PMID: 8944631Nov 1, 1996Paper

Mercuric chloride uncouples glutamate uptake from the countertransport of hydroxyl equivalents

The American Journal of Physiology
T N Nagaraja, N Brookes

Abstract

The cotransport of sodium and glutamate by system X(AG)- is believed to be coupled to the countertransport of potassium and hydroxyl ion equivalents. Accordingly, the uptake of glutamate or D-aspartate in astrocytes is accompanied by an intracellular acidification. Here, we report that HgCl2 blocks the glutamate-induced acidification with an approximate 50% inhibitor concentration (IC50) of 55 nM, an order of magnitude below its IC50 for inhibition of glutamate uptake. At 100 nM HgCl2, glutamate-induced acidification was abolished, whereas glutamate uptake was unaffected. D-Aspartate-induced acidification was equally sensitive to HgCl2, indicating that HgCl2 blocked a transporter-mediated, rather than a receptor-mediated, acidification. Unaltered responses to acute acid and alkaline loads showed that HgCl2 was not acting indirectly via a change in pH regulation. We conclude that HgCl2 acted directly on the glutamate transporter to uncouple the uptake of glutamate from the export of hydroxyl equivalents. In contrast, two other sulfhydryl reagents, p-chloromercuribenzensulfonate and N-ethylmaleimide, failed to discriminate between glutamate-induced acidification and glutamate uptake. An additional effect of > or = 100 nM HgCl2, i...Continue Reading

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Citations

Sep 30, 2006·The Journal of Physiology·Simen Gylterud OweDavid Attwell
May 12, 1998·The American Journal of Physiology·T N Nagaraja, N Brookes
May 23, 2001·Progress in Neurobiology·N C Danbolt
Mar 22, 2001·Toxicology in Vitro : an International Journal Published in Association with BIBRA·T A Toimela, H Tähti

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