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Volume 16, Number 21,
Issue of November 1, 1996
pp. 6722-6731
Copyright ©1996 Society for Neuroscience
Anion Conductance Behavior of the Glutamate Uptake Carrier in
Salamander Retinal Glial Cells
Received May 23, 1996; revised Aug. 13, 1996; accepted Aug. 16, 1996.
Brian Billups,
David Rossi, and
David Attwell
Department of Physiology, University College London, London WC1E
6BT, United Kingdom
Glutamate uptake is driven by the cotransport of Na+
ions, the countertransport of K+ ions, and either the
countertransport of OH or the cotransport of
H+ ions. In addition, activating glutamate uptake carriers
has been shown to lead to activation of an anion conductance present in
the carrier structure. Here we characterize the ion selectivity and
gating of this anion conductance. The conductance is small with
Cl as the permeant anion, but it is large with
NO3 or ClO4 present, undermining
the earlier use of NO3 and ClO4 to
suggest that OH countertransport rather than
H+ cotransport helps drive uptake. Activation of the anion
conductance can be evoked by extra- or intracellular glutamate and can
occur even when glutamate transport is inhibited. By running the
carrier backward and detecting glutamate release with AMPA receptors in
neurons placed near the glial cells, we show that anion flux is not
coupled thermodynamically to glutamate movement, but
OH /H+ transport is. The possibility that cell
excitability is modulated by the anion conductance associated with
glutamate uptake suggests a target for therapeutic drugs to reduce
glutamate release in conditions like epilepsy.
Key words:
glutamate;
transporter;
anion conductance;
uptake;
pH;
glial cell
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