Fig. 1.
Glutamate–H2O2-dependent modulation of striatal DA release is blocked by glibenclamide. (A) Glibenclamide (Glib; 3 μM) caused a significant increase in evoked DA release (P < 0.01, glibenclamide vs. control; n = 5). (B) Applied voltage waveform and representative voltammograms of DA obtained during DA calibration (DA cal; 1 μM) and at maximum evoked [DA]o during stimulation (10 Hz, 30 pulses) in normal aCSF (control) and in the presence of glibenclamide in the same striatal slice. Sampling interval was 100 ms; voltage scan rate was 800 V/s. (C) In the presence of glibenclamide, the usual effects of MCS (1 mM), GYKI-52466 (GYKI; 50 μM), and picrotoxin (100 μM) on DA release were prevented (P 0.05, each agent vs. glibenclamide alone; n = 5). Data are given as mean ± SEM, illustrated as percentage of same-site control. Solid bars indicate the stimulation period.