Skip to main content
. Author manuscript; available in PMC: 2022 Jan 14.
Published in final edited form as: Handb Exp Pharmacol. 2009;(192):85–112. doi: 10.1007/978-3-540-69248-5_4

Fig. 2.

Fig. 2

Agonist-stimulated 86Rb+ from mouse brain synaptosomes. Acetylcholine (ACh)-stimulated ion (86Rb+) efflux from synaptosomes prepared from mouse brain was done as described in Marks et al. (2007). The left panel of this figure demonstrates that 4 log units of agonist (ACh) were required to elicit maximal ion flux. These data are fit best by a two-site model indicating that higher and lower sensitivity components of the ion flux response exist. The right hand panels of the figure illustrate the effects of α4 and β gene deletion on the ion flux responses. Both α4 and β2 gene deletion resulted in total elimination of both the higher and lower sensitivity components of the ion flux response to ACh. ACh-stimulated release from synaptosomes prepared from mice that were heterozygous for the null mutations (α4+/− and β2+/−) showed intermediate levels of ion flux. These results demonstrate that α4β2* nAChRs are responsible for both components of the ion flux response