Figure 9. SLAMR is not enriched in dorsal CA1 after MWM training as well as not required for spatial learning and memory.

A. Experimental design. B. Latency of mice in MWM during 1 week of training. C. Distance during the first trial or a single swimming session. D. RT-qPCR results show that lncRNA SLAMR is not increased in dorsal CA1 1 hr after finishing a single session of swimming exercise, 1 day or 1 week of training in MWM (n=4 per group). E. Schematic representation of SLAMR genetic manipulation for MWM study. F. Latency values did not show any differences between groups during the learning and long-term memory test. Also, no differences in distance and velocity values indicated behavioral changes induced by the genetic manipulation of SLAMR. G-H. Test results in percentage of time spent in target quadrant and platform crossings show no differences between groups for consolidation of spatial memory. Data shown as MEAN±SEM. I. Representative heat maps indicated normal exploratory behavior during the test session for all three conditions. J. Model of SLAMR during consolidation. Top panel: Learning increases SLAMR expression which reciprocally regulates KIF5C expression. KIF5C transports and deposits SLAMR throughout the dendrite and in spines. Bottom panel left: Model of a vesicle containing SLAMR and identified interactor CaMKII, along with numerous other proteins, lncRNAs, microRNAs, and mRNAs as suggested by the pulldown experiments. Red hairpin indicates binding region to CaMKII/Vimentin. Bottom panel right: Stimulated dendritic spine showing structural plasticity, the active recruitment of SLAMR, phosphorylation of CaMKII and increased local protein synthesis. SLAMR participates in this role in fear memory but not spatial memory.