Search results for "Synaptosome"

showing 10 items of 31 documents

Benzodiazepine receptor binding: the interactions of some non-benzodiazepine drugs with specific [3H] diazepam binding to rat brain synaptosomal memb…

1978

The interaction of several non-benzodiazepine drugs with [3H] diazepam binding to benzodiazepine receptors in rat brain synaptosomal membranes was investigated. Baclofen, benzoctamine, hydroxyzine, chlorpromazine, haloperidol, imipramine, and amitriptyline displace specific [3H] diazepam binding, but the concentrations needed are too high to explain pharmacological effects of these drugs by an interaction with benzodiazepine receptors. The most potent non-benzodiazepine drug for inhibiting specific [3H] diazepam binding was methaqualone (IC50 value of 150 micrometer). It is suggested that interactions with benzodiazepine receptors may account for the anxiolytic and anticonvulsive side effec…

Malemedicine.drug_classReceptors DrugPharmacologyIn Vitro TechniquesAnxiolyticBinding Competitivechemistry.chemical_compoundmedicineAnimalsDrug InteractionsBenzodiazepine receptor bindingPharmacologyBenzodiazepineDiazepam bindingDiazepamMembranesGABAA receptorBrainGeneral MedicineRatsBaclofenAnalepticchemistryBenzoctaminemedicine.drugSynaptosomesNaunyn-Schmiedeberg's archives of pharmacology
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A homeostatic mechanism counteracting K+-evoked choline release in adult brain

2002

Choline (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10-fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7-120 mm). The K(+) -evoked Ch release was Ca(2+) -independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K(+) -induced Ch efflux was absent. Also, under in vivo conditions, …

Malemedicine.medical_specialtyMicrodialysisMicrodialysisIn Vitro TechniquesHippocampusBiochemistryCholineCellular and Molecular Neurosciencechemistry.chemical_compoundInternal medicinePotassium Channel BlockersmedicineExtracellularAnimalsHomeostasisCholine4-AminopyridineRats WistarNeurotransmitterBrain ChemistrySynaptosomeMembrane potentialDose-Response Relationship DrugBrainBiological TransportDepolarizationHemicholinium 3RatsEndocrinologychemistryPotassiumExtracellular SpaceAcetylcholineSynaptosomesmedicine.drugJournal of Neurochemistry
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[3H]-DA release evoked by low pH medium and internal H+ accumulation in rat hypothalamic synaptosomes: involvement of calcium ions

2003

The pH fluctuations have been often interpreted as an insufficient regulation or as a consequence of the onset of pathological events, such as ischemia, in which a significant decrease in pH levels occurs. Neurotransmitter release appears to be affected by pH drop significantly. In this study, we investigated the effect of an extracellular and an intracellular acidification on tritiated dopamine release ([3H]-DA release), from superfused rat hypothalamic synaptosomes. When compared to basal release, extracellular acidification, due to a reduction in the external pH of the nominally carbonic-free superfusion media, provoked a significant increase in [3H]-DA release that showed a sensitivenes…

Malemedicine.medical_specialtySodium-Hydrogen ExchangersNigericinDopamineHypothalamusIonophoreIntraterminal acidificationchemistry.chemical_elementIn Vitro TechniquesCalciumCalcium in biologyPotassium ChlorideAmiloridehypothalamic synaptosomesCellular and Molecular Neurosciencechemistry.chemical_compoundDopamineInternal medicinemedicineExtracellularlow pHCalcium dependenceAnimalsChelationRats WistarNeurotransmitterIonophoresCell BiologyHydrogen-Ion ConcentrationRatsNeuroprotective AgentsEndocrinologychemistryNigericinSettore BIO/14 - Farmacologiadopamine releaseSuperfused synaptosome[3H]-DA outflowSettore MED/26 - NeurologiaCalciumProtonsExtracellular SpaceSynaptosomesmedicine.drugNeurochemistry International
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A presynaptic excitatory M1 muscarine receptor at postganglionic cardiac noradrenergic nerve fibres that is activated by endogenous acetylcholine.

