Synaptosomes
Mostrando 25-36 de 155 artigos, teses e dissertações.
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25. Immunological characterization of papain-induced fragments of Clostridium botulinum type A neurotoxin and interaction of the fragments with brain synaptosomes.
After treatment of Clostridium botulinum type A neurotoxin with papain, three fragments (Mrs, 101,000, 45,000, and 43,000) were purified by hydrophobic and ion-exchange chromatography with a high-performance liquid chromatographic system. Immunoblotting analyses with monoclonal antibodies showed that the 101,000-dalton fragment consisted of the light chain a
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26. Saturable binding of halothane to rat brain synaptosomes.
The hypothesis that volatile anesthetics act directly on or bind specifically to membrane proteins remains controversial. In earlier in situ electron probe microanalysis studies in cardiac muscle we showed preferential partitioning of halothane into mitochondria. To determine whether partitioning represents saturable binding or simple solubility, a photoaffi
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27. Membrane depolarization and carbamoylcholine stimulate phosphatidylinositol turnover in intact nerve terminals.
Synaptosomes, purified from rat cerebral cortex, were prelabeled with [3H]inositol to study phosphatidylinositol turnover in nerve terminals. Labeled synaptosomes were either depolarized with 40 mM K+ or exposed to carbamoylcholine (carbachol). K+ depolarization increased the level of inositol phosphates in a time-dependent manner. The inositol trisphosphate
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28. Regulation of cytosolic free calcium concentration by intrasynaptic mitochondria.
By the use of digitonin permeabilized presynaptic nerve terminals (synaptosomes), we have found that intrasynaptic mitochondria, when studied "in situ," i.e., surrounded by their cytosolic environment, are able to buffer calcium in a range of calcium concentrations close to those usually present in the cytosol of resting synaptosomes. Adenine nucleotides and
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29. Pulsatile release of acetylcholine by nerve terminals (synaptosomes) isolated from Torpedo electric organ.
1. Electrophysiological detection of acetylcholine (ACh) release by synaptosomes from the electric organ of Torpedo was searched for by laying the isolated nerve terminals on a culture of Xenopus embryonic muscle cells (myocytes), and by recording the ACh-induced inward currents in the myocytes. 2. Whole-cell recording in one of the myocytes revealed rapid i
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30. Tityustoxin K alpha blocks voltage-gated noninactivating K+ channels and unblocks inactivating K+ channels blocked by alpha-dendrotoxin in synaptosomes.
Two nonhomologous polypeptide toxins, tityustoxin K alpha (TsTX-K alpha) and tityustoxin K beta (TsTX-K beta), purified from the venom of the Brazilian scorpion Tityus serrulatus, selectively block voltage-gated noninactivating K+ channels in synaptosomes (IC50 values of 8 nM and 30 nM, respectively). In contrast, alpha-dendrotoxin (alpha-DTX) and charybdoto
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31. Co-operative action of calcium ions in dopamine release from rat brain synaptosomes.
1. The release of [3H]dopamine from isolated presynaptic nerve terminals (synaptosomes) prepared from rat striata was measured as a function of the external Ca2+ concentration ([Ca2+]o). 2. In synaptosomes depolarized by the addition of 50 mM-K+, release of [3H]dopamine increased in a highly non-linear manner with [Ca2+]o. The release could be described as a
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32. Botulinum toxin type A blocks the morphological changes induced by chemical stimulation on the presynaptic membrane of Torpedo synaptosomes.
The action of botulinum neurotoxin on acetylcholine release, and on the structural changes at the presynaptic membrane associated with the transmitter release, was studied by using a subcellular fraction of cholinergic nerve terminals (synaptosomes) isolated from the Torpedo electric organ. Acetylcholine and ATP release were continuously monitored by chemilu
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33. The early time course of potassium-stimulated calcium uptake in presynaptic nerve terminals isolated from rat brain.
K-stimulated (voltage-dependent) 45Ca uptake in rat brain synaptosomes was measured at times ranging from 0.1 to 10 s, in experiments that employed a rapid-mixing device to initiate and terminate radiotracer uptake. The rapid mixing did not disrupt the functional integrity of the synaptosomes, as judged by their ability to take up Ca. In solutions containing
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34. Differences in attachment between herpes simplex type 1 and type 2 viruses to neurons and glial cells.
Fractions of nerve cell perikarya, synaptosomes, and astrocytic glia were prepared from human, monkey , rabbit, rat, and mouse brain tissue. The herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) binding capacity of these fractions was studied. Pretreatment of fractions with one type of HSV and the subsequent testing of adsorption of homotypic and hetero
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35. Diphenylhydantoin and potassium transport in isolated nerve terminals
The antiepileptic action of diphenylhydantoin (DPH) has been explained by two different theories: (a) that DPH stimulates the Na-K pump; (b) that DPH specifically blocks the passive translocation of sodium. Since electrophysiological experiments have recently suggested abnormal synaptic mechanisms as the basis for epileptogenic discharges, the action of DPH
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36. Abnormal sodium transport in synaptosomes from brain of uremic rats.
The causes of central nervous system (CNS) dysfunction in uremia are not well known and are not completely reversed by dialysis. This problem was investigated in synaptosomes, which are membrane vesicles from synaptic junctions in the brain. We measured Na uptake under conditions of control, veratridine stimulation, and tetrodotoxin inhibition, in synaptosom