Brain, Vol. 119, No. 6, 2021-2027, 1996
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research-article |
Tumour necrosis factor-
increases intracellular Ca2+ and induces a depolarization in cultured astroglial cells
Department of Neurology, Heinrich-Heine University Düsseldorf, Germany
Correspondence to:
Correspondence to: Dr H. Köller, Department of Neurology, Heinrich-Heine University, PO Box 101007, D-40001 Düsseldorf, Germany
Tumour necrosis factor (TNF)-
, a strong immune mediator, is released within the brain during inflammatory diseases and contributes to immunological activation of glial cells. Here we report that, in astrocytes, TNF- also affects the intracellular Ca2+ homeostasis and basic electrophysiological properties such as the membrane potential. Using the Ca2+ indicator dye fura-2 in a cell culture model, we found that TNF- (10–1000 U ml–1), but not interleukin 1 or 6, induced a slow but more than two-fold increase of the intracellular Ca2+ concentration, which could be blocked by Co2+ (1.0 mM), verapamil (100 µM) or omission of external Ca2+. This intracellular Ca2+ increase was accompanied by a marked decrease of the membrane potential by 35 mV. CSF of patients with bacterial meningitis, known to contain large amounts of TNF-, induced a similar depolarization of astrocytes, which was markedly reduced by a neutralizing anti-TNF- antibody. We conclude that TNF- induces an increase of intracellular Ca2+ and a depolarization in astrocytes with the consequence of disturbing voltage-dependent glial functions such as regulation of local ion concentrations and glutamate uptake. During inflammatory CNS diseases this immuno-electrical coupling may contribute to an impairment of neuronal function.
tumour necrosis factor a; cultured astrocytes; intracellular calcium; meningitis; cerebrospinal fluid
Received February 2, 1996. Revised May 23, 1996. Accepted June 25, 1996.
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