Search results for "toxin"

showing 10 items of 1434 documents

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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Intermittent cortical stimulation evokes sensitization to cocaine and enduring changes in matrix and striosome neuron responsiveness

2005

Both the behavioral sensitization syndrome and the changes in the responsiveness of striatal neurons evoked by chronic cocaine exposure may be linked to enhanced neocortical activity, yet a direct demonstration of the effects of cortical stimulation on these parameters is lacking. We have found that repeated stimulation of the rat prelimbic cortex with picrotoxin (0.25 microg/0.25 microl, five injections on alternate days followed by 7-day withdrawal) contributed to increase c-Fos protein expression in the striosomes of the dorsolateral striatum, while producing the opposite effect in the matrix compartment, after a single exposure to cocaine (25 mg/kg). Moreover, rats exposed to cortical s…

MaleMicroinjectionsStriosomeInfralimbic cortexPrefrontal CortexStimulationStriatumMotor ActivityGABA AntagonistsRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundCocainemedicineAnimalsPicrotoxinPrefrontal cortexNeuronsBehavior AnimalImmunohistochemistryStimulation ChemicalRatsNeostriatumStereotypy (non-human)medicine.anatomical_structurechemistryNeuronStereotyped BehaviorPsychologyProto-Oncogene Proteins c-fosNeurosciencePicrotoxinSynapse
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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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Identification of Patulin from

2019

The identification and characterization of fungal commensals of the human gut (the mycobiota) is ongoing, and the effects of their various secondary metabolites on the health and disease of the host is a matter of current research. While the neurons of the central nervous system might be affected indirectly by compounds from gut microorganisms, the largest peripheral neuronal network (the enteric nervous system) is located within the gut and is exposed directly to such metabolites. We analyzed 320 fungal extracts and their effect on the viability of a human neuronal cell line (SH-SY5Y), as well as their effects on the viability and functionality of the most effective compound on primary ent…

MaleNeuronsCell SurvivalPrimary Cell CulturePenicilliummicrobiomeComplex MixturesMycotoxinsEnteric Nervous SystemArticleMice Inbred C57BLMicePatulinCell Line TumorAnimalsHumansgastrointestinal systemFemaleCalcium SignalingfungiReactive Oxygen SpeciesfusariumMolecules (Basel, Switzerland)
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Nicotinic and muscarinic modulation of 5-hydroxytryptamine (5-HT) release from porcine and canine small intestine

1992

Strips of porcine and canine small intestine were incubated in vitro and the release of 5-hydroxytryptamine (5-HT) was determined by HPLC with electrochemical detection. The spontaneous outflow of 5-HT from the porcine and canine small intestine largely reflects calcium-dependent 5-HT secretion from enterochromaffin cells which are under a spontaneous neuronal, excitatory input as indicated by the inhibitory effect (30-40%) of tetrodotoxin. In both species, nicotine enhanced the release of 5-HT in a concentration-dependent manner by a maximum of about 50% at 100 microM. This effect was blocked by the nicotine receptor antagonist hexamethonium, but not by the subtype-selective nicotine recep…

MaleNicotineSerotoninmedicine.medical_specialtySwineScopolamineHexamethonium CompoundsTetrodotoxinReceptors NicotinicBiologyHexamethoniumNicotine03 medical and health scienceschemistry.chemical_compoundDogs0302 clinical medicineInternal medicineIntestine SmallDrug DiscoveryMuscarinic acetylcholine receptorEnterochromaffin CellsmedicineOxotremorineAnimalsGenetics (clinical)030304 developmental biology0303 health sciencesMuscarineOxotremorineParasympatholyticsGeneral MedicineHydroxyindoleacetic AcidBungarotoxinsReceptors MuscarinicAcetylcholine3. Good healthNicotinic agonistEndocrinologyParasympathomimeticschemistryEnterochromaffin cellMolecular MedicineCalciumFemaleHexamethoniumDimethylphenylpiperazinium Iodide030217 neurology & neurosurgeryAcetylcholinemedicine.drugThe Clinical Investigator
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Role of Ca2+-Activated K+ Channels on Adrenergic Responses of Human Saphenous Vein

