Search results for "neurotoxin"

showing 10 items of 53 documents

Effect of beta-N-oxalylamino-L-alanine on cerebellar cGMP level in vivo.

1993

Beta-N-oxalylamino-L-alanine (BOAA), a non-protein amino acid present in the seeds of Lathyrus Sativus (LS), is one of several neuroactive glutamate analogs reported to stimulate excitatory receptors and, in high concentrations, cause neuronal degeneration. In the present study, the in vivo acute effects of synthetic BOAA and LS seed extract were investigated on rat cerebellar cyclic GMP following intraperitoneal (10-100 mg/kg) or oral (100 mg/kg) administration of subconvulsive doses of toxin. Furthermore, the BOAA content in LS seeds and in the cerebellum of injected rats was determined by high performance liquid chromatograph analysis. A dose- and time-dependent increase of cerebellar cy…

Malemedicine.medical_specialtyCerebellumAdministration OralStimulationBiologyBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundKynurenic acidIn vivoInternal medicineCerebellummedicineNeurotoxinAnimalsRats WistarCyclic guanosine monophosphateCyclic GMPChromatography High Pressure LiquidLathyrismGlutamate receptorAmino Acids DiaminoGeneral Medicinemedicine.diseaseRatsEndocrinologymedicine.anatomical_structurechemistrybeta-AlanineInjections IntraperitonealNeurochemical research
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Pregnenolone sulfate, a naturally occurring excitotoxin involved in delayed retinal cell death.

2002

The present study was designed to investigate the neurosteroid pregnenolone sulfate (PS), known for its ability to modulate NMDA receptors and interfere with acute excitotoxicity, in delayed retinal cell death. Three hours after exposure of the isolated and intact retina to a 30-min PS pulse, DNA fragmentation as assessed by genomic DNA gel electrophoresis and a modified in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method appeared concurrently with an increase in superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels. At 7 h, the increased amount of DNA laddering was accompanied by a higher number of TUN…

Malemedicine.medical_specialtyNeurotoxinsExcitotoxicityApoptosisDNA FragmentationDNA ladderingBiologymedicine.disease_causeBiochemistryReceptors N-Methyl-D-AspartateThiobarbituric Acid Reactive SubstancesRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundAdjuvants ImmunologicSuperoxidesInternal medicinemedicineTBARSIn Situ Nick-End LabelingAnimalsCycloheximideRats WistarProgesteroneProtein Synthesis InhibitorsTUNEL assayEstradiolL-Lactate DehydrogenaseDehydroepiandrosterone SulfateSuperoxide DismutaseRatsEndocrinologychemistryApoptosisPregnenolonePregnenoloneDNA fragmentationLipid PeroxidationPregnenolone sulfateReactive Oxygen Speciesmedicine.drugJournal of neurochemistry
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Acute ammonia intoxication induces an NMDA receptor-mediated increase in poly(ADP-ribose) polymerase level and NAD+ metabolism in nuclei of rat brain…

2004

Acute ammonia toxicity is mediated by excessive activation of NMDA receptors. Activation of NMDA receptors leads to activation of poly(ADP-ribose) polymerase (PARP) which mediates NMDA excitotoxicity. PARP is activated following DNA damage and may lead to cell death via NAD+ and ATP depletion. The aim of the present work was to assess whether acute ammonia intoxication in vivo leads to increased PARP in brain cells nuclei and to altered NAD+ and superoxide metabolism and the contribution of NMDA receptors to these alterations. Acute ammonia intoxication increases PARP content twofold in brain cells nuclei.NAD+ content decreased by 55% in rats injected with ammonia. This was not due to decre…

Malemedicine.medical_specialtyPoly ADP ribose polymeraseExcitotoxicityBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundNAD+ NucleosidaseAmide SynthasesAmmoniaSuperoxidesInternal medicinemedicineAnimalsNeurotoxinRats WistarReceptorBrain ChemistryCell NucleusProtein Synthesis InhibitorsSuperoxideNAD+ ADP-RibosyltransferaseBrainProteinsNADMolecular biologyRatsEndocrinologychemistryTyrosineNMDA receptorNAD+ kinasePoly(ADP-ribose) PolymerasesJournal of Neurochemistry
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Early-onset tolerance in rat global cerebral ischemia induced by a mitochondrial inhibitor

2000

It was studied whether a subtoxic dose of the mitochondrial neurotoxin, 3-nitropropionic acid (3-NPA), can initiate early-onset tolerance induction for subsequent ischemic injury. Wistar rats were pretreated for 3 h by intraperitoneal 3-NPA (20 mg/kg body weight; n=13) or solvent (n=12). Fifteen minutes global cerebral ischemia was induced by bilateral carotid artery occlusion and hypobaric hypotension. rCBF and tissue hemoglobin oxygen saturation were measured by laser Doppler scanning and a microspectrophotometric method. Ischemic insult and brain temperature were identical in both groups. Body weight and neurological scores recovered in the pretreated group but further deteriorated in th…

Malemedicine.medical_specialtyTime FactorsNeurotoxinsIschemiaConvulsantsMotor ActivityHippocampal formationBrain IschemiaCentral nervous system diseaseBrain ischemiaProsencephalonInternal medicinemedicineAnimalsNeurotoxinRats WistarNeuronsNeocortexbusiness.industryGeneral NeuroscienceNitro Compoundsmedicine.diseaseMitochondriaRatsTolerance inductionNeuroprotective Agentsmedicine.anatomical_structureEndocrinologyReperfusion InjuryAnesthesiaPropionatesbusinessReperfusion injuryNeuroscience Letters
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Binding Sites for Neurotoxins and Cholinergic Ligands in Peripheral and Neuronal Nicotinic Receptors Studies with Synthetic Receptor Sequencesa

