Fig. 1. Delayed outward currents of mouse hippocampal neurons and patterns of changes observed during and after exposure to 100 μm1S,3R-ACPD. These currents demonstrate the immediate increase in current amplitude seen on application of 1S,3R-ACPD, and acceleration of delayed current inactivation observed after the exposure to agonist. Note that the changes in inactivation rate and steady-state amplitude were most evident at voltages positive to approximately −10 mV.A1, Control currents recorded under conditions that will maximize observation of delayed outward currents,ID,IK, and various forms ofIK(Ca), and minimize the contribution of IA (see Results). Currents were recorded at voltages between −50 and +40 mV (in 10 mV increments), as illustrated in the schematic. A2, Currents recorded 1 min after initiating exposure to 100 μm1S,3R-ACPD. A3, Currents recorded 10 min after termination of the 3-min-long exposure to 1S,3R-ACPD. B1, Voltage dependence of fractional inactivation of delayed outward currents [1 − (Iend/Ipeak)], illustrating the 1S,3R-ACPD-induced increase seen at voltages positive to −10 mV and the broad bell-shape of the change in fractional inactivation with voltage (difference). B2, Ratio of mean fractional inactivation for each test voltage; 1S,3R-ACPD increased mean fractional inactivation by ∼35% except at the most positive voltage. Data are mean ± SD; n = 7. Statistical significance is indicated in this and all subsequent figures: ns, not significant; *p < 0.05; **p < 0.01; and ***p < 0.001.