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. Author manuscript; available in PMC: 2016 Dec 1.
Published in final edited form as: Neuropharmacology. 2015 May 6;99:273–284. doi: 10.1016/j.neuropharm.2015.04.022

Fig. 2.

Fig. 2

Functional characterization of mutations on PKA putative sites in the α4 subunit with nicotine used as agonist. (A) Family of nicotine-induced macroscopic currents for mutation α4S471Dβ2 and the wild-type α4β2 nAChR. Calibration bars are shown for all family of currents, horizontal bars indicate time (5 s) and vertical bars indicate the inward current (500 nA). (B) Dose-response relationships obtained by voltage-clamp using nicotine as agonist. Nicotine dose-response curves were determined using seven nicotine concentrations (0.1, 1, 3, 10, 30, 100 and 300 M). The responses were normalized to the maximum response (I/Imax). (C) Comparison of the nicotine-induced macroscopic peak currents of the mutations and wild-type receptor shown in nA (n=6-17) (** p<0.005).