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Science (New York, N.Y.) Jul 1979Erythrosin B is a member of a class of fluorescein dyes that are suggested to elicit hyperkinesis when ingested by susceptible children. We found that erythrosin B...
Erythrosin B is a member of a class of fluorescein dyes that are suggested to elicit hyperkinesis when ingested by susceptible children. We found that erythrosin B inhibits dopamine uptake in rat caudate synaptosomes "uncompetitively" in the 10- to 800-micromolar range. Half maximal inhibition of uptake occurred at 45 micromolar. Uncompetitive inhibition denotes a decrease in efficacy of the dopamine membrane transport mechanism with an increase in affinity of dopamine to the carrier. Erythrosin B also decreased nonsaturable binding of dopamine to the synaptosome membrane. The inhibitory action of erythrosin B on dopamine uptake is consistent with the hypothesis that erythrosin B can act as a central excitatory agent able to induce hyperkinetic behavior.
Topics: Animals; Biological Transport; Caudate Nucleus; Dopamine; Erythrosine; Fluoresceins; Kinetics; Rats; Synaptosomes
PubMed: 451609
DOI: 10.1126/science.451609 -
Journal of the Autonomic Nervous System Apr 1996Synaptosomes are nerve-end particles (NEP) isolated by using the technique of differential centrifugation. The synaptosome offers a good model for biochemical and...
Synaptosomes are nerve-end particles (NEP) isolated by using the technique of differential centrifugation. The synaptosome offers a good model for biochemical and pharmacological studies of the nerve endings. No report has been made on synaptosome isolation from the urinary bladder. The purpose of our work was to develop the use of synaptosome in the research of neurophysiology and neuropharmacology of the urinary bladder. Synaptosome-rich fraction was prepared from tissue homogenate of male Wistar rat urinary bladder by differential centrifugation (1000, 17,000 and 100,000 g) with discontinuous sucrose gradient. Electron microscopy showed synaptosomes as thin-walled bags containing a large number of synaptic vesicles. Two types of synaptosomes were easily discerned: those containing small agranular vesicles, and those containing dense-cored vesicles. The acetylcholine, norepinephrine, epinephrine and dopamine contents in the preparation were measured by the method of high-performance liquid chromatography. The respective concentrations were 300.4 +/- 30.1, 962.8 +/- 58.5, 617.3 +/- 59.8 and 1354.8 +/- 144.2 pmol/mg synaptosomal protein. In conclusion, it has been demonstrated that synaptosome-rich fractions can be prepared from the rat urinary bladder. Thus it is possible to apply this methodology for the investigation of the neurobiology of urinary bladders.
Topics: Animals; Autonomic Pathways; Cell Fractionation; Male; Microscopy, Electron; Neurotransmitter Agents; Rats; Rats, Wistar; Synaptosomes; Urinary Bladder
PubMed: 8740663
DOI: 10.1016/0165-1838(95)00122-0 -
Molecular Pharmacology Jan 1976
Topics: Animals; Brain; Calcium Radioisotopes; Chlortetracycline; Fatty Acids; In Vitro Techniques; Membranes; Metals; Phospholipids; Propranolol; Rats; Synaptosomes
PubMed: 1256439
DOI: No ID Found -
International Journal of Radiation... Nov 2018It is considered that exposure to static magnetic fields (SMF) may have both detrimental and therapeutic effect, but the mechanism of SMF influence on the living...
PURPOSE
It is considered that exposure to static magnetic fields (SMF) may have both detrimental and therapeutic effect, but the mechanism of SMF influence on the living organisms is not well understood. Since the adenosine triphosphatases (ATPases) and acetylcholinesterase (AChE) are involved in both physiological and pathological processes, the modulation of Na/K-ATPase, ecto-ATPases and AChE activities, as well as oxidative stress responses were followed in synaptosomes isolated from rats after chronic exposure toward differently oriented SMF.
MATERIAL AND METHODS
Wistar albino rats were randomly divided into three experimental groups (six animals per group): Up and Down group - exposed to upward and downward oriented SMF, respectively, and Control group. After 50 days, the rats were sacrificed, and synaptosomes were isolated from the whole rat brain and used for testing the enzyme activities and oxidative stress parameters.
RESULTS
Chronic exposure to 1 mT SMF significantly increased ATPases, AChE activities, and malondialdehyde (MDA) level in both exposed groups, compared to control values. The significant decrease in synaptosomal catalase activity (1.48 ± 0.17 U/mg protein) induced by exposure to the downward oriented field, compared to those obtained for Control group (2.60 ± 0.29 U/mg protein), and Up group (2.72 ± 0.21 U/mg protein).