1990

Rabbit atria were isolated with the extrinsic right vagus and sympathetic nerves intact and perfused with Tyrode solution. Noradrenaline overflow evoked by sympathetic nerve stimulation (SNS) at 3 Hz for 3 min was determined before, during, and after vagus nerve stimulation (VNS), also at 3 Hz and for 3 min. The VNS pulses preceded the SNS pulses by 3, 100 and 233 ms. Acetylcholine overflow was determined after labelling of the transmitter stores with [14C]choline. Pirenzepine 80 nmol/l failed to alter the muscarinic inhibition of noradrenaline overflow when the vago-sympathetic impulse intervals were 3 and 233 ms. At an interval of 100 ms VNS did not significantly inhibit noradrenaline ove…

Malemedicine.medical_specialtyanimal structuresSympathetic Nervous Systemmedicine.medical_treatmentStimulationBiologychemistry.chemical_compoundNorepinephrineNorepinephrineInternal medicineMuscarinic acetylcholine receptormedicineReaction TimeAnimalsCarbon RadioisotopesPharmacologyMuscarineHeartVagus NerveGeneral MedicineMuscarinic acetylcholine receptor M1PirenzepineReceptors MuscarinicAcetylcholineElectric StimulationEndocrinologynervous systemchemistrycardiovascular systemExcitatory postsynaptic potentialAutonomic Fibers PostganglionicFemaleRabbitsAcetylcholineVagus nerve stimulationmedicine.drugSynaptosomesNaunyn-Schmiedeberg's archives of pharmacology
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Abnormal accumulation of autophagic vesicles correlates with axonal and synaptic pathology in young Alzheimer's mice hippocampus

2012

Dystrophic neurites associated with amyloid plaques precede neuronal death and manifest early in Alzheimer's disease (AD). In this work we have characterized the plaque-associated neuritic pathology in the hippocampus of young (4- to 6-month-old) PS1(M146L)/APP(751SL) mice model, as the initial degenerative process underlying functional disturbance prior to neuronal loss. Neuritic plaques accounted for almost all fibrillar deposits and an axonal origin of the dystrophies was demonstrated. The early induction of autophagy pathology was evidenced by increased protein levels of the autophagosome marker LC3 that was localized in the axonal dystrophies, and by electron microscopic identification…

Pathologymedicine.medical_specialtyNeuriteClinical NeurologyHippocampusMice TransgenicPlaque AmyloidAmyloid plaquesBiologyHippocampal formationHippocampusDystrophic neuritesPathology and Forensic MedicineAmyloid beta-Protein PrecursorMiceCellular and Molecular NeuroscienceAlzheimer DiseaseAutophagyNeuritesmedicineElectron microscopyLC3AnimalsSenile plaquesMicroscopy ImmunoelectronNeuronsSynaptosomeOriginal PaperPS1/APP transgenic miceCytoplasmic VesiclesAutophagymedicine.diseaseAxonsDisease Models AnimalPresynaptic terminalsAxoplasmic transportNeurology (clinical)Alzheimer's disease
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Modulation of neuronal phospholipase D activity under depolarizing conditions

1999

Neuronal phospholipase D (PLD) activity was hypothesized to be involved in vesicle trafficking and endocytosis and, possibly, transmitter release. We here report that prolonged depolarization of rat hippocampal slices by potassium chloride (KCl) or 4-aminopyridine inhibited PLD activity. Similarly, PLD activity in rat cortical synaptosomes was significantly inhibited by depolarizing agents including veratridine and ouabain. Inhibition of calcium/calmodulin kinase II (CaMKII) which positively modulates synaptosomal PLD activity [Sarri et al. (1998) FEBS Lett. 440, 287-290] by KN-62 caused a further reduction of PLD activity in depolarized synaptosomes. Depolarization-induced inhibition of PL…

Phosphatidylinositol 45-DiphosphateTime FactorsBiophysicschemistry.chemical_elementCalciumHippocampusBiochemistryOuabainMembrane PotentialsPotassium Chloridechemistry.chemical_compoundStructural BiologyCa2+/calmodulin-dependent protein kinaseSynaptosomeElectrochemistryPhospholipase DGeneticsmedicineAnimalsPhospholipase D activityEnzyme InhibitorsRats WistarMolecular BiologyProtein Kinase CProtein Synthesis InhibitorsSynaptosomePhospholipase DCalcium/calmodulin-dependent protein kinase IINeomycinDepolarizationPhosphatidylinositol-45-bisphosphateCell BiologyRatsCell biologyenzymes and coenzymes (carbohydrates)chemistryCalcium-Calmodulin-Dependent Protein KinasesDepolarizationlipids (amino acids peptides and proteins)VeratridineSynaptosomesmedicine.drugFEBS Letters
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The neurobiological bases for the pharmacotherapy of nicotine addiction.

