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Specificity and Reversibility of the Inhibition by HgCl 2 of Glutamate Transport in Astrocyte Cultures
Author(s) -
Brookes N.
Publication year - 1988
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1988.tb10581.x
Subject(s) - astrocyte , glutamate receptor , neuroscience , chemistry , excitatory amino acid transporter , biophysics , biochemistry , biology , central nervous system , receptor
Inhibition of glutamate transport is a potential indirect cause of excitotoxic damage by glutamate in the CNS. The mercuric ion, the form in which metallic mercury vapor is believed to exert its neurotoxic action, is a known inhibitor of amino acid transport. This study examines the specificity with which HgCl 2 inhibits glutamate transport in mouse cerebral astrocytes by means of comparative measurements of 2‐deoxyglucose uptake. Uptake of 2‐deoxyglucose is an index of glucose utilization that reflects the function of Na + ,K + ‐ATPase and hexokinase, and is sensitive to Na + entry. The kinetic parameters, ionic dependence, and substrate specificity of glutamate transport in these astrocyte cultures were consistent with the commonly occurring system designated X A g . Acute exposure to 0.5 μ M HgCl 2 inhibited by 50% the initial rate of glutamate transport but did not affect 2‐deoxyglucose uptake. Glutamate transport was not detectably inhibited by Al 2+ , Pb 2+ , Co 2+ , Sr 2+ , Cd 2+ , or Zn 2+ (10 μ M as chlorides). The inhibitory action of 0.5 μ M HgCl 2 on glutamate transport was rapidly reversible. The action of 1–2 μ M HgCl 2 was progressive when exposures were extended to 1–3 h, and was more slowly reversible. These results suggest that Hg 2+ can impair glial glutamate transport reversibly at exposure levels that do not compromise some other vital cell functions.