1995

Molecular Sequence DataNeurotoxinsIn Vitro TechniquesReceptors NicotinicLigandsBinding CompetitiveGeneral Biochemistry Genetics and Molecular BiologyStructure-Activity RelationshipGanglion type nicotinic receptorSpecies SpecificityHistory and Philosophy of ScienceConsensus SequenceEnzyme-linked receptorAnimalsAmino Acid SequenceBinding siteReceptorNeuronsBinding SitesSequence Homology Amino AcidChemistryGeneral NeuroscienceAntibodies MonoclonalPeripheralCell biologyNicotinic agonistCholinergicAlpha-4 beta-2 nicotinic receptorPeptidesSequence AlignmentAnnals of the New York Academy of Sciences
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Novel approaches in diagnosis and therapy of Creutzfeldt-Jakob disease.

2000

The scrapie prion protein, PrP(Sc), as well as its peptide fragment, PrP106-126, are toxic on neuronal cells, resulting in cell death by an apoptotic, rather than necrotic mechanism. The apoptotic process of neuronal cells induced by prion protein supports diagnosis and offers potential targets for therapeutic intervention of the prion diseases. Among the cerebrospinal fluid (CSF) proteins, which may serve as markers of neuronal cell death associated with prion diseases, the 14-3-3 protein(s) turned out to be the most promising one. A new sensitive assay allows the detection of even small changes in the normally low levels of these proteins. In vitro, the toxic effects displayed by PrP(Sc) …

NeuronsAgingCell DeathPrPSc ProteinsNeurotoxicityMemantinePrPSc ProteinsScrapieBiologyPharmacologymedicine.diseaseVirologyCreutzfeldt-Jakob Syndromenervous system diseasesPrion DiseasesmedicineNeurotoxinAnimalsHumansFlupirtineReceptor14-3-3 proteinDevelopmental Biologymedicine.drugMechanisms of ageing and development
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Differences in the temperature dependencies of uptake of botulinum and tetanus toxins in Aplysia neurons

1992

The respective neuroselective actions of botulinum type A (BoNT) and tetanus (TeTx) neurotoxins on cholinergic and non-cholinergic synapses of Aplysia are mainly due to differences in their extracellular neuronal targetting. Further information was gained on this neuroselectivity by examining the temperature dependencies of binding, internalization and intracellular action of both toxins. After reduction of temperature from 22 degrees C to 10 degrees C, the binding of neither BoNT nor TeTx was significantly altered whereas the neuronal uptake of BoNT, but not of TeTx, was prevented. Although TeTx internalization could be detected at the low temperature, its intracellular activity was greatl…

NeuronsBotulinum ToxinsGeneral Neurosciencemedia_common.quotation_subjectTemperatureBiologybiology.organism_classificationAcetylcholineSynapseTetanus ToxinAplysiaAplysiamedicineExtracellularBiophysicsAnimalsNeurotoxinCholinergicInternalizationNeuroscienceAcetylcholineIntracellularmedia_commonmedicine.drugNeuroscience Letters
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Neurodegeneration in excitotoxicity, global cerebral ischemia, and target deprivation: A perspective on the contributions of apoptosis and necrosis.

1998

In the human brain and spinal cord, neurons degenerate after acute insults (e.g., stroke, cardiac arrest, trauma) and during progressive, adult-onset diseases [e.g., amyotrophic lateral sclerosis, Alzheimer's disease]. Glutamate receptor-mediated excitotoxicity has been implicated in all of these neurological conditions. Nevertheless, effective approaches to prevent or limit neuronal damage in these disorders remain elusive, primarily because of an incomplete understanding of the mechanisms of neuronal death in in vivo settings. Therefore, animal models of neurodegeneration are crucial for improving our understanding of the mechanisms of neuronal death. In this review, we evaluate experimen…

NeuronsProgrammed cell deathNecrosisCell DeathGeneral Neurosciencemedicine.medical_treatmentNeurodegenerationNeurotoxinsGlutamate receptorExcitotoxicityApoptosisAxotomyBiologymedicine.diseasemedicine.disease_causeNeuroprotectionBrain IschemiaBrain ischemiaNecrosisNerve DegenerationmedicineAnimalsmedicine.symptomAxotomyNeuroscienceBrain research bulletin
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Neurotoxic effects of ochratoxin A on the subventricular zone of adult mouse brain

2014

Ochratoxin A (OTA), a mycotoxin that was discovered as a secondary metabolite of the fungal species Aspergillus and Penicillium, is a common contaminant in food and animal feed. This mycotoxin has been described as teratogenic, carcinogenic, genotoxic, immunotoxic and has been proven a potent neurotoxin. Other authors have previously reported the effects of OTA in different structures of the central nervous system as well as in some neurogenic regions. However, the impact of OTA exposure in the subventricular zone (SVZ) has not been assessed yet. To elucidate whether OTA affects neural precursors of the mouse SVZ we investigated, in vitro and in vivo, the effects of OTA exposure on the SVZ …

Ochratoxin Aanimal diseasesCellular differentiationSubventricular zoneAnatomyBiologyToxicologyNeural stem cellCell biologychemistry.chemical_compoundmedicine.anatomical_structurenervous systemNeuroblastchemistryIn vivomedicineNeurotoxinViability assayJournal of Applied Toxicology
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Isolation and cytotoxic activity of neurotoxin from the mucus of Actinia equina (Anthozoa, Cnidaria).

2011

Parole chiave: cytotoxicity cnidaria neurotoxin
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