2007

Nicotine, the major psychoactive agent present in tobacco, acts as a potent addictive drug both in humans and laboratory animals, whose locomotor activity is also stimulated. A large body of evidence indicates that the locomotor activation and the reinforcing effects of nicotine may be related to its stimulatory effects on the mesolimbic dopaminergic function. Thus, it is now well established that nicotine can increase in vivo DA outflow in the nucleus accumbens and the corpus striatum. The stimulatory effect of nicotine on DA release most probably results from its ability to excite the neuronal firing rate and to increase the bursting activity of DA neurons in the substantia nigra pars com…

RAT STRIATAL SYNAPTOSOMESNicotineINDUCED BEHAVIORAL SENSITIZATIONmedia_common.quotation_subjectSubstantia nigraStriatumNicotinic AntagonistsBiologyNucleus accumbensPharmacologyReceptors NicotinicNicotineDrug DiscoverySUSTAINED-RELEASE BUPROPIONmedicineLOCOMOTOR STIMULANT ACTIONAnimalsHumansNicotinic Agonistsmedia_commonPharmacologyMIDBRAIN DOPAMINE NEURONSPars compactaAddictionNIGRA PARS COMPACTAFACILITATES SMOKING CESSATIONTobacco Use DisorderSUBUNIT MESSENGER-RNAAntidepressive AgentsVentral tegmental areaVENTRAL TEGMENTAL AREANicotinic agonistmedicine.anatomical_structurenervous systemmedicine.drugSEROTONIN(2C) RECEPTORS BLOCKSCurrent pharmaceutical design
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SANS (USH1G) expression in developing and mature mammalian retina

2008

AbstractThe human Usher syndrome (USH) is the most common form of combined deaf-blindness. Usher type I (USH1), the most severe form, is characterized by profound congenital deafness, constant vestibular dysfunction and prepubertal-onset of retinitis pigmentosa. Five corresponding genes of the six USH1 genes have been cloned so far. The USH1G gene encodes the SANS (scaffold protein containing ankyrin repeats and SAM domain) protein which consists of protein motifs known to mediate protein–protein interactions. Recent studies indicated SANS function as a scaffold protein in the protein interactome related to USH.Here, we generated specific antibodies for SANS protein expression analyses. Our…

Retinal degenerationScaffold proteinBlotting WesternNerve Tissue ProteinsBiologyRibbon synapseRats Inbred WKYPhotoreceptor cellRetinaMiceXenopus laevisAntibody SpecificityCiliogenesisConnecting ciliumRetinitis pigmentosamedicineAnimalsCiliaEye ProteinsCentrosomeRetinaCiliogenesisPhotoreceptor cellsCiliumImmune SeraCiliary BodyFibroblastsmedicine.diseaseSynapseSensory SystemsCell biologyRatsMice Inbred C57BLOphthalmologymedicine.anatomical_structureSynapsesRetinal developmentsense organsUsher SyndromesUsher syndromePhotoreceptor Cells VertebrateSynaptosomesVision Research
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Depletion of cytosolic GSH decreases the ATP levels and viability of synaptosomes from aged mice but not from young mice

1995

The effect of glutathione depletion on the viability of freshly isolated synaptosomes from whole brain was investigated in young and aged mice. Aging did not influence the GSH and ATP levels and the viability of these synaptosomes. However depletion of glutathione caused by the cytosolic glutathione inhibitor diethyl maleate (1 mM) resulted in a significant decline, after 60 min of incubation, in ATP levels and viability in the synaptosomes from aged mice but not in those from young mice. When synaptosomes were incubated in the presence of the mitochondrial glutathione inhibitor ethacrynic acid (0.2 mM) there was a similar decline in glutathione, ATP levels and synaptosomal viability, both …

SenescenceAgingmedicine.medical_specialtyRatónBiologyMitochondrionMiceRandom Allocationchemistry.chemical_compoundAdenosine TriphosphateCytosolInternal medicinemedicineAnimalsIncubationSynaptosomeGlutathioneGlutathioneIn vitroMitochondriaCytosolEthacrynic AcidEndocrinologychemistryFemaleEnergy MetabolismSynaptosomesDevelopmental BiologyMechanisms of Ageing and Development
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Thirty years of synaptosome research.

1993

Detached synapses (synaptosomes), first isolated by the author in 1958 and identified as such in 1960, are sealed presynaptic nerve terminals often with a portion of the target cell--sometimes amounting to a complete dendritic spine--adhering to their external surface. They can be prepared in high yield from brain tissue and also in decreasing yield from spinal cord, retina, sympathetic ganglia, myenteric plexus and electric organs. They are sealed structures which, under metabolizing conditions, respire, take up oxygen and glucose, extrude Na+, accumulate K+, maintain a normal membrane potential and, on depolarization, release transmitter in a Ca(2+)-dependent manner. They thus provide an …

SynaptosomeNervous systemMembrane potentialNeurotransmitter AgentsHistologyDendritic spineGeneral NeuroscienceResearchModels NeurologicalDepolarizationCell BiologyBiologySynaptic vesicleSynapsemedicine.anatomical_structureSynapsesmedicineBiophysicsCentrifugation Density GradientAnimalsAnatomyNeuroscienceMyenteric plexusSynaptosomesJournal of neurocytology
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