Search results for "Neurotoxin"

showing 10 items of 53 documents

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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An Integrated Pharmacophore/Docking/3D-QSAR Approach to Screening a Large Library of Products in Search of Future Botulinum Neurotoxin A Inhibitors

2020

Botulinum toxins are neurotoxins produced by Clostridium botulinum. This toxin can be lethal for humans as a cause of botulism

0301 basic medicineModels MolecularBotulinum ToxinsDatabases FactualNeuromuscular transmissionQuantitative Structure-Activity RelationshipPharmacologymedicine.disease_cause01 natural sciencesType Alcsh:ChemistryModelsClostridium botulinumbotulinum neurotoxin ABotulismBotulinum Toxins Type Alcsh:QH301-705.5Spectroscopyfood and beveragesGeneral MedicineBotulinum neurotoxinComputer Science ApplicationsdockingPharmacophoreQuantitative structure–activity relationshipStatic ElectricityChemicalbotulinum neurotoxin A virtual screening docking 3D-QSAR molecular dynamicsMolecular Dynamics SimulationArticleCatalysisInorganic ChemistrySmall Molecule Libraries03 medical and health sciencesDatabasesmedicinePhysical and Theoretical ChemistryMolecular BiologyFactual3D-QSARVirtual screening010405 organic chemistrybusiness.industryfungiOrganic ChemistryMolecularHydrogen Bondingmedicine.diseasevirtual screeningmolecular dynamics0104 chemical sciences030104 developmental biologyModels Chemicallcsh:Biology (General)lcsh:QD1-999Docking (molecular)Clostridium botulinumbusinessInternational Journal of Molecular 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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The CB1 cannabinoid receptor mediates excitotoxicity-induced neural progenitor proliferation and neurogenesis.

2007

Endocannabinoids are lipid signaling mediators that exert an important neuromodulatory role and confer neuroprotection in several types of brain injury. Excitotoxicity and stroke can induce neural progenitor (NP) proliferation and differentiation as an attempt of neuroregeneration after damage. Here we investigated the mechanism of hippocampal progenitor cell engagement upon excitotoxicity induced by kainic acid administration and the putative involvement of the CB1 cannabinoid receptor in this process. Adult NPs express kainate receptors that mediate proliferation and neurosphere generation in vitro via CB1 cannabinoid receptors. Similarly, in vivo studies showed that excitotoxicity-induce…

medicine.medical_specialtyKainic acidCannabinoid receptorNeurotoxinsExcitotoxicityKainate receptorBiologymedicine.disease_causeBiochemistryNeuroprotectionHippocampuschemistry.chemical_compoundMiceReceptor Cannabinoid CB1Epidermal growth factorInternal medicinemedicineAnimalsMolecular BiologyCell ProliferationMice KnockoutNeuronsKainic AcidStem CellsNeurogenesisCell BiologyEndocannabinoid systemCell biologyNerve RegenerationEndocrinologynervous systemchemistrylipids (amino acids peptides and proteins)Fibroblast Growth Factor 2The Journal of biological chemistry
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Differential effect of beta-N-oxalylamino-L-alanine, the Lathyrus sativus neurotoxin, and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate …

2000

We studied the effect of beta-oxalylamino-L-alanine, a glutamate analog present in Lathyrus sativus seeds and implicated in the etiopathogenesis of neurolathyrism, and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate on the extracellular levels of aspartate, glutamate and taurine in the primary motor cortex of freely moving rats. We found that while both neurotoxins increase the level of aspartate and glutamate, only (+/-)-alpha(-amino-3-hydroxy-5-methylisoxazole-4-propionate is able to modulate the level of taurine. GYKI-52466, a non-competitive non-NMDA antagonist, inhibited beta-oxalylamino-L-alanine-induced increase of aspartate, but not that of glutamate. Conversely, this ant…

MaleTaurineTaurineMicrodialysisGlutamic AcidTetrodotoxinReceptors N-Methyl-D-AspartateRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundGlutamate aspartate transporterNeurotoxinAnimalsNeurotransmitteralpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAlaninechemistry.chemical_classificationAspartic AcidbiologyGlutamate receptorMotor CortexAmino Acids DiaminoBrainCell BiologyCorpus StriatumAmino acidRatschemistryBiochemistrybiology.proteinPotassiumbeta-AlanineNMDA receptorExtracellular SpaceExcitatory Amino Acid AntagonistsNeurochemistry international
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Minireview: Nicotinic Acetylcholine Receptors on Hippocampal Neurons: Distribution on the Neuronal Surface and Modulation of Receptor Activity

1997

The recent development of a technique that uses infrared microscopy for the visualization of well-defined areas on the surface of neurons, and a computerized system of micromanipulators led to the discovery that functional nicotinic acetylcholine receptors (nAChRs) are expressed at higher density on the dendrites than on the soma of rat hippocampal neurons. The finding that the expression of alpha-bungarotoxin-sensitive, alpha 7-bearing, nAChRs and dihydro-beta-erythroidine-sensitive, alpha 4 beta 2 nAChRs tends to increase along the dendritic length suggests that these receptors may be highly involved in the integration of synaptic functions in hippocampal neurons. The present report also …

