Speaker: Prof. Huimin Wang, East China Normal University
Abstract of the Talk
Memories are dynamic rather than static. After retrieval or reactivation, memories enter into a labile state, requiring the process of reconsolidation. However, the underling molecular mechanisms are not fully understood. By employing an inducible and reversible protein knockout technique, we can manipulate the activity of αCaMKII in the mouse forebrain in the time scale of minutes. By studying 1-month-old fear memories, we find that CaMKII plays important roles during long term memory reconsolidation. We show that rapid shift of αCaMKII activity within the immediate 10min after retrieval significantly disrupts post-reactivation long-term memories (PR- LTM), including hippocampal-dependent and amygdale-dependent memories, suggesting a critical time window for αCaMKII activation during memory reconsolidation. Moreover, we show that αCaMKII-induced PR-LTM deficit is only restricted to the memory that is retrieved while leaving other memories intact. Further we demonstrate that αCaMKII-induced PR-LTM deficit seems long-lasting since there is no spontaneous recovery observed even two weeks after second recall. Systematic analysis suggests that αCaMKII-induced protein degradation during reconsolidation may serve as a mechanism for memory reorganization. Taken together, we propose that the initial destabilization of memory traces during memory reconsolidation requires CaMKII-dependent protein degradation processes.
Biography
Professor Huimin Wang, obtained her M.D. from Medical School of Zhejiang University. She received her Ph.D. in Pharmacology from Rutgers University (the State University of New Jersey) and Robert Wood Johnson Medical School of University of Medicine and Dentistry of New Jersey. She held positions at Children’s Hospital affiliated to the Medical School of Zhejiang University, Princeton University, and Boston University.