Fig. 5: Kisspeptin and AVPV-Kisspeptin neurons differentially affect aggressive behavior in IST mice.
Schematic drawings depicting the detailed protocols followed in experiments (Exp) A and D. Please note that each individual Exp has used different cohorts of animals. AVPV: anteroventral periventricular nucleus; Cetr: Cetrorelix (GnRHR antagonist, 0.5 mg/Kg); Deso: deslorelin (GnRHR agonist, 300 ng/Kg); Kp-10: Kisspeptin-10 (0.52 μg/Kg); RI: resident-intruder; Sex: sexual behavior test; WO: Washout (neither behavior nor injection) (A) Kisspeptin (Kp-10, 0.52 μg/Kg, pink bars) reduced the total percentage of time spent on aggression (two-tailed Student’s t test t(10) = 2.51, p = 0.04) as well as the number of attacks (Wilcoxon test W = −39, p = 0.04), increased the attack latency (t(10) = 2.53, p = 0.02), tended to elevate time spent on social investigation (t(10) = 2.05, p = 0.06) and home cage exploration (t test t(10) = 2.13, p = 0.06) in IST mice (B). Maximal z-projection of DAPI (magenta) and kisspeptin (green, Alexa-fluor 488 anti-rabbit) in the anteroventral periventricular nucleus (AVPV) confirming viral deletion of kisspeptin neurons (t(10) = 2.29, p = 0.02) and reduction on fiber densities (Mann–Whitney U test U = 1, p = 0.005) (C). Finally, the deletion of kisspeptin neurons in the AVPV (Kiss-del, pink) abolished the rise in aggression levels seen in controls regarding the percentage of time spent on aggression (Two-way ANOVA Training effect: F(2,22) = 20.10, p < 0.0001; Deletion effect: F(1,11) = 4.16, p = 0.06; TrainingxDeletion: F(2,22) = 4.55, p = 0.02) and number of attacks (Training effect: F(2,22) = 3.93, p = 0.03; Deletion effect: F(1,11) = 0.006, p = 0.93; TrainingxDeletion: F(2,22) = 0.34, p = 0.77) (D), without affecting social, exploratory (E) and sexual behavior (F). *p < 0.05, **<0.01 vs vehicle or control (Ctrl); #<0.5 vs RI1; ## <0.1 vs RI1. Data are presented as mean + s.e.m. Scale bar 100 μm.
