Anion Conductance Behavior of the Glutamate Uptake Carrier in Salamander Retinal Glial Cells

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 stru...

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Bibliographic Details
Published in:The Journal of neuroscience 1996-11, Vol.16 (21), p.6722-6731
Main Authors: Billups, Brian, Rossi, David, Attwell, David
Format: Article
Language:English
Subjects:
Amino Acid Transport System X-AG
Animals
Anions - metabolism
Biological Transport - drug effects
Biological Transport - physiology
Carrier Proteins - metabolism
Chlorides - metabolism
Electric Conductivity
Excitatory Amino Acid Agonists - pharmacology
Glutamate Plasma Membrane Transport Proteins
Glutamates - metabolism
Glutamates - pharmacology
Hydrogen-Ion Concentration
Ion Channel Gating - physiology
Neuroglia - drug effects
Neuroglia - metabolism
Nitrates - metabolism
Patch-Clamp Techniques
Potassium - metabolism
Retina - cytology
Sodium - metabolism
Sodium - pharmacology
Symporters
Urodela
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Summary: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.
ISSN:0270-6474
1529-2401
DOI:10.1523/jneurosci.16-21-06722.1996