0000000000075241
AUTHOR
Christopher Volk
A proton-translocating H+-ATPase is involved in C6 glial pH regulation.
AbstractGlial cells extrude acid equivalents to maintain pHi. Although four mechanisms have been described so far, pHi-control under physiological conditions is still not sufficiently explained. We therefore investigated whether a H+-translocating ATPase is involved in glial pHi homeostasis using an established glial cell line (C6 glioma). In the absence of bicarbonate, the inhibition of H+-ATPases by NEM led to a pHi decrease. The application of a more specific inhibitor (NBD-Cl) showed that the H+-ATPase involved is of the vacuolar type. Inhibition went along with delayed cell swelling. Together with the fact that glial acidification was far more pronounced in Na+-free media, this may ser…
Inhibition of lactate export by quercetin acidifies rat glial cells in vitro
The relationship between glial lactate release and glial intracellular pH (pH i) regulation is studied using C6 glioma cells and rat astrocytes in vitro, and the lactate transport inhibitors quercetin and a-cyano-4-hydroxycinnamate (CHC). pHi is measured using 2′,7′bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The results show that lactate release is mediated partly by a specific lactate transport system inhibitable by quercetin (50 mM), but not by CHC (5 mM). Inhibition by quercetin results in a significant 3‐4-fold increase of intracellular lactate and a decrease of intracellular pH to 6.9. A participation of quercetin-inhibitable lactate transport in glial pHi-regulation is suggested…
Neuron-Glial Interaction During Injury and Edema of the CNS
During injury and ischemia of the CNS mediator compounds are released or activated which cause secondary swelling and damage of nerve cells. Such mediators are glutamate, acidosis, free fatty acids, or high extracellular potassium. Glial homeostatic mechanisms are activated to prevent the secondary injury from these mediators. The glial clearance mechanisms have been studied in detail using in vitro systems allowing for a close control of the glial environment. Current evidence suggests glial swelling to occur together with glutamate uptake or in response to extracellular acidosis. Glial swelling, therefore, is rather the result of homeostatic mechanisms than an indication of glial demise.