Skip to main content
. 2010 Jul 12;107(29):13141–13146. doi: 10.1073/pnas.1004829107

Fig. 4.

Fig. 4.

Working memory impairments caused by increased inhibition in the Nf1+/− mice. (A–C) Delayed win-shift radial arm maze errors, summed across 10 d of task performance, are compared between Nf1+/− (n = 12) and WT (n = 12) mice for training phase errors (P = 0.883, t test), testing phase within-phase errors (P = 0.047, t test), and testing phase across-phase errors (P = 0.403, t test). (D) Nf1+/− mice make more testing phase within-phase errors during the first 6 d of the task (RM ANOVA genotype × day × error; P = 0.024, *P < 0.05, Tukey’s post hoc). (E) Picrotoxin improves within-phase errors (P = 0.009) in Nf1+/− mice (RM ANOVA drug × genotype × day × error). Comparisons made across four groups: saline (n = 20) and picrotoxin (n = 18) treated Nf1+/− mice and saline (n = 20) and picrotoxin treated WT mice (n = 19). (F) In the operant delayed nonmatch to sample task, Nf1+/− mice (n = 12) show impaired accuracy (RM ANOVA genotype × delay × %correct P = 0.043) compared with WT (n = 10). (G) Picrotoxin improves accuracy in Nf1+/− mice (n = 11, RM ANOVA drug × genotype × delay × %correct P = 0.037) compared to WT (n = 9). (Left) Accuracy of Nf1+/− and WT mice administered saline or picrotoxin (0.025 mg/kg) in a counterbalanced within-subject design. (Right) Within-subject percent change in accuracy at the 3–6 s delay (*P < 0.05; one-tailed t test). Error bars represent SEM.