Figure 2. Presynaptic α6* nAChRs in striatum mediate hypersensitive, nicotine-stimulated DA release in α6^L9’S transgenic mice.

(A–C) Hypersensitive DA release in striatum of α6^L9’S transgenic mice is α6*-dependent. Striata (‘ST’; dorsal striatum and dorsal aspects of nucleus accumbens) from WT and α6^L9’S mice were dissected and synaptosomes were prepared. DA release was stimulated with a range of nicotine concentrations (3 nM, 10 nM, 30 nM, 100nM, 300 nM, 1 µM, 10 µM), and a concentration-response relation for each mouse line (n = 6 mice / line) is shown for total release (A). To determine the relative contribution of α6* and non-α6* receptors, striatal synaptosome samples were incubated with αCtxMII (50 nM). α6* independent release is shown in (C), and αCtxMII-sensitive (α6* dependent) release is shown in (B).

(D–F) Hypersensitive DA release in olfactory tubercle of α6^L9’S transgenic mice is α6*-dependent. Olfactory tubercle (‘OT’) was dissected from WT and α6^L9’S mice, and samples were processed as in (A–C).

(G and H) Quantification of hypersensitive DA release in striatum (G) and olfactory tubercle (H). Average nicotine EC₅₀ values for each concentration response curve from (A–F) are shown.

(I–K) α6* nAChRs do not participate in nicotine-stimulated GABA release in striatum. ST and OT were dissected and combined, followed by synaptosome preparation. GABA release was stimulated by nicotine at the following concentrations: 100 nM, 300 nM, 1 µM, 3 µM, 10 µM, 30 µM, 100 µM, and 300 µM. Total (I) release, and αCtxMII-sensitive (J) and resistant (K) components are shown.

Data are expressed as mean ± SEM. *, p < 0.05.