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J Neurophysiol 88: 1407-1419, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 88 No. 3 September 2002, pp. 1407-1419
Copyright ©2002 by the American Physiological Society

GAT-1 and Reversible GABA Transport in Bergmann Glia in Slices

L. Barakat and A. Bordey

Department of Neurosurgery, Yale University, New Haven, Connecticut 06520-8082

Barakat, L. and A. Bordey. GAT-1 and Reversible GABA Transport in Bergmann Glia in Slices. J. Neurophysiol. 88: 1407-1419, 2002. Although glial GABA uptake and release have been studied in vitro, GABA transporters (GATs) have not been characterized in glia in slices. Whole cell patch-clamp recordings were obtained from Bergmann glia in rat cerebellar slices to characterize carrier-mediated GABA influx and efflux. GABA induced inward currents at -70 mV that could be pharmacologically separated into GABAA receptor and GAT currents. In the presence of GABAA/B/C receptor blockers, mean GABA-induced currents measured -48 pA at -70 mV, were inwardly rectifying between -70 and +50 mV, were inhibited by external Na+ removal, and were diminished by reduction of external Cl-. Nontransportable blockers of GAT-1 (SKF89976-A and NNC-711) and a transportable blocker of all the GAT subtypes (nipecotic acid) reversibly reduced GABA-induced transport currents by 68 and 100%, respectively. A blocker of BGT-1 (betaine) had no effect. SKF89976-A and NNC-711 also suppressed baseline inward currents that likely result from tonic GAT activation by background GABA. The substrate agonists, nipecotic acid and beta -alanine but not betaine, induced voltage- and Na+-dependent currents. With Na+ and GABA inside the patch pipette or intracellular GABA perfusion during the recording, SKF89976-A blocked baseline outward currents that activated at -60 mV and increased with more depolarized potentials. This carrier-mediated GABA efflux induced a local accumulation of extracellular GABA detected by GABAA receptor activation on the recorded cell. Overall, these results indicate that Bergmann glia express GAT-1 that are activated by ambient GABA. In addition, GAT-1 in glia can work in reverse and release sufficient GABA to activate nearby GABA receptors.




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