Skip to main content
. Author manuscript; available in PMC: 2011 May 1.
Published in final edited form as: Neuropsychopharmacology. 2010 Aug 25;35(12):2324–2338. doi: 10.1038/npp.2010.130

Figure 7. ACh stimulated [86Rb+] efflux from thalamic synaptosomes and [125I]-epibatidine binding to particulate fractions.

Figure 7

A. Crude thalamic synaptosomes were prepared from wild-type (WT), heterozygous (HET), β2 subunit knock out (KO) and tr(CT) mice. Concentration effect curves for [86Rb+] efflux were biphasic for both WT and HET mice and absent in the KO animals. tr(CT) samples exhibited partial functional recovery relative to the KO, with high sensitivity (HS) to ACh. This HS tr(CT) component is comparable to that derived from WT animals. The high ACh sensitivity component (HS) is indicated by a long dashed line and the low ACh sensitivity component (LS) is indicated by a short dashed line.

B. [125I]-epibatidine binding to particulate fractions derived from thalamic synaptosomes from each of the genotypes indicates a progressive decline in cytisine sensitive (CS) epibatidine binding between WT and HET mice, an absence of binding in KO samples and a partial recovery in the tr(CT) mice.