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 Previous Article
Journal of Neuroscience, Vol 13, 402-411, Copyright © 1993 by Society for Neuroscience
Characterization of the glutamate transporter in retinal cones of the tiger salamander
S Eliasof and F Werblin
University of California, Berkeley 94720.
L-Glutamate elicits an inwardly rectifying current at hyperpolarized
potentials in isolated retinal cones of the tiger salamander, as measured
under whole-cell patch clamp. Evidence presented in this article supports
the notion that cones possess a high-affinity glutamate transporter. This
glutamate-elicited current shows no desensitization over a period of
several minutes, and has an affinity (Km) of 10 microM. The inward current
is mimicked by the amino acids L- aspartate, D-aspartate, L-cysteate, and
to a lesser extent D-glutamate. It is neither blocked by the glutamate
receptor antagonists kynurenic acid (1 mM),
6-cyano-7-nitroquinoxaline-2,3-dione (100 microM), or 2-
amino-5-phosphonovalerate (100 microM), nor elicited by the glutamate
receptor agonists (100 microM each) kainate, quisqualate, NMDA, or 2-
amino-4-phosphonobutyrate. The glutamate-elicited current was reduced by
the glutamate transport blockers dihydrokainate (DHKA), DL-threo-
beta-hydroxyaspartate (beta HA), and L-trans-pyrrolidine-2,4- dicarboxylic
acid. When glutamate was present on both sides of the membrane, the
blockers reduced both uptake and release; the blocker- sensitive current as
a function of membrane potential represents the transport current-voltage
relation (I-V), and the reversal potential of the I-V represents the
transporter equilibrium potential. This potential was a function of the
equilibrium potential for glutamate. DHKA and beta HA depolarized
horizontal cells in a retinal slice, and abolished their light responses,
suggesting that in the absence of glutamate transport, glutamate
concentrations in the cleft rise to a level that saturates the postsynaptic
receptors. The high capacity of the cone glutamate transporter is well
suited for the rapid removal of glutamate from the synaptic cleft required
for the signaling of a light onset to postsynaptic cells.
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