Article Figures & Data
Figures
- Figure 1.
Mecamylamine-induced withdrawal signs in wild-type, β4-/-, and β2-/- mice. A, Total nicotine withdrawal signs in control mice (+/+, black bars) treated with saline (n = 6) or nicotine (n = 21), β4-/- mice (white bars) treated with saline (n = 4) or nicotine (n = 18), and β2-/- mice (gray bars) treated with saline (n = 7) or nicotine (n = 7) during the 20 min immediately after mecamylamine injection. B, Comparison of different withdrawal signs between wild-type (black bars) and β4-/- mice (white bars). The Other bar refers to other symptoms such as leg shakes, head nods, rear leg digging, and cage scratching. *p < 0.05 versus saline for the same genotype (ANOVA and Newman-Keuls post hoc comparisons) (A) versus +/+ (B).
- Figure 2.
Epibatidine binding in wild-type and β4-/- mouse brain sections. A-E, MHb level. F, G, IPN level. A, Saline-treated (Veh) β4+/+ mouse. B, Saline-treated (Veh) β4-/- mouse. C, Nicotine-treated (Nic) β4+/+ mouse. D, Nicotine-treated (Nic) β4-/- mouse. E, β2-/- mouse. F, Saline-treated (Veh) β4+/+ mouse; epibatidine binding has been competed with cytisine. G, Saline-treated (Veh) β4-/- mouse; epibatidine binding has been competed with cytisine. H, Quantification of epibatidine binding in striatum (Str), prefrontal cortex (PFC), and dentate gyrus (DG). n = 3-6 per group. *p < 0.05; #p < 0.1; Student's t test versus corresponding saline. A two-factor ANOVA analysis of the data indicated that there was a significant effect of genotype (Str, PFC, and DG, p < 0.05) and treatment (Str and PFC, p < 0.01; DG, p < 0.05) but no treatment × genotype interaction (p > 0.6 in all cases), confirming that β4-/- mice up regulate epibatidine binding sites during chronic nicotine treatment. Cx, Cortex; SC, superior colliculus.
