Inhibition of glutamate uptake increased the amplitude and duration of stimulus-evoked, NMDA receptor–mediated EPSCs. A, Currents recorded in the presence and in the absence of 300 μm PDC are shown. B, PDC increased the peak current (control = −137 ± 44 pA; PDC = −214 ± 53 pA; n = 7;p = 0.006). C, PDC increased the time to peak (control = 89 ± 14 msec; PDC = 171 ± 20 msec; p = 0.002). D, PDC increased the decay time (D₃₇) (control = 256 ± 49 msec; PDC = 1257 ± 95 msec;p = 0.00003). E, Currents recorded in normal extracellular solution (see Materials and Methods) and in solution containing 115 mm Li⁺ and 0 Na⁺ are shown. The Li⁺ solution prolonged D₃₇ from 168 ± 28 to 1268 ± 330 msec (n = 5; p= 0.02). Cells were held at −30 mV. For these experiments, all extracellular solutions contained 150 μm picrotoxin, 10 μm strychnine, 5 μm NBQX, and 1 μml-AP-4, blocking any effects of extracellular glutamate accumulation on AMPA and KA receptors or on mGluR6 on bipolar cell dendrites in the outer plexiform layer.