Ex vivoprotective effects of nicotinamide and 3-aminobenzamide on rat synaptosomes treated with Aβ(1-42)

2014 ◽  
Vol 32 (7) ◽  
pp. 557-564 ◽  
Author(s):  
Ezgi Turunc Bayrakdar ◽  
Guliz Armagan ◽  
Yigit Uyanikgil ◽  
Lutfiye Kanit ◽  
Ersin Koylu ◽  
...  
Keyword(s):  
Rat Synaptosomes

ω-Agatoxins differentially block calcium channels in locust, chick and rat synaptosomes

1992 ◽  
Vol 20 (2) ◽  
pp. 263-270 ◽  
Author(s):  
J.M. Pocock ◽  
V.J. Venema ◽  
M.E. Adams
Keyword(s):  
Calcium Channels ◽  
Rat Synaptosomes

A new perspective on the role of CuZn superoxide dismutase (SOD1)

2007 ◽  
Vol 2 (3) ◽  
pp. 337-350 ◽  
Author(s):  
Paolo Mondola ◽  
Rosalba Seru ◽  
Simona Damiano ◽  
Mariarosaria Santillo
Keyword(s):  
Superoxide Dismutase ◽  
Biological Action ◽  
Gh3 Cells ◽  
Oxygen Species ◽  
Cuzn Superoxide Dismutase ◽  
New Perspective ◽  
Rat Synaptosomes ◽  
Lateral Sclerosis ◽  
Dependent Mechanism

AbstractThe CuZn superoxide dismutase (SOD1), a member of a group of isoenzymes involved in the scavenger of superoxide anions, is a dimeric carbohydrate free protein, mainly localized in the cytosol. The reactive oxygen species (ROS) are involved in many pathophysiological events correlated with mutagenesis, cancer, degenerative processes and aging. In the first part of this mini-review the well known role of SOD1 and ROS are briefly summarized. Following, a potential novel biological action that SOD1 could exert is described, based on the recent researches demonstrating the secretion of this enzyme in many cellular lines. Moreover, the role of impaired mutant SOD1 secretion, associated with cytoplasmic toxic inclusion, which occurs in familial amyotrophic lateral sclerosis (ALS), is summarized. In addition, a depolarization-dependent release of SOD1 in pituitary GH3 cells and in rat synaptosomes through a calcium and SNARE-dependent mechanism is reported.

ATP and ADP hydrolysis in fish, chicken and rat synaptosomes

2001 ◽  
Vol 128 (4) ◽  
pp. 731-741 ◽  
Author(s):  
Maria Rosa Chitolina Schetinger ◽  
Vânia Lúcia Pimentel Vieira ◽  
Vera Maria Morsch ◽  
Daniela Balz
Keyword(s):  
Rat Synaptosomes

Effects of neuroleptics on glutaminase from rat synaptosomes

1988 ◽  
Vol 13 (6) ◽  
pp. 535-538 ◽  
Author(s):  
A. D. Sherman ◽  
M. Hamrah ◽  
J. Mott
Keyword(s):  
Rat Synaptosomes

DETERMINATION OF BRAIN-SPECIFIC ANTIGENS IN SHORT TERM CULTIVATED RAT ASTROGLIAL CELLS AND IN RAT SYNAPTOSOMES

1975 ◽  
Vol 25 (6) ◽  
pp. 867-870 ◽  
Author(s):  
Elisabeth Bock ◽  
O. S. Jørgensen ◽  
L. Dittmann ◽  
L. F. Eng
Keyword(s):  
Short Term ◽  
Astroglial Cells ◽  
Specific Antigens ◽  
Rat Synaptosomes

Relationship between energy expenditure and ion channel density in the turtle and rat brain

1989 ◽  
Vol 257 (6) ◽  
pp. R1354-R1358 ◽  
Author(s):  
R. A. Edwards ◽  
P. L. Lutz ◽  
D. G. Baden
Keyword(s):  
Energy Consumption ◽  
Energy Expenditure ◽  
Ion Channel ◽  
Rat Brain ◽  
Receptor Interaction ◽  
Na Channel ◽  
Apparent Difference ◽  
Na Channels ◽  
Channel Density ◽  
Rat Synaptosomes

Synaptosomes were isolated from turtle and rat brains to determine whether differences in brain ion channel densities accounted for the turtle's ability to survive anoxia compared with the mammal. The Na(+)-channel binding neurotoxin brevetoxin showed high-affinity specific binding in both turtle and rat synaptosomes, suggesting specific ligand-receptor interaction. The maximum binding capacity (Bmax) value for the turtle was only about one-third of that found for the rat synaptosomes, suggesting that the turtle synaptosome has a correspondingly lower Na+ channel density than the rat. This apparent difference in Na+ channel density is not reflected in metabolic rates, since at the same temperature (31 degrees C) the O2 consumption of both the rat and turtle synaptosome was almost identical. The large reductions in energy expenditure seen in synaptosomes incubated in Na(+)-free media and in media containing ouabain (approximately 50% turtle, 80% rat) are probably related to the halting of transmembrane Na(+)-K+ exchange. The greater reduction in the rat may be related to the apparent greater density of Na+ channels in the rat brain. However, compared with the 90% reduction in brain metabolism that occurs when the turtle brain becomes anoxic, the differences in ion channel density and in the costs of ion pumping between the rat and turtle brain are trivial. Closing Na+ channels with tetrodotoxin and increasing Na+ channel activation with veratridine caused substantial decreases and increases in synaptosome energy consumption, respectively. This suggests that the modulation of ion channel conductance has a significant effect on metabolic cost and may be an important mechanism to reduce energy consumption and electrical activity in the anoxic turtle brain, while still maintaining ionic gradients.

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