Figure 1
From: Npas4 impairs fear memory via phosphorylated HDAC5 induced by CGRP administration in mice
Effects of CGRP administration on general behavior and memory performance. Open field test analysis, showing locomotor activity (A), rearing activity (B) and time spent in the center area (C) (Welch’s t test, p = 0.0412), 24 h after CGRP i.c.v. (D) The mean escape latency in the Morris water maze task. Escape latencies were recorded during training session trials on days 1–4 (left). Changes in the percentage of time spent in the target quadrant during a 90-s testing period on day 5, 24 h after CGRP administration (right) (Welch’s t test, saline; p = 0.0129, CGRP; p = 0.0115). (E) CGRP effects on working memory performance in the Y maze test. (F) Step-through latency (in s) 24 h after foot shock (0.2 mA) (Welch’s t test, p = 0.0040). (G) The freezing time (s) during a contextual fear learning test. Fear conditioning was followed by CGRP administration (0, 0.1, 0.3, and 0.5 nmol), and freezing behavior was observed, 24 h after administration (One-way ANOVA, F3,26 = 16.13, with Tukey’s test). (H) CGRP antagonist, CGRP8-37 (0.5 nmol), blocked the CGRP (0.5 nmol)-mediated decrease in freezing time during a contextual fear learning test. CGRP8-37 was administered into the brain, simultaneously with CGRP (Two-way ANOVA, interaction, F1,22 = 14.3, p = 0.001; CGRP, F1,22 = 22.02, p = 0.0001; CGRP 8–37, F1,22 = 13.14, p = 0.0015, One-way ANOVA, F3,24 = 5.11, with Tukey’s test). Each bar indicates the mean ± SEM, with, significant differences shown as inserts. *p < 0.05, **p < 0.01. Numbers in parentheses indicate the animal numbers for each group. All mice were for each experiment were separate cohorts.
