Abstract
Electrophysiological interaction between GABAergic transmission and encapsulate astrocytes is still unclear. Astrocytes could be affected by GABA spillover that could attribute to regulating extracellular Cl− of synaptic clefts by causing passive and/or active Cl− transport in themselves. To characterize GABA-induced currents and [Cl−]i alterations in CA1 astrocytes, whole cell patch-clamp recordings and simultaneous Cl− imaging using fluorescent Cl− indicator MEQ were obtained from mice (P17-30) hippocampal slices. The Cl− concentration in intracellular solution was adjusted to physiological condition (40 mM). GABA-induced inward currents were observed from -100 to +40 mV. Picrotoxin (PTX) reduced, but failed to abolish these inward currents. Additional application of GABA transporter (GAT) inhibitors abolished the residual slow decay currents, suggesting that the GABA-induced inward currents were consisting of GABAA receptor and GAT mediated currents. Cl− imaging using MEQ revealed that GABA decreased [Cl−]i in a large part of cells, which was blocked by PTX. [Cl−]i increases were also observed in some cells accompanied by the large PTX-insensitive currents, suggesting Cl− influx associated with GABA transport at GABAergic synapses. These data indicate that both GABAA receptors and GATs activation depolarize CA1 astrocytes. Not only Cl− efflux by GABAA receptor-channels but also Cl− influx by GATs exist and the Cl− efflux/influx balance may differ cell by cell, hence it could modify synaptic environment. [J Physiol Sci. 2008;58 Suppl:S129]
