Please use this identifier to cite or link to this item:
https://hdl.handle.net/10316/4857
Title: | Effect of Glucose Deprivation and Acute Glutamate Exposure in Cultured Retinal Cells | Authors: | Rego, Ana Cristina Areias, Filipe Miguel Santos, Maria Sancha Oliveira, Catarina R. |
Keywords: | Ca2+uptake; cell injury; energy charge; glucose deprivation; glutamate; membrane potential; retinal cells | Issue Date: | 1998 | Citation: | Experimental Neurology. 153:1 (1998) 128-134 | Abstract: | The relationship between bioenergetics and the glutamate system was analyzed in a neuronal model of retinal cells in culture, submitted to glucose deprivation and exposed to glutamate for 2 h, and compared with exposure to glutamate in the presence of glucose. Under glucose deprivation, a reduction (about 1.1-fold) in the energy charge of the cells occurred, probably as a result of a decrement (by about 75%) in the cellular redox efficacy, as determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) test. In the absence of glucose, exposure of retinal cells to 10 [mu]M glutamate potentiated the reduction in the energy charge (by about 1.2-fold) and induced a significant increase in the uptake of45Ca2+by the cells (1.3-fold), although no significant changes were observed in the presence of glucose. Under glucose deprivation, 100 [mu]M glutamate caused an irreversible cell membrane damage, as shown by the significant increase in lactate dehydrogenase (LDH) leakage (about 1.8-fold). A significant increase in membrane depolarization, measured by the reduction of [3H]tetraphenylphosphonium+([3H]TPP+) uptake, was also observed after glutamate exposure in the absence of glucose. In the presence of glucose, high glutamate concentrations (10 mM) induced a major increase in Ca2+entry into the cells and membrane depolarization, without affecting the energy charge or cell survival. In contrast, in the absence of glucose, 10 mM glutamate did not alter Ca2+accumulation by the cells and a smaller decrease in membrane potential occurred, as compared to 100 [mu]M glutamate exposure. Data shown in this study suggest that during a prolonged (2 h) and acute exposure to high glutamate (10 mM), under glucose deprivation conditions, the neuronal systems have "adaptive" mechanisms that allow the survival of cells. These findings may have implications in neuronal degeneration occurring during brain ischemia. | URI: | https://hdl.handle.net/10316/4857 | DOI: | 10.1006/exnr.1998.6865 | Rights: | openAccess |
Appears in Collections: | FMUC Medicina - Artigos em Revistas Internacionais |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
filed159ccebb12c48bfbd71f5501b98696a.pdf | 129.31 kB | Adobe PDF | View/Open |
SCOPUSTM
Citations
5
checked on Oct 7, 2024
WEB OF SCIENCETM
Citations
5
checked on Oct 2, 2024
Page view(s) 50
498
checked on Oct 15, 2024
Download(s) 50
602
checked on Oct 15, 2024
Google ScholarTM
Check
Altmetric
Altmetric
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.