Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Estrogen suppresses the impact of glucose deprivation on astrocytic calcium levels and signaling independently of the nuclear estrogen receptor

Item Type:Article
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

Repository Staff Only: item control page

Open Access
MDC Library