Figure 10.
[ahx5–24]NPY elicits opposing effects on AP firing patterns. A, AP trains evoked by depolarizing current steps in a PN in which [ahx5–24]NPY (1 μm; inset, top left; blue) enhanced the rebound outward current relative to control (inset; black). Similar numbers of step-evoked APs (here, 9 APs each; full trace not shown) were compared in control (black) and in [ahx5–24]NPY (blue). Treatment with the Y2R agonist nearly doubled the latency between the first two APs (black and blue bars above traces). B, Interspike interval plotted against AP number in a train, compared in control and in [ahx5–24]NPY (1 μm), from neurons responding to the Y2R agonist as in A (rebound current increased >10%; two-way repeated-measures ANOVA; treatment: F(1,40) = 4.124, p = 0.0490; AP number: F(4,40) = 7.021, p = 0.0002; interaction: F(4,40) = 4.617, p = 0.0037; n = 9 cells, 9 rats). In these PNs, [ahx5–24]NPY (1 μm) significantly increased the interval between the first two current step-evoked APs, from 33.8 ± 9.5 to 80.1 ± 9.5 ms (Bonferroni's post-test). C, Representative AP trains evoked by depolarizing current steps in a PN as in A in which [ahx5–24]NPY (1 μm; blue) inhibited the KIR and Ih but did not affect the outward rebound current (inset, top left). In this example, 7 and 8 APs were evoked by current steps in control and drug, respectively (full trace not shown). Inset, Bottom left, Change in latency of initial APs. D, Interspike interval plotted against AP number in trains, compared in control and in [ahx5–24]NPY (1 μm), from neurons where [ahx5–24]NPY did not enhance the outward rebound current (two-way repeated-measures ANOVA; treatment: F(1,45) = 29.95, p < 0.0001; AP number: F(4,45) = 20.03, p < 0.0001; interaction: F(4,45) = 0.5365, p = 0.7096; n = 10 cells, 7 rats). In these PNs, Y2R activation significantly decreased the interval between the first and second APs and between the second and third APs (Bonferroni's post-test). *p < 0.05, **p < 0.01, ***p < 0.001.