Figure 5. Tacr3 agonist mediates the slow EPSP.
(A–C) The slow EPSP was abrogated by an NKB receptor (Tacr3) antagonist SB222,200 (A) and the NKB receptor antagonist cocktail SDZ-NKT 343 (1 µM), GR94,800 (1 µM) and SB222,200 (3 µM) (Tacr1, 2 and 3 antagonists, respectively) (B). Furthermore, Tacr3 agonist senktide pretreatment completely occluded the slow EPSP (C), demonstrating that the slow EPSP was mediated by the Tacr3. A hyperpolarizing bias was used to repolarize the membrane potential to −70 mV when the senktide response reached the maximal depolarization (C2). (D) Bar graphs summarizing the effects of Tacr3 agonist and antagonists on the slow EPSP. Comparisons between different treatments were performed using a one-way ANOVA analysis (F(3, 20) = 31.6, p<0.0001) with the Newman-Keuls’s post hoc test. *** indicates p<0.005 vs. control. (E–F) Depolarization induced by senktide (250 nM) perfused on two separate occasions in a Kiss1ARH neuron. The R2/R1 ratio was 0.65 (E, upper trace), which was not different from the ratio from photostimulation (E, lower trace). (F) Bar graphs summarizing R2/R1 ratios (Un-paired t-test, t(14)= 0.0408, p = 0.9680).