Astrocytes are involved in maintenance of synaptic microenvironment by glutamate uptake and K+clearance. These processes are associated with net charge transfer across the membrane and therefore can be recorded as glutamate transporter (IGluT) and K+(IK) currents. It has been previously shown that the blockade of IKwith BaCl2enhances the IGluT. Here we show that activity-dependent facilitation (5 stimuli at 50 Hz) of IGluTwas not significantly different in BaCl2compared to facilitation of IGluTisolated by post-hoc subtraction of IK. Nevertheless, BaCl2abolished the activity-dependent prolongation of τdecay, which was observed for IGluTisolated by post-hoc subtraction of IK. This finding suggests that activity-dependent accumulation of extracellular K+([K+]o) causes astrocytic depolarization, which is responsible for the increase in τdecayof IGluT.The blockade of inward rectifying K+channels (Kir) with BaCl2makes astrocytic membrane potential insensitive to [K+]oelevation and thus abolishes this increase. Blockade of IGluTwith glutamate transporter blocker, DL-threo-β-benzyloxyaspartic acid (TBOA) did not significantly affect the amplitude of IKbut decreased its τdecay. However, activity dependent facilitations of both amplitude and τdecayof IKwere larger in TBOA, than in the control conditions. We suggest that activity-dependent accumulation of extracellular glutamate can enhance release of K+. Thus activity-dependent changes in [K+]ocan affect glutamate dwell-time in the synaptic cleft, and vice versa, extracellular glutamate accumulation can affect [K+]otime-course. Our finding is important for understanding of the astrocytic mechanisms in glutamate excitotoxicity and in diseases related to disruption of K+homeostasis (e.g. stroke, migraine, and epilepsy).