Fast synaptic transmission requires a rapid removal of the released neurotransmitter from the extracellular space. Glial glutamate transporters strongly contribute to glutamate removal. In this work we investigated short-term plasticity of synaptically-activated, glutamate transporter-mediated currents (STCs) in cortical layer 2/3 astrocytes. STCs were elicited by local electrical stimulation in layer 4 in the presence of ionotropic glutamate, GABAA, and GABAB receptor antagonists and recorded using whole-cell patch-clamp approach. In experiments with low [Na+]i (5 mM) intrapipette solution, STCs induced by paired-pulse stimulation demonstrated paired-pulse facilitation (PPF) at short (<250 ms) inter-stimulus intervals (ISIs) and paired-pulse depression (PPD) at longer (500–5000 ms) ISIs. In experiments with high [Na⁺]i (20 mM) intrapipette solution, PPF of STCs at short ISIs was significantly reduced, while PPD at longer ISIs was not affected. In addition, STC kinetics were slowed in the presence of high [Na⁺]i. Exogenous GABA has been shown to increase [Na⁺]i via GABA transporters (GATs). Exogenous GABA reduced the mean STC amplitude, decreased PPF at short ISIs, and slowed STC kinetics. In experiments with the low but not the high [Na⁺]i intrapipette solution, GAT blockers, decreased PPF at short ISIs both at room and at near physiological temperatures, suggesting that endogenous GABA is capable to modulate short-term plasticity of STCs via GATs. We conclude that 1) short-term plasticity of STCs is dependent on [Na⁺]i and 2) GATs may influence glutamate transporter activity and thus the rate and efficacy of glutamate removal.