Examination of the Role of the Muscarinic Acetylcholine Receptor M1 Subtype in Reactivation-Induced Object Memory Modification
Previously stored memory traces can become modifiable once again following memory reactivation. Reactivation can cause the memory trace to destabilize—a protein degradation-dependent process seemingly mediated by proteasome activity—and permits synaptic modifications before reconsolidation. Reactivated memory traces can be “erased” or strengthened, but little is known about mechanisms facilitating qualitative memory changes (i.e., information integration). We hypothesize that muscarinic acetylcholine receptor activation, specifically of the M1 subtype, facilitates reactivation-induced memory updating, due to its established role in object memory destabilization and new learning. In the present thesis, we developed a new object memory modification task for rats in order to observe direct behavioural change as a result of qualitative memory updating. By employing this task, we found that M1 receptor activation, and intact signalling of its downstream messengers associated with proteasome recruitment, within perirhinal cortex are required for reactivation-induced object memory updating.