such as the extracellular signal-related protein kinase (ERK) pathway. This study explored the kinetics, calcium-dependency and intracellular signals following application of capsaicin and l…

MaleMAPK/ERK pathwayHot TemperaturePatch-Clamp TechniquesStatistics as TopicTRPV1BiologyMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundBAPTAGanglia SpinalNitrilesButadienesAnimalsDrug InteractionsEnzyme InhibitorsPhosphorylationExtracellular Signal-Regulated MAP KinasesProtein kinase AProtein kinase CNeuronsAnalysis of VarianceDose-Response Relationship DrugGeneral NeuroscienceMEK inhibitorRatsCell biologychemistryBiochemistryCapsaicinMitogen-activated protein kinasebiology.proteinCalciumFemaleCapsaicinNeuroscience
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Ion Pairing with Bile Salts Modulates Intestinal Permeability and Contributes to Food–Drug Interaction of BCS Class III Compound Trospium Chloride

2013

In the current study the involvement of ion pair formation between bile salts and trospium chloride (TC), a positively charged Biopharmaceutical Classification System (BCS) class III substance, showing a decrease in bioavailability upon coadministration with food (negative food effect) was investigated. Isothermal titration calorimetry provided evidence of a reaction between TC and bile acids. An effect of ion pair formation on the apparent partition coefficient (APC) was examined using (3)H-trospium. The addition of bovine bile and bile extract porcine led to a significant increase of the APC. In vitro permeability studies of trospium were performed across Caco-2-monolayers and excised seg…

MaleMagnetic Resonance SpectroscopyNortropanesPharmaceutical ScienceBenzilatesBile Acids and SaltsFood-Drug InteractionsGlycochenodeoxycholic AcidDrug DiscoverymedicineAnimalsHumansRats WistarTaurodeoxycholic AcidChromatographyUssing chamberTrospium chlorideChemistryIsothermal titration calorimetryPermeationDrug interactionRatsBioavailabilityIntestinal AbsorptionCaco-2Permeability (electromagnetism)Molecular MedicineCattleCaco-2 Cellsmedicine.drugMolecular Pharmaceutics
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NMDA glutamate but not dopamine antagonists blocks drug-induced reinstatement of morphine place preference.

2004

The effects of dopaminergic and glutamatergic antagonists on the drug-induced reinstatement of a previously extinguished morphine conditioned place preference (CPP) in mice were evaluated. Following extinction of a place preference induced by morphine (40 mg/kg), a non-contingent injection of the dopaminergic antagonists SCH 23390 (0.125, 0.5 mg/kg), raclopride (0.3, 1.2 mg/kg), haloperidol (0.1, 0.2 mg/kg) and the dopamine (DA) release inhibitor CGS 10746B (1, 10 mg/kg) or glutamatergic NMDA antagonists memantine (10, 20, 40 mg/kg) and MK-801 (0.1, 0.2, 0.3 mg/kg) alone or with 10 mg/kg morphine was given. Neither the dopaminergic nor the glutamatergic antagonists alone reinstated the plac…

MaleMice Inbred StrainsPharmacologyReceptors N-Methyl-D-AspartateExtinction PsychologicalGlutamatergicMiceDopaminemedicineHaloperidolAnimalsDrug InteractionsRacloprideAnalysis of VarianceBehavior AnimalDose-Response Relationship DrugMorphineChemistryGeneral NeuroscienceDopaminergicMemantineConditioned place preferenceAnalgesics OpioidNMDA receptorConditioning OperantDopamine AntagonistsExcitatory Amino Acid Antagonistsmedicine.drugBrain research bulletin
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Aspirin protects striatal dopaminergic neurons from neurotoxin-induced degeneration: an in vivo microdialysis study.

