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. Author manuscript; available in PMC: 2010 May 10.
Published in final edited form as: Brain Res. 2008 Nov 12;1250:88–100. doi: 10.1016/j.brainres.2008.10.076

Figure 4. Changes in nAChR binding and nicotine-stimulated dopamine release from PN10 to PN42 in striatum.

Figure 4

Rats were sacrificed either at PN10 (PreSal; PreNic) or at PN42 (PreSal/AdolSal; PreNic/AdolSal); the effect of age is shown for animals never receiving nicotine (PreSal v. PreSalAdolSal), and for those receiving prenatal nicotine (PreNic v. PreNicAdolSal). Means were analyzed by two-way ANOVA for age and treatment; F ratios and significance shown for those comparisons with a significant main effect. Unless noted, there were no significant interactions between parameters. For those with a significant main effect, we proceeded to analyze the four treatment means by one-way ANOVA and Tukey’s post-test. Means +/− S.E.M. are shown (N=9–11); *p<0.05; **p<0.01; ***p<0.001. A. Binding of 0.5 nM [3H]epibatidine, in the presence of 50 nM αCtxMII to inhibit binding to α6* nAChRs; age effect F(1,27) = 141.45; p<0.0001. B. Emax values for total nicotine-stimulated dopamine release from striatal synaptosomes; age effect F(1,29) = 32.24; p<0.0001. C. Emax values for the conotoxin-resistant release (in the presence of 50 nM αCtxMII, leaving α4β2*-mediated release); age effect F(1,29) = 20.92; p<0.0001. D. Emax values for the conotoxin-sensitive release (conotoxin-resistant release subtracted from total release; mediated by α6*-nAChRs); age effect F(1,29) = 9.57; p<0.005.