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1

Sphingolipid derivatives modulate intracellular Ca2plus in rat synaptosomes

100%
Miguel B. G., Calcerrada M. C., Catalan R. E., Martinez A. M.
Acta Neurobiologiae Experimentalis
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2001
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tom 61
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nr 2
2

Is lead toxicosis a reflection of altered energy metabolism in brain synaptosomes ?

84%
Rafalowska U., Struzynska L., Dabrowska-Bouta B., Lenkiewicz A.
Acta Neurobiologiae Experimentalis
|
1996
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tom 56
|
nr 2
3
Content available remote

Age-related changes of Na plus, K plus - ATPase, Ca plus2 - ATPase and Mg plus2 - ATPase activities in rat brain synaptosomes

84%
Torlinska T., Grochowalska A.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 2
Cerebral metabolism of glucose, one of the determinants of tissue ATP level, is crucial for central nervous system function. The activity of P-type pumps, namely Na+, K+ - ATPase, Ca+2 - ATPase and Mg+2 - ATPase were examined in brain synaptosomes of 5 - day, 3 - month and 18 - month - old rats to determine if changes in enzyme activity related to aging are potentially associated with alterations in glucose homeostasis. Activities of all the ATPases studied in isolated brain synaptosomes were expressed in µmol of Pi liberated from ATP by 1 mg of synaptosome protein during one hour. Serum glucose concentration was measured by the glucose oxidase method and insulin level was estimated by the RIA. Our results demonstrate that 18 - month - old rats are characterized by hyperglycemia and hyperinsulinemia. Their serum glucose concentration was significantly increased approx. 62.3% and 135.8 % as compared to 3 - month - old rats and 5 - day, newborn rats, respectively. An enormous increase in serum insulin concentration in the old, hyperglycemic rats was observed concomitantly. As a result of these changes the insulin - to - glucose ratio in the old rats was greatly increased approx. (270% and 230%) compared to young, mature and newborn rats. Hyperglycemia and hyperinsulinemia occurring in the old rats, had a different impact on activities of the ATPases tested. Our results have revealed that Na+, K+ - ATPase activity remains almost unchanged with age, the activity of Ca+2 - ATPase decreases, whereas that of Mg+2 - ATPase increases significantly in old, insulin resistant rats. In conclusion it seems that changes in activity of different P - type pumps may differ with aging and that adaptation of specific ATPases to internal environment alterations is not identical.
4
Content available remote

In vivo and in vitro effects of hyperglycemia on Naplus-Kplus, Caplus2, Mgplus2-dependent ATPases activity in brain synaptosomes of aging rats

67%
Torlinska T., Grochowalska A., Kupisz J., Skoracka J., Kojo S.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
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nr 7
145-158
Cerebral metabolism of glucose, one of the determinants of tissue ATP level, is crucial for the CNS function. The activity of P-type pumps: Na+, K+-ATPase, Ca+2-ATPase and Mg+2-ATPase were examined in rat brain synaptosomes to determine if changes in the enzyme activity related to aging are potentially associated with alterations in glucose homeostasis. Male Wistar rats (newborn, 3- and 18-month-old) were sacrificed by decapitation and synaptic plasma membranes were isolated from brains. In vivo study demonstrated that 18-month-old rats were characterized by hyperglycemia, hyperinsulinemia and increased total antyoxidative status (TAS) level. These conditions had a different impact on activities of the ATPases tested in vivo: only the activity of Ca+2-ATPase decreased whereas that of Mg+2-ATPase increased significantly. In vitro experiments, prior incubation of isolated synaptosomes with glucose of concentrations corresponding to normoglycemia in vivo (4.5 - 6.5 mM), stimulated Ca+2-ATPase activity, whereas higher glucose concentrations (10.0 - 12.5 mM) inhibited significantly the enzyme activity. The most sensitive to hyperglycemia appeared Na+, K+-ATPase in old rats synaptosomes with the progressive decline starting at 6.5 mM glucose. The activity of Mg+2-ATPase was not inhibited in vitro even at high glucose concentrations that may explain the increased in vivo, activity of this enzyme in old, hyperglycemic rats.
5

Modulation of GABA transport in synaptosomes by histamine

67%
Waskiewicz J., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1992
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tom 52
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nr 2
6

Acute lead toxicity and energy metabolism in rat brain synaptosomes

67%
Struzynska L., Dabrowska-Bouta B., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1997
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tom 57
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nr 4
7

Protective role of L-methionine against free radical damage of rat brain synaptosomes

67%
Slyshenkov V. S., Shevalye A. A., Liopo A. V., Wojtczak L.
Acta Biochimica Polonica
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2002
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tom 49
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nr 4
Incubation of rat brain synaptosomal/mitochondrial fraction with ieri-butyl- hydroperoxide resulted in accumulation of the lipid peroxidation product, conjugated dienes, damage of the synaptosomal membrane as evidenced by leakage of lactate dehydrogenase, and decrease of the total content of glutathione and of the GSH/GSSG ratio. This treatment also produced a considerable decrease of the ouabain-sensitive ATPase activity and a much smaller diminution of the activities of glutathione reductase and glutathione transferase. Preincubation of the synaptosomal/mitochon- drial fraction with 0.5 or 1.0 mM L-methionine significantly protected against lipid peroxidation, membrane damage and changes in the glutathione system produced by low (1 mM) concentrations of ieri-butylhydroperoxide and completely prevented inac- tivation of ouabain-sensitive ATPase, glutathione reductase and glutathione transferase by such treatment. The importance of L-methionine in antioxidant protec­tion is discussed.
8

Effect of acute hepatic encephalopathy on [3 H]dopamine release from rat cerebral cortex and striatum in vitro: role of Ca2plus

59%
Borkowska H. D., Oja S. S., Hilgier W., Saransaari P., Albrecht J.
Acta Neurobiologiae Experimentalis
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2000
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tom 60
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nr 1
Hepatic encephalopathy (HE) is characterized by motor symptoms associated with disturbed functions of the dopaminergic systems, but the underlying mechanisms are not clear. A previous study from our laboratories revealed that HE, induced in rats by repeated treatment with thioacetamide, enhanced the 50 mM potassium (KC1) -stimulated release of newly loaded [3H]dopamine in both striatal and frontal cerebral cortical slices in the presence of Ca2+. In the present study we compared the effects of HE on dopamine release in striatal and frontal cerebral cortical slices and synaptosomes in the presence and absence of Ca2+. HE enhanced the KCl-stimulated [3H]dopamine release from striatal and frontal cortical synaptosomes in the presence of Ca2+ to the same extent as in slices prepared from the respective brain regions. In the absence of Ca2+ a slight reduction in dopamine release was observed in frontal cortical synaptosomes from HE rats when compared to control rats, while no effect of HE on the release was discernible in frontal cortical and striatal slices and striatal synaptosomes. We conclude that in both brain regions studied HE stimulates dopamine exocytosis triggered by Ca2+ influx without affecting the release mediated by means of plasma membrane transporters or exocytosis involving intraterminal Ca2+.
9

The effect of lead on dopamine, GABA and histidine spontaneous and KCI-dependent releases from rat brain synaptosomes

59%
Struzynska L., Rafalowska U.
Acta Neurobiologiae Experimentalis
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1994
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tom 54
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nr 3
10

Plasma membrane phospholipid asymmetry and its maintenance

51%
Roelofsen B., Vermeulen W. P., Op den Kamp J.A.F.
Biophysics of Membrane Transport
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1994
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tom 12
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nr 2
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