A rapid method for preparing synaptosomes: Comparison, with alternative procedures

Dodd, Peter R.; Hardy, John; Oakley, Arthur E.; Edwardson, James A.; Perry, Elaine K.; Delaunoy, J. P.

doi:10.1016/0006-8993(81)91086-6

Cited by 388 publications

(178 citation statements)

References 21 publications

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“…Rats were housed in standard conditions (12-hr light-dark cycle, temperature 21 ± 2'C, and humidity 50 ± 10%), four per cage. After decapitation, 0.9-1.0 g cerebrum (excluding pons, medulla, and the main part ofhippocampus) was dissected out on ice and purified synaptosomes prepared as described in detail elsewhere (Komulainen and Bondy, 1987) by the modified method of Gray and Whittaker (1962) (Dodd et al, 1981). Synaptosomes were suspended in 25 mM Hepes buffer, pH 7.4, containing NaCl 125 mM, KCI 5 mM, NaH2PO.…”

Section: Methodsmentioning

confidence: 99%

Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms

Komulainen

Bondy

1987

Toxicology and Applied Pharmacology

119

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Increased Free Intrasynaptosomal CaH by Neurotoxic Organometals: Distinetive Mechanisms. KOMULAINEN, H., AND BONDY. S. c. (1987). Toxico/. Appl. Pharmacol. 88,[77][78][79][80][81][82][83][84][85][86] Effects of several alkylmetals on free intrasynaptosomal Ca 2 + concentration, [Ca2+],, were studied in vitro using the fluorescent Ca 2 + indicator fura-2. Neurotoxic alkylmetals methylmercury than TET while dimethyltin and methyl tin were inactive. These results indicate that neurotoxic derivatives of alkylmetals studied increase [Caz+];. This occurs mainly either by nonspecific increase (Met-Hg, TET) ofCa 2 + leakage through the plasma membrane and/or specific interference with the mechanisms regulating Ca 2 + fluxes through the plasma membrane (TEL). '9 1987 Academic Press, Inc.The organometals methylmercury (Met-Hg), triethyllead (TEL) (Seawright et al.. 1984; Walsh and Tilson, 1984), triethyltin (TET), and trimethyltin (TMT) (Reuhl and Cranmer, l 984;Reiter and Ruppert, 1984) are neurotoxic but the underlying biochemical mechanisms causing impaired cell function and neuronal death are not as yet fully established. Trialkyltin and trialkyllead are thought to affect primarily mitochondria and thus energy metabolism of the cell (Aldridge, 1984;Bierkamper and Bassett, 1984). They

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Section: Methodsmentioning

confidence: 99%

Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms

Komulainen

Bondy

1987

Toxicology and Applied Pharmacology

119

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“…All tissues were placed into screw-capped microcentrifuge tubes, stored at -20° for 24 hr, and subsequently stored at -70° until used. A relatively slow freezing rate was intended to maintain the integrity of subcellular structures [ 11]. Each tissue was weighed and homogenized in 10 vol.…”

Section: Tissue Preparationmentioning

confidence: 99%

Regional selectivity in ethanol-induced pro-oxidant events within the brain

Bondy¹,

Guo²

1995

Biochemical Pharmacology

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Abst.ract-Sewral biochemical para1!1eters that reflect the presence of excess levels of reactive oxygen species were modulated m the brams of rats exposed acutely or subchronically to ethanol. These parameters included depression of cytosolic glutathione (GSH) concentration and of glutamine syntheta~e l~vds. How~ver, using these in?ices, there was a significant difference in susceptibility to ethanol m different bram reg10ns. After dietary exposure to ethanol for 12 days, these indices were sel~ctively depressed in the striatum but not in the cerebral cortex or cerebellum. Eighteen hours after a smgle acute dose of ethanol (4.5 g/kg body wt), the striatum was also the only one of these areas in which proteolytic activity. was el~vated by etha.nol treatment. Two injections of acetaldehyde (300 mg/ kg), given 18 and 2 hr pnor to tissue preparation, caused a specific reduction of glutamine synthetase in the striatum and a decrease of GSH levels in both striatum and cerebellum. Taken together, the results suggest a distinctive vulnerability of the striatum to ethanol-promoted oxidative events. Rather than ethanol exerting effects directly, the metabolite acetaldehyde may be the primary agent responsible for these chan~.es.

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“…The samples were frozen in a -80° freezer. A relatively slow freezing rate of the samples was achieved by placing them in a styrofoam box in order to maintain the integrity of synaptosomal structure [35].…”

Section: Chemicalsmentioning

confidence: 99%

Three weeks' exposure of rats to dearomatized white spirit modifies indices of oxidative stress in brain, kidney, and liver

Lam¹,

Østergaard²,

Guo

et al. 1994

Biochemical Pharmacology

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A rapid method for preparing synaptosomes: Comparison, with alternative procedures

Cited by 388 publications

References 21 publications

Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms

Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms

Regional selectivity in ethanol-induced pro-oxidant events within the brain

Three weeks' exposure of rats to dearomatized white spirit modifies indices of oxidative stress in brain, kidney, and liver

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