Skip to main content
Fig. 3 | Molecular Autism

Fig. 3

From: Targeting the RHOA pathway improves learning and memory in adult Kctd13 and 16p11.2 deletion mouse models

Fig. 3

Exploration activity in the a open field test, b novel object location and c novel object recognition of the Kctd13+/− and the 16p11.2 Del/+b mouse models with or without fasudil treatment. a The Kctd13+/− animals showed no alteration compared to their wt littermate whereas the Del/+ mice showed increase exploratory activity in the distance travelled during the exploration of the open field for 30 min, which was not affected by the fasudil treatment. b For NOL test, recognition index reflects the ability of mice to distinguish the new location of an object from the familiar one after a 5 min retention delay. We observed again that the 16p11.2 Del/+ male mice showed a deficit in object location memory compared to their wt littermate but the Kctd13 heterozygotes were no longer defective. c In the NOR test, the mutant animals from the Kctd13+/− [non-treated wt (n = 12), treated wt (n = 11), non-treated Kctd13+/− (n = 14) and treated Kctd13+/− (n = 10)] or the 16p11.2 Del/+ model [non-treated wt (n = 17), treated wt (n = 9), non-treated Del/+ (n = 13) and treated Del/+ (n = 13)] were challenged to recognize the new object from the familiar object after a 3 h delay. Kctd13+/− and the Del/+ mutant mice were both impaired to recognize the new object compared to their respective wt littermates in the non-treated group. The fasudil treatment was able to restore the object recognition in the Kctd13+/− line (*p < 0.05; **p < 0.01; ***p < 0.001)

Back to article page
\