CONCLUSIONS
It could be concluded that chronic exposure to differently oriented SMF increases ATPases and AChE activities in rat synaptosomes. Since brain ATPases and AChE have important roles in the pathogenesis of several neurological diseases, SMF influence on the activity of these enzymes may have potential therapeutic importance.
Topics: Acetylcholinesterase; Adenosine Triphosphatases; Animals; Magnetic Fields; Male; Oxidative Stress; Rats; Rats, Wistar; Synaptosomes; Time Factors
PubMed: 30238840
DOI: 10.1080/09553002.2018.1518611 -
Journal of Neural Transmission. General... 1989The neuroactive sulphur-containing amino acids L-cysteate (CA), L-cysteine sulphinate (CSA), L-homocysteine sulphinate (HSA), S-sulpho-L-cysteine (SC) and L-homocysteate...
The neuroactive sulphur-containing amino acids L-cysteate (CA), L-cysteine sulphinate (CSA), L-homocysteine sulphinate (HSA), S-sulpho-L-cysteine (SC) and L-homocysteate (HCA) evoked the release of previously accumulated D-[3H]aspartate from rat brain cerebrocortical and cerebellar synaptosome fractions in a manner that was wholly Ca2+-independent. However, analysis of endogenous release by hplc revealed the presence of both Ca2+-dependent and -independent component of L-glutamate release but only a Ca2+-independent component of L-aspartate release. CA, CSA, HSA and SC but not HCA evoked the release of previously accumulated [3H]GABA from synaptosome fractions by a mechanism shown to comprise both a Ca2+-dependent and -independent component. The specific antagonists of the N-methyl-D-aspartate (NMDA) receptor, 3-[(+/-)-2-carboxypiperazin-4-yl]propyl-l-phosphonic acid (CPP) and the relatively selective competitive quisqualate (QUIS)/kainate (KA) receptor antagonist, 6-cyano-7-dinitroquinoxalinedione (CNQX), were ineffective in blocking the excitatory sulphur amino acid-evoked release of either D-[3H]aspartate, [3H]GABA or of endogenous established transmitter amino acids.
Topics: Amino Acids; Amino Acids, Sulfur; Animals; Brain; Male; Neurotransmitter Agents; Rats; Rats, Inbred Strains; Receptors, Amino Acid; Receptors, Cell Surface; Synaptosomes
PubMed: 2572244
DOI: 10.1007/BF01249229 -
Journal of Neurochemistry Aug 1986The effect of the neurotoxic pigment bilirubin on the membrane potential of rat brain synaptosomes was studied by using the tetraphenylphosphonium ion (TTP+) technique....
The effect of the neurotoxic pigment bilirubin on the membrane potential of rat brain synaptosomes was studied by using the tetraphenylphosphonium ion (TTP+) technique. Bilirubin induces a rapid depolarization of synaptosomes, as reflected by an efflux of previously accumulated [3H]TTP+. This phenomenon persisted when the membrane potential across either the plasma membrane of the synaptosome or the inner membrane of the entrapped mitochondria was selectively depressed, thus indicating that both components of the synaptosomal membrane potential were affected by bilirubin. Bovine serum albumin, used at a albumin/bilirubin molar ratio of 1:1, had the capacity to completely prevent and reverse the effect of bilirubin. This fact demonstrates that the bilirubin-induced TPP+ release from synaptosomes is a reversible process that requires the presence of bilirubin interacting with the synaptosomal membranes. These results, together with the inhibition by bilirubin of [3H]TPP+ and [2-14C]acetate uptake by synaptosomal plasma membrane vesicles isolated from rat brain, suggest that bilirubin depresses the membrane potential across the synaptosomal plasma membrane by a mechanism involving alterations in ion permeability. This effect could be of relevance in the pathogenesis of bilirubin encephalopathy.
