Article ID Journal Published Year Pages File Type
9989660 Neurobiology of Disease 2005 11 Pages PDF
Abstract
Glucose deprivation of astrocytes results in an elevation of cytosolic calcium concentration ([Ca2+]i) [Kahlert, S., Reiser, G., 2000. Requirement of glycolytic and mitochondrial energy supply for loading of Ca2+ stores and InsP3-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 μM 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. 17β-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 17β-estradiol.
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