2006

Background We studied the participation of K + channels on the adrenergic responses in human saphenous veins as well as the intervention of dihydropyridine-sensitive Ca 2+ channels on modulation of adrenergic responses by K + channels blockade. Methods Saphenous vein rings were obtained from 40 patients undergoing coronary artery bypass surgery. The vein rings were suspended in organ bath chambers for isometric recording of tension. Results Iberiotoxin (10 −7 mol/L), an inhibitor of large conductance Ca 2+ -activated K + channels, and charybdotoxin (10 −7 mol/L), an inhibitor of both large and intermediate conductance Ca 2+ -activated K + channels, enhanced the contractions elicited by elec…

MaleNifedipineCharybdotoxinAdrenergicStimulationIn Vitro TechniquesApaminMuscle Smooth VascularNorepinephrinePotassium Channels Calcium-Activatedchemistry.chemical_compoundInternal MedicinemedicineHumansSaphenous VeinChannel blockerbusiness.industryDihydropyridineMiddle AgedIberiotoxinCalcium Channel BlockersElectric StimulationchemistryVasoconstrictionMuscle TonusAnesthesiaBiophysicsFemalemedicine.symptombusinessMuscle contractionmedicine.drugAmerican Journal of Hypertension
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Neuroprotective Properties of Mildronate, a Small Molecule, in a Rat Model of Parkinson’s Disease

2010

Previously, we have found that mildronate [3-(2,2,2-trimethylhydrazinium) propionate dihydrate], a small molecule with charged nitrogen and oxygen atoms, protects mitochondrial metabolism that is altered by inhibitors of complex I and has neuroprotective effects in an azidothymidine-neurotoxicity mouse model. In the present study, we investigated the effects of mildronate in a rat model of Parkinson’s disease (PD) that was generated via a unilateral intrastriatal injection of the neurotoxin 6-hydroxydopamine (6‑OHDA). We assessed the expression of cell biomarkers that are involved in signaling cascades and provide neural and glial integration: the neuronal marker TH (tyrosine hydroxylase); …

MaleNitric Oxide Synthase Type IIlcsh:ChemistryUbiquitinNeurotoxinlcsh:QH301-705.5Receptor Notch3SpectroscopyNeuronsReceptors NotchbiologyGlial fibrillary acidic proteinMicrofilament ProteinsGeneral MedicineComputer Science ApplicationsCell biologySubstantia NigraNitric oxide synthaseNeuroprotective Agentsmedicine.anatomical_structureBiochemistryNeurogliaNeurogliaMethylhydrazinesneuroimmunological biomarkersTyrosine 3-Monooxygenasesmall moleculeSubstantia nigraParkinson’s disease; 6-OHDA model; neuroimmunological biomarkers; mildronate; small moleculeNeuroprotectionArticleCatalysisInorganic ChemistryGlial Fibrillary Acidic ProteinmedicineAnimalsParkinson Disease SecondaryRats WistarPhysical and Theoretical ChemistryOxidopamineMolecular BiologyTyrosine hydroxylase6-OHDA modelCalcium-Binding ProteinsmildronateOrganic ChemistryCorpus StriatumRatslcsh:Biology (General)lcsh:QD1-999nervous systemParkinson’s diseasebiology.proteinBiomarkersInternational Journal of Molecular Sciences
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Sulfhydryl G Proteins and Phospholipase A2-Associated G Proteins Are Involved in Adrenergic Signal Transduction in the Rat Pineal Gland

2001

The rat pineal gland with its circadian noradrenaline-regulated melatonin rhythm is an excellent model for studying adrenergic signal transduction with respect to cAMP and cGMP formation. The stimulatory G(s) proteins play a well-established role in this process. In contrast, the potential roles of the inhibitory G(i) proteins, the functionally unclear other G(o) proteins, and a number of G protein subtypes are not known. The present study examines the effects on beta(1)- and beta(1)-plus-alpha(1)-stimulated cAMP and cGMP formation of a number of G protein modulators in rat pinealocyte suspension cultures. The effects of the nitric oxide donor sodium nitroprusside on cGMP were also examined…

