Damage to the hippocampus (HPC) typically causes retrograde amnesia for contextual fear conditioning. Reinstating the conditioning over several sessions, however, can mitigate the retrograde amnesic effects. Reinstatements, thus, establish a sufficiently strong memory in non-HPC systems to no longer require the HPC for expression, meaning that it has become HPC independent. This thesis aimed to determine the structures comprising the non-HPC system supporting reinstated context fear memory. The contribution of the perirhinal cortex (PRH) and the anterior cingulate cortex (ACC) were examined because of their established role in context memory. Initially, it was demonstrated that HPC damage indeed causes retrograde amnesia for single session, but not reinstated, contextual fear conditioning. Then, it was demonstrated that combined HPC and PRH damage causes retrograde amnesia for reinstated contextual fear conditioning, whereas combined HPC and ACC damage had lesser effects. Therefore, the PRH is a key structure within the non-HPC memory system for reinstated context fear memory.
Author Keywords: anterior cingulate cortex, contextual fear conditioning, hippocampus, memory, perirhinal cortex, retrograde amnesia