Figure 1.

Acetylcholine and nicotine currents in IPR neurons of WT and α5KO mice. A, Example traces of ACh (1 mm) current responses in WT and α5^KO IPR neurons performed in voltage clamp at a holding potential of −75 mV. B, Mean ACh responses are significantly larger in WT compared with α5^KO neurons (Mann–Whitney U = 70.0, p < 0.0001). C, Example responses of IPR neurons from WT and α5^KO mice to 100 μm, 300 μm and 1 mm ACh. D, Quantitative comparison of current responses of WT and α5^KO neurons show significant differences are maintained across this range of ACh concentrations (F_1,34 = 16.6, p = 0.0003). E, Example traces of current responses to ACh stimulation in IPR neurons from WT and α5^KO mice in the presence of the synaptic blockers APV, CNQX, and bicuculline. F, Quantification of ACh currents in the presence of synaptic blockers demonstrates that marked differences persist in the direct ACh response in WT compared with α5^KO neurons (Mann–Whitney U = 4.0, p = 0.005). G, Example traces of ACh current responses in WT and α5^KO neurons before and after bath application of the α4β2* nAChR antagonist DHβE (10 μm). H, DHβE significantly reduces the mean current amplitude of responses to ACh in both WT and α5^KO neurons (Wilcoxon W = −45.0, p = 0.004). I, Example traces of nicotine (1 μm) current responses in WT and α5^KO IPR neurons. J, Mean nicotine responses are significantly larger in WT compared with α5^KO neurons (Mann–Whitney U = 31.0, p = 0.005). See Figure 1-1 (in table form). *p < 0.05, **p < 0.01, ****p < 0.0001.