Figure 3.
Choline signals evoked by nicotine and ABT-089. a, b, Representative traces of cholinergic signals obtained after pressure ejections of nicotine (4 nmol) or ABT-089 (4 nmol). c, Dose-dependent increases in cholinergic activity after nicotine and ABT-089. Compared with nicotine, ABT-089 generated higher signal amplitudes at lower doses (40 and 200 pmol; *p < 0.05, unpaired t test). d, e, Cholinergic signals evoked by ABT-089 were characterized by faster rise times and faster signal decay (t50) when compared with nicotine (*p < 0.05; **p < 0.01, unpaired t test). f, Dose–response curves for nicotine- and ABT-089-evoked choline signal amplitudes indicate a higher ED50 value for ABT-089 (0.047 nmol; nicotine: 1.48 nmol; error bars indicate SEM). As ABT-089 was robustly more potent than nicotine, in terms of peak amplitude (see Introduction for justification of the focus on this measure), an additional low dose (4 pmol) of ABT-089 needed to be tested in a separate group of animals (n = 3) to calculate the ED50 (see data point closest to the abscissa).