Figure 4
Adolescent PDE11A knockout (KO) mice demonstrate impairments in the consolidation of long-term memories (LTMs) for social experiences. (a) As measured in C57BL/6J and PDE11A wild-type male and female mice, PDE11A4 mRNA expression significantly increases in ventral CA1 and subiculum (vCA1, vSub) between postnatal day 7 (P7) and P21 (n=4–6/age). The specificity of the probe was confirmed using sections from PDE11A knockout (KO) mice. Whereas, PDE11A4 mRNA levels then stabilize (vCA1), or subsequently decrease (vSub), between P21 and P28, (b) PDE11A4 protein expression in the hippocampus significantly increases every week from P7 to P28 (n=4–6/age). No further increase in expression is observed between P28 and young adulthood (n=11–14/age). The specificity of the antibody was verified using hippocampal tissue from PDE11A KO mice. Consistent with the fact that adolescent PDE11A4 protein expression is equivalent to levels observed in young adults, adolescent PDE11A KO mice exhibit similar phenotypes to adult PDE11A KO mice. (c) Adolescent PDE11A KO mice show normal short-term memory (STM) 1 h after social odor recognition (SOR) training but (d) no LTM 24 h after SOR training (n=22–30/genotype). (e) Similarly, adolescent PDE11A KO mice show no LTM for social transmission of food preference (n=19–25/genotype). Post hoc, *vs P7, familiar odor, or novel food, P<0.005–0.001; #vs P14 or WT within odor/food, P<0.02–0.001. @vs P21, P<0.001. Brightness and contrast adjusted for graphical clarity.