MaleNitroprussideArylamine N-AcetyltransferaseG proteinAdrenergicWasp VenomsPhospholipaseBiologyNitric OxidePertussis toxinBenzylisoquinolinesPineal GlandPhospholipases APinealocyteRats Sprague-DawleyPhenylephrineAlkaloidsEndocrinologyPhospholipase A2GTP-Binding ProteinsCyclic AMPAnimalsp-Methoxy-N-methylphenethylamineVirulence Factors BordetellaCyclic GMPSulfhydryl ReagentsIsoproterenolAdrenergic beta-AgonistsRatsReceptors AdrenergicPhospholipases A2Pertussis ToxinBiochemistryEthylmaleimideMastoparanbiology.proteinIntercellular Signaling Peptides and ProteinsAnimal Science and ZoologySignal transductionPeptidesAdrenergic alpha-AgonistsSignal TransductionGeneral and Comparative Endocrinology
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Nitric oxide induces muscular relaxation via cyclic GMP-dependent and -independent mechanisms in the longitudinal muscle of the mouse duodenum

2003

The aim of this study was to investigate, in mouse duodenum, the role of nitric oxide (NO) in the relaxation of longitudinal muscle evoked by nerve activation and the coupled action mechanism. Electrical field stimulation (EFS; 0.5ms, 10-s train duration, supramaximal voltage, at various frequencies) under nonadrenergic noncholinergic conditions evoked muscular relaxation occasionally followed, at the higher stimulus frequencies, by rebound contractions. Inhibition of the synthesis of NO by Nω-nitro-L-arginine methyl ester (L-NAME; 100μM) virtually abolished the evoked relaxation. The relaxation was reduced also by apamin (0.1μM) and by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1μM)…

MaleNitroprussideCancer Researchmedicine.medical_specialtyPotassium ChannelsDuodenumPhysiologyMuscle RelaxationClinical BiochemistryNonadrenergic noncholinergic relaxationStimulationStimulus (physiology)Inhibitory postsynaptic potentialApaminSettore BIO/09 - FisiologiaBiochemistryNitric oxideMicechemistry.chemical_compoundInternal medicineK+ -channelmedicineAnimalsCyclic GMPMolecular BiologyDose-Response Relationship DrugMuscle SmoothNitric oxideElectric StimulationDose–response relationshipEndocrinologychemistryTetrodotoxinSodium nitroprussideMouse duodenummedicine.drugNitric Oxide
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Spontaneous mechanical activity and evoked responses in isolated gastric preparations from normal and dystrophic (mdx) mice

2002

This study examined whether alterations of the spontaneous and evoked mechanical activity are present in the stomach of the mdx mouse, the animal model for Duchenne muscular dystrophy. The gastric mechanical activity from whole-organ of normal and mdx mice was recorded in vitro as changes of intraluminal pressure. All gastric preparations developed spontaneous tone and phasic contractions, although the tone of the mdx preparations was significantly greater. Atropine reduced the tone of the two preparations by the same degree. Nomega-nitro-l-arginine methyl ester (l-NAME) significantly increased the tone and spontaneous contractions only in the stomach from normal animals, but did not affect…

MaleNitroprussideDuchenne muscular dystrophymedicine.medical_specialtymdx mouseContraction (grammar)PhysiologyDuchenne muscular dystrophyTetrodotoxinCholinergic AgonistsSettore BIO/09 - FisiologiaContractilityMicechemistry.chemical_compoundOrgan Culture TechniquesInternal medicinemedicineAnimalsNitric Oxide Donorsmdx mouseAnesthetics LocalEnzyme InhibitorsNeuroscience (all)Endocrine and Autonomic SystemsChemistryStomachStomachGastroenterologyMuscle SmoothNitric oxideAnatomyMuscular Dystrophy AnimalGastric smooth musclemedicine.diseaseElectric StimulationMuscular Dystrophy DuchenneGastric mechanical activityAtropineNG-Nitroarginine Methyl Estermedicine.anatomical_structureEndocrinologyMice Inbred mdxTetrodotoxinCholinergicCarbacholMuscle Contractionmedicine.drug
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