Figure 3.

Heteromeric nAChRs cells mediate ACh responses in A17 and RB cells. (A–F) Representative traces of current responses induced by localized puffs of ACh (1 mM, 1 s) at the IPL in A17 (left) and in RB cells (right) in control conditions and in the presence of (A) the nicotinic receptor blocker mecamylamine (Mec 2 μM), (B) muscarinic receptor antagonist scopolamine (Sco 10 μM), (C) heteromeric nAChR antagonist tetramethylpiperidine-4-yl-heptanoate (TMPH 10 μM), (D) homomeric nAChR antagonist methylcaconitine (MLA 10 nM) or α₄β₂ antagonists (E) dihydro-β-erythroiodine (DHβE 10 μM) and (F) erysodine (Ery 10 μM). Vertical scale bars represent 50 pA for A17 cell responses and 5 pA for RB cell traces, and horizontal bars depict 1 s of time. (G) Bar graph summarizing the effects of cholinergic receptor antagonists on the ACh-induced currents in A17 (gray bars) and RB cells (white bars). Two-tailed paired t-tests, ^*p < 0.05, ^**p < 0.01, and ^***p < 0.001. For A17 cells, significant differences were observed between Mec and TMPH if tested vs. the effects of Sco, MLA or DHβE. For RB cells, differences were significant when comparing the influence of Mec and TMPH vs. Sco or MLA (One-Way ANOVA on ranks and Dunn's method for multiple comparisons).