Item Type: | Article |
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Title: | Estrogen suppresses the impact of glucose deprivation on astrocytic calcium levels and signaling independently of the nuclear estrogen receptor |
Creators Name: | Arnold, S. |
Abstract: | Glucose deprivation of astrocytes results in an elevation of cytosolic calcium concentration ([Ca2+](i)) [Kablert, S., Reiser, G., 2000. Requirement of glycolytic and mitochondrial energy supply for loading of Ca2+ stores and InsP(3)-mediated Ca2+ signaling in rat hippocampus astrocytes. J. Neurosci. Res. 61, 409-420; Silver, I.A., Deas, J., Erecinska, M., 1997. Ion homeostasis in brain cells: differences in intracellular ion responses to energy limitation between cultured neurons and glial cells. Neuroscience 78, 589-601] equivalent to an impairment of astrocytic energy metabolism and function. Superfusion of fura-2 loaded primary cortical astrocytes with glucose-free solution triggered a slow and progressive, 56-fold increase of the [Ca2+](i) from 60 nM up to 3.3 mu M within 2 h. Re-addition of glucose led to a rapid drop of [Ca2+](i), yet [Ca2+](i) did not fully recover to the low levels recorded prior to glucose deprivation and, moreover, astrocytic Ca2+ signaling was impaired: adenosine 5'-triphosphate (ATP) and uridine 5-triphosphate (UTP) were no longer able to trigger a transient Ca2+ response as recorded in controls. 17 beta-estradiol protected astrocytes from the glucose deprivation-induced [Ca2+](i) increase and the impaired signaling independently of the nuclear estrogen receptor, as the antiestrogen tamoxifen and the protein synthesis inhibitor cycloheximide did not impede the protective effect of 17 beta-estradiol. |
Keywords: | Astrocytes, Glucose Deprivation, Calcium, Estrogen |
Source: | Neurobiology of Disease |
ISSN: | 0969-9961 |
Publisher: | Elsevier |
Volume: | 20 |
Number: | 1 |
Page Range: | 82-92 |
Date: | October 2005 |
Official Publication: | https://doi.org/10.1016/j.nbd.2005.02.002 |
PubMed: | View item in PubMed |
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