2006

The effect of aspirin on dopaminergic neuronal damage induced by in vivo infusion of 1-methyl-4-phenylpiridinium iodide (MPP(+)) and 6-hydroxydopamine (6-OHDA) was studied in rats, using microdialysis. Rat striata were perfused with 1 mM MPP(+) or 6-OHDA for 10 min, causing peak levels of dopamine (DA) in the dialytic fluid, after 40 min. After 24 h, 1 mM MPP(+) was perfused again for 10 min and DA levels measured in the dialytic fluid, as an index of neuronal cell integrity. Pretreatment with Aspidol (lysine acetylsalicylate), 180 mg/kg i.p., 1 h before MPP(+) or 6-OHDA perfusion, did not modify DA extracellular output, on day 1, but restored MPP(+)-induced DA release on day 2, indicating …

MaleMicrodialysisTyrosine 3-MonooxygenaseDopamineMicrodialysisNeurotoxinsPharmacologyNeuroprotectionSettore BIO/09 - FisiologiaRats Sprague-Dawleychemistry.chemical_compoundIn vivoHydroxybenzoatesNeurotoxinAnimalsDrug InteractionsMolecular BiologyChromatography High Pressure LiquidNeuronsAnalysis of VarianceAspirinGeneral NeuroscienceMPTPDopaminergicImmunohistochemistryCorpus StriatumRatsNeuroprotective Agentsnervous systemchemistryAnesthesiaNerve DegenerationNeurology (clinical)Aspirin in vivo microdialysisPerfusionOxidopamineDevelopmental Biology
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Effects of risperidone on the acquisition and reinstatement of the conditioned place preference induced by MDMA

2013

Some users of 3,4-methylenedioxymethylamphetamine (MDMA or ecstasy) abuse this drug and/or become concerned about their use. These individuals would benefit greatly from the development of pharmacological strategies to reduce MDMA consumption. We have previously observed that antipsychotics block acquisition and expression of the conditioned place preference (CPP) induced by MDMA, though they do not modify priming-induced reinstatement of MDMA-induced CPP after extinction. In the present study we have evaluated the capacity of the mixed serotonin (5-HT2A)/dopamine (DA D2) antagonist risperidone to block acquisition and reinstatement of MDMA induced-CPP. Adolescent male mice conditioned with…

MaleN-Methyl-34-methylenedioxyamphetamineEcstasyPharmacologyMiceRewardDopamineConditioning Psychologicalmental disordersmedicineAnimalsDrug InteractionsSerotonin Plasma Membrane Transport ProteinsDopamine Plasma Membrane Transport ProteinsRisperidoneDose-Response Relationship DrugGeneral NeuroscienceAge FactorsAntagonistMDMAExtinction (psychology)RisperidoneCorpus StriatumConditioned place preferenceAnimals NewbornHallucinogensSerotoninPsychologypsychological phenomena and processesAntipsychotic Agentsmedicine.drugBrain Research Bulletin
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Role of GABAergic antagonism in the neuroprotective effects of bilobalide

2006

Bilobalide, a constituent of Ginkgo biloba, has neuroprotective properties. Its mechanism of action is unknown but it was recently found to block GABA(A) receptors. The goal of this study was to test the potential role of a GABAergic mechanism for the neuroprotective activity of bilobalide. In rat hippocampal slices exposed to NMDA, release of choline indicates breakdown of membrane phospholipids. NMDA-induced choline release was almost completely blocked in the presence of bilobalide (10 microM) and under low-chloride conditions. Bicuculline (100 microM), a competitive antagonist at GABA(A) receptors, reduced NMDA-induced choline release to a small extent (-23%). GABA (100 microM) partiall…

MaleN-MethylaspartateBrain EdemaCyclopentanesIn Vitro TechniquesPharmacologyBicucullineInhibitory postsynaptic potentialHippocampusArticlegamma-Aminobutyric acidCholineGABA AntagonistsRats Sprague-Dawleychemistry.chemical_compoundBilobalideExcitatory Amino Acid AgonistsmedicineAnimalsPicrotoxinDrug InteractionsFuransMolecular Biologygamma-Aminobutyric AcidChemistryGABAA receptorGeneral NeuroscienceBicucullineGABA receptor antagonistBridged Bicyclo Compounds HeterocyclicRatsGinkgolidesNeuroprotective Agentsnervous systemNonlinear DynamicsMechanism of actionArea Under CurveGABAergicNeurology (clinical)medicine.symptomSynaptosomesDevelopmental Biologymedicine.drugBrain Research
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Intensity of GABA-evoked responses is modified by nitric oxide-active compounds in the subthalamic nucleus of the rat: a microiontophoretic study.