Topics: Animals; Bilirubin; Brain; Carbonyl Cyanide m-Chlorophenyl Hydrazone; Cell Membrane Permeability; Male; Membrane Potentials; Mitochondria; Onium Compounds; Organophosphorus Compounds; Potassium; Rats; Rats, Inbred Strains; Serum Albumin, Bovine; Synaptic Membranes; Synaptosomes
PubMed: 3734784
DOI: 10.1111/j.1471-4159.1986.tb04510.x -
Journal of Neurochemistry May 1990Synaptosome preparations were utilized to characterize the release and compartmentalization of immunoreactive insulin (IRI) in the adult rat brain. Depolarization of... (Comparative Study)
Comparative Study
Synaptosome preparations were utilized to characterize the release and compartmentalization of immunoreactive insulin (IRI) in the adult rat brain. Depolarization of synaptosomes by elevation of the external potassium ion concentration elicited release of IRI from the synaptosomes into the incubation medium. This release was reduced or eliminated under three conditions known to prevent depolarization-induced Ca2+ flux: elevating the external MgCl2, adding CoCl2, and eliminating external Ca2+ with EGTA. Depolarization of synaptosomes by veratridine also elicited release of synaptosomal IRI. This release was inhibited by tetrodotoxin. The amount of IRI released under depolarizing conditions represented 3-7% of that contained in the synaptosomes. High levels of IRI release also were observed upon removal of external Na+ to allow depolarization-independent influx of external Ca2+ into the synaptosomal compartment. The Ca2+ dependency of synaptosomal IRI release suggests IRI is stored in the adult rat brain in synaptic vesicles within nerve endings from which it can be mobilized by exocytosis in association with neural activity.
Topics: Animals; Brain; Buffers; Electrochemistry; Insulin; Pancreas; Potassium Chloride; Radioimmunoassay; Rats; Synaptosomes; Veratridine
PubMed: 2182775
DOI: 10.1111/j.1471-4159.1990.tb01219.x -
Biochemical and Biophysical Research... Mar 1987The binding ability of Cl. botulinum neurotoxin to synaptosomes upon treatment with various enzymes (neuraminidase, trypsin, and beta-bungarotoxin containing...
The binding ability of Cl. botulinum neurotoxin to synaptosomes upon treatment with various enzymes (neuraminidase, trypsin, and beta-bungarotoxin containing phospholipase A2 activity) was studied. When synaptosomes were treated with neuraminidase, their ability to bind toxin decreased; trypsin and beta-bungarotoxin had slightly week or no effect. The decrease in toxin-binding ability of synaptosomes was paralleled by a release of sialic acid from the synaptosomes by the neuraminidase treatment. The toxin-binding ability of synaptosomes treated with neuraminidase was lower than untreated ones at a high concentration of sodium chloride. The binding of the toxin to synaptosomes occurred at least at the two types of structural sites, one site which contained sialic acid, and other site which was sensitive to high ionic strength. It may be possible that another binding state except these is present at the synapse.
Topics: Animals; Binding Sites; Botulinum Toxins; Cerebellum; In Vitro Techniques; Neuraminidase; Neurotoxins; Phospholipases A; Phospholipases A2; Rats; Rats, Inbred Strains; Synaptosomes; Trypsin
PubMed: 3566763
DOI: 10.1016/0006-291x(87)90339-1 -
Pharmacology & Toxicology May 1989Interaction of lead with the serotonergic system has been studied in vitro in rat brain synaptosomal fraction prepared from cortical tissue. Synaptosomes were loaded...
Interaction of lead with the serotonergic system has been studied in vitro in rat brain synaptosomal fraction prepared from cortical tissue. Synaptosomes were loaded with 3H-5-HT and spontaneous and K+-evoked release of the amine was examined in the presence and the absence of calcium. It was shown that lead itself induced the release of 3H-5-HT (EC50 = 27 microM). This effect decreased (40%) in the presence of calcium without modification of the EC50. Moreover, lead markedly inhibited the K+-evoked release of 3H-5-HT observed in the presence of calcium. This effect was obtained either in the presence of lead or using synaptosomes pretreated with lead and washed. These results indicate that lead interferes with neuronal 5-HT release by mechanism(s) involving calcium.
Topics: Animals; Calcium; Cerebral Cortex; Evoked Potentials; In Vitro Techniques; Lead; Male; Potassium; Rats; Rats, Inbred Strains; Serotonin; Synaptosomes
PubMed: 2771873
DOI: 10.1111/j.1600-0773.1989.tb00687.x -
Psychopharmacology Aug 1977The effect of di-n-propylacetate (DPA) on the 'binding' of gamma-aminobutyric acid (GABA) to a synaptosome-enriched fraction of rat cerebral cortex has been examined...
The effect of di-n-propylacetate (DPA) on the 'binding' of gamma-aminobutyric acid (GABA) to a synaptosome-enriched fraction of rat cerebral cortex has been examined using differential centrifugation and double-isotope liquid scintillation spectrometry. DPA at 10(-4) M caused a slight decrease in GABA binding. This effect could explain in part the in vivo anticonvulsant and behavioral effects of this drug when administered to animals in high systemic doses.
Topics: Aminobutyrates; Animals; Cerebral Cortex; In Vitro Techniques; Male; Nerve Tissue Proteins; Rats; Synaptosomes; Valerates; Valproic Acid; gamma-Aminobutyric Acid
PubMed: 408853
DOI: 10.1007/BF00492360