Figure 4.

Concomitant exposure to concentrations of N,N-decane-1,10-diyl-bis-3-picolinium diiodide (bPiDI) and α-CtxMII produces inhibition of nicotine-evoked [³H]dopamine overflow not different from that after exposure to either antagonist alone. (A) Striatal slices were superfused in the absence or presence of mecamylamine (MEC; 10 µM), α-CtxMII (1 nM), bPiDI (1 µM), or α-CtxMII + bPiDI for 36 min. Superfusion continued for an additional 36 min following addition of nicotine (10 µM) to the buffer. Control represents nicotine-evoked [³H]dopamine overflow in the absence of antagonist. Data are expressed as mean ± SEM of % basal fractional release. * indicates significant difference from control (nicotine alone; P < 0.05). # indicates significant difference from all other antagonist conditions. n = 6 rats. (B) Time course of nicotine-evoked [³H]dopamine fractional release in the absence and presence of MEC, bPiDI, α-CtxMII or α-CtxMII + bPiDI. Data are expressed as fractional release as a percent of basal [³H]outflow. Arrow indicates the time point at which nicotine was added to the superfusion buffer. Mean basal [³H]outflow was 1.14 ± 0.02 fractional release as percentage of tissue [³H]content. DA, dopamine.