Figure 3.

Results from the Morris Water Maze learning trials (A–C) and memory (probe) trial (D–F) for the 15-day survival study (means ± SEM). Rats were subjected to sham- or midline fluid percussion injury (mFPI), and naïve controls were used. The animals were treated with either antisecretory factor (AF)-16 as the active, treatment compound or an inactive control compound (scramble). There was a clear effect on both latency (A) and path length (B) by the brain injury, without influencing the swim speed (C) with the exception of sham-injured, scramble-treated animals that swam significantly slower than all other treatment groups on the fourth day of the trials [p < 0.05, (C)]. AF-16 treatment significantly decreased the latency to find the platform and path length on the second day of the learning trials compared to scramble-treated, brain-injured controls [p < 0.05, (A,B)]. The memory (probe) trial at 72 h following the last learning trial showed that scramble-treated, brain-injured animals had significantly longer latency to find the platform area than the naïve and sham-injured treatment groups [p < 0.05, (D)]. Both naïve treatment groups had significantly more passes through the platform area than sham operated or injured groups [p < 0.05, (E)]. Scramble-treated, brain-injured animals spent significantly less time in the correct quadrant compared to all other groups [p < 0.05, (F)]. Treatment with AF-16 in brain-injured animals did not significantly reduce the latency to reach the area originally harboring the hidden platform [p = 0.23, (D)], increase the passes (E), or increase the time spent in the platform area (F).