2009

We have previously described modulatory effects of nitric oxide (NO)-active drugs on subthalamic nucleus (STN) neurons. In this study, the effects of microiontophoretically applied NO-active compounds on GABA-evoked responses were investigated in subthalamic neurons extracellularly recorded from anesthetized rats: 45 of 62 cells were excited by S-nitroso-glutathione (SNOG), an NO donor, whereas 28 of 43 neurons were inhibited by N-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor. Nearly all neurons responding to SNOG and/or L-NAME showed significant inhibitory responses to the administration of iontophoretic GABA. In these cells, the changes induced by NO-active drugs in the magnitud…

MaleNOS inhibitormedicine.drug_classBiophysicsAction PotentialsGlutamic AcidPharmacologyNeurotransmissionInhibitory postsynaptic potentialBicucullineNitric OxideSettore BIO/09 - FisiologiaNitric oxideGABA AntagonistsCellular and Molecular Neurosciencechemistry.chemical_compoundSubthalamic NucleusmedicineAnimalsDrug InteractionsNitric Oxide DonorsEnzyme InhibitorsRats Wistargamma-Aminobutyric AcidNeuronssubthalamic nucleus GABA SNOG L-NAMEIontophoresisBicucullineIontophoresisReceptor antagonistElectric StimulationRatsSubthalamic nucleusNG-Nitroarginine Methyl Esternervous systemchemistryS-Nitrosoglutathionemedicine.drugJournal of neuroscience research
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The gamma(2)-MSH peptide mediates a central analgesic effect via a GABA-ergic mechanism that is independent from activation of melanocortin receptors.

2001

Using the latency for tail-flick after thermal stimulation we have assessed the effects of alpha-, gamma(1)- and gamma(2)-MSH on nociceptive threshold in the mice. Intracisternal injections of gamma(2)-MSH induced a distinct analgesia, while gamma(1)-MSH in the same doses gave only a minor analgesia. Intracisternal alpha-MSH instead gave a short-term hyperalgesia. The effect of gamma(2)-MSH was not blocked by any of the MC(4)/MC(3)receptor antagonist HS014, naloxone or by the prior intracisternal administrations of gamma(1)-MSH. However, the gamma(2)-MSH analgesic response was completely attenuated by treating animals with the GABA(A)antagonist bicuculline. The gamma(2)-MSH analgesic effect…

MaleNarcotic Antagonists(+)-NaloxonePharmacologyGABA Antagonistschemistry.chemical_compoundMiceEndocrinologyDrug Interactionsgamma-Aminobutyric AcidAnalgesicsMice Inbred BALB Cintegumentary systemMuscimolNaloxoneReceptors MelanocortinNociceptorsGeneral MedicineReceptor antagonistNeurologyHyperalgesiamedicine.symptomhormones hormone substitutes and hormone antagonistsmedicine.drugPain ThresholdTailendocrine systemmedicine.medical_specialtyanimal structuresmedicine.drug_classCatalepsyBicucullinePeptides CyclicCellular and Molecular Neurosciencegamma-MSHMelanocortin receptorInternal medicinemedicineAnimalsGABA ModulatorsGABA AgonistsCatalepsyDiazepamEthanolEndocrine and Autonomic SystemsAntagonistCentral Nervous System DepressantsBicucullinemedicine.diseaseEndocrinologyMuscimolchemistryReceptors Corticotropinalpha-MSHNeuropeptides
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