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. 2018 Mar 23;596(9):1549–1574. doi: 10.1113/JP275478

Figure 10. Post‐junctional neural responses in tamoxifen treated adult iAno1+/– control and an iAno1−/− animals.

Figure 10

A–D, responses to EFS (1 pulse delivered at arrows; 5 Hz delivered at horizontal bars) of a gastric fundus from a tamoxifen treated iAno1+/– animal. A, under control conditions, EFS evoked a frequency‐dependent biphasic neural response consisting of a transient EJP followed by a more sustained IJP (dashed line; n = 11). B, l‐NNA (100 μm) inhibited the IJP at 1 and 5 Hz. C, in the presence of l‐NNA and neostigmine (1 μm), EFS caused a depolarization in membrane potential and produced a EJP followed by a large and sustained frequency‐dependent depolarization in membrane potential (dashed lines). D, atropine (1 μm) inhibited the EFS evoked EJP and the slow sustained depolarization in membrane potential caused by neostigmine. E–H, EFS evoked neural responses of the gastric fundus from a tamoxifen treated iAno1–/– animal. E, under control conditions, EFS evoked little or no post‐junctional responses at 1 or 5 Hz (n = 27). F, L‐NNA (100 μm) did not alter the EFS responses observed under control conditions. G, in the presence of L‐NNA, neostigmine (1 μm) produced membrane depolarization and EFS evoked a large and sustained depolarization in membrane potential (dashed lines). H, atropine (1 μm) repolarized membrane potential and inhibited the EFS evoked sustained depolarization in membrane potential at all frequencies of EFS tested.