SerotoninMicrocystinsBacterial ToxinsNeurotoxinsReceptors NicotinicHippocampal formationPharmacologyHippocampusModels BiologicalBiochemistryGanglion type nicotinic receptormedicineAnimalsReceptorEvoked PotentialsMolecular Biologygamma-Aminobutyric AcidAcetylcholine receptorNeuronsCyanobacteria ToxinsChemistryCell BiologyAcetylcholineRatsmedicine.anatomical_structureNicotinic agonistnervous systemMarine ToxinsSomaAlpha-4 beta-2 nicotinic receptorInfrared microscopyNeuroscienceJournal of Receptors and Signal Transduction
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Structural brain network fingerprints of focal dystonia

2019

Background: Focal dystonias are severe and disabling movement disorders of a still unclear origin. The structural brain networks associated with focal dystonia have not been well characterized. Here, we investigated structural brain network fingerprints in patients with blepharospasm (BSP) compared with those with hemifacial spasm (HFS), and healthy controls (HC). The patients were also examined following treatment with botulinum neurotoxin (BoNT). Methods: This study included matched groups of 13 BSP patients, 13 HFS patients, and 13 HC. We measured patients using structural-magnetic resonance imaging (MRI) at baseline and after one month BoNT treatment, at time points of maximal and minim…

Dystoniagraph theory610 Medical sciencesblepharospasm610 Medizinbotulinum neurotoxinlcsh:Neurology. Diseases of the nervous systemlcsh:RC346-429Original ResearchMRIstructural brain networks
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Novel imine antioxidants at low nanomolar concentrations protect dopaminergic cells from oxidative neurotoxicity.

2009

Strong evidence indicates that oxidative stress may be causally involved in the pathogenesis of Parkinson's disease. We have employed human dopaminergic neuroblastoma cells and rat primary mesencephalic neurons to assess the protective potential of three novel bisarylimine antioxidants on dopaminergic cell death induced by complex I inhibition or glutathione depletion. We have found that exceptionally low concentrations (EC(50) values approximately 20 nM) of these compounds (iminostilbene, phenothiazine, and phenoxazine) exhibited strong protective effects against the toxicities of MPP(+), rotenone, and l-buthionine sulfoximine. Investigating intracellular glutathione levels, it was found t…

Antioxidantmedicine.medical_treatmentDopamineGlutathione reductaseNeurotoxinsBiologymedicine.disease_causeProtein oxidationBiochemistryAntioxidantsLipid peroxidationRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumormedicineAnimalsHumansCells CulturedMembrane Potential MitochondrialCell DeathDose-Response Relationship DrugNeurotoxicityParkinson DiseaseRotenoneGlutathionemedicine.diseaseGlutathioneMitochondriaRatsSubstantia NigraOxidative StressNeuroprotective AgentschemistryBiochemistryElectron Transport Chain Complex ProteinsCytoprotectionNerve DegenerationIminesOxidation-ReductionOxidative stressJournal of neurochemistry
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Reduction of red-green discrimination by dopamine D1 receptor antagonists and retinal dopamine depletion

1996

AbstractReduction of wavelength discrimination ability in the 560–640 nm range, but not in the 404–540 nm range, has been demonstrated in goldfish after intravitreal injection of D1-dopamine receptor antagonists. Intravitreal injection of the dopaminergic neurotoxin 6-OH-dopamine severely reduced wavelength discrimination ability in the 540–661 nm range within 3 days. Discrimination ability could be reconstituted by the Dl-agonist SKF 38393. Animals recovered from injection of 6-OH-dopamine within 14–16 days. No change of wavelength discrimination was induced by 6-OH-dopamine in the 461–540 nm range. We conclude that under photopic conditions dopamine modulates retinal mechanisms involved i…

DopamineWavelength discriminationRetinaHydroxydopamineschemistry.chemical_compoundDiscrimination PsychologicalDopamine receptor D1OpticsDopamineGoldfishmedicineAnimalsNeurotoxinDopamine receptorsNeurotransmitterRetinabusiness.industryReceptors Dopamine D1DopaminergicRetinalSensory SystemsOphthalmologymedicine.anatomical_structurechemistryDopamine receptorDopamine AgonistsBiophysicssense organsbusinessColor Perceptionmedicine.drugVision Research
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A single mutation in the recombinant light chain of tetanus toxin abolishes its proteolytic activity and removes the toxicity seen after reconstituti…

1994

Specific proteolysis by the tetanus toxin light chain of a vesicle-associated membrane protein (VAMP) involved in exocytosis is thought to underlie its intracellular blockade of neurotransmitter release. To substantiate this mechanism, recombinant light chain was expressed as a maltose binding protein-light chain fusion product in Escherichia coli. After purification of affinity chromatography and cleavage with factor Xa, the resultant light chain was isolated and its identity confirmed by Western blotting and N-terminal sequencing. It exhibited activity similar to that of the native light chain in proteolyzing its target in isolated bovine small synaptic vesicles and in hydrolyzing a 62-re…

medicine.medical_treatmentRecombinant Fusion ProteinsMolecular Sequence DataNeurotoxinsGlutamic AcidMaltose bindingNerve Tissue ProteinsIn Vitro TechniquesImmunoglobulin light chainBiochemistrySynaptic vesicleExocytosislaw.inventionR-SNARE ProteinsMiceStructure-Activity RelationshipAffinity chromatographyGlutamatesTetanus ToxinlawThermolysinEndopeptidasesmedicineEscherichia coliAnimalsAmino Acid SequenceProteaseBase SequenceChemistryMembrane ProteinsMolecular biologyPeptide FragmentsRecombinant DNAMutagenesis Site-DirectedCattleBiochemistry
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