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J Biol Chem, Vol. 274, Issue 2, 889-895, January 8, 1999
-Aminobutyric Acid (GABA) Transporters by
Extracellular GABA
From the Department of Neurobiology, University of Alabama at
Birmingham, Birmingham, Alabama 35294-0021
-Aminobutyric acid (GABA) transporters on
neurons and glia at or near the synapse function to remove GABA from
the synaptic cleft. Recent evidence suggests that GABA transporter
function can be regulated, although the initial triggers for such
regulation are not known. One hypothesis is that transporter function
is modulated by extracellular GABA concentration, thus providing a
feedback mechanism for the control of neurotransmitter levels at the
synapse. To test this hypothesis, GABA uptake assays were performed on
primary dissociated rat hippocampal cultures that endogenously express
GABA transporters and on mammalian cells stably expressing the cloned
rat brain GABA transporter GAT1. In both experimental systems,
extracellular GABA induces chronic changes in GABA transport that occur
in a dose-dependent and time-dependent manner.
In addition to GABA, ACHC and nipecotic acid, both substrates of GAT1,
up-regulate transport; GAT1 transport inhibitors that are not
transporter substrates down-regulate transport. These changes occur in
the presence of blockers of both GABAA and
GABAB receptors, occur in the presence of protein synthesis
inhibitors, and are not influenced by intracellular GABA. Surface
biotinylation experiments reveal that the increase in transport is
correlated with an increase in surface transporter expression. This
increase in surface expression is due, at least in part, to a slowing
of GAT1 internalization in the presence of extracellular GABA. These data suggest that the GABA transporter fine-tunes its function in
response to extracellular GABA and would act to maintain a constant
level of neurotransmitter at the synaptic cleft.
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