Our findings and theoretical predictions suggest that the forgetting mechanisms targeting recent memories or reactivated long-term memories are different from those targeting “dormant” long-term memories. In our current studies on the forgetting of recent (or “active”) memories, we explore the role of memory interference.

It has been generally assumed that interference from new learning underpins the loss of recently acquired memories, and that it contributes little to the loss of long-term memories. We have proposed that the hippocampus plays a critical role in preventing interference. Our theory is supported by the observation that amnesic patients with hippocampal damage seem to suffer from enhanced interference, while their ability to encode memories remains intact: reducing the amount of stimulation after memory encoding can boost memory retention in these patients. In healthy adults, this effect, albeit weaker, can also be detected.

We replicated this basic effect in rats, establishing what we called “The Black Box Effect”: We found that exposing rats to a familiar dark chamber after learning promotes long-term memory persistence in an object recognition task. Departing from this finding, we developed a rat model of hippocampal amnesia to test whether impaired function of the hippocampus leads to heightened interference for object memories, i.e., whether the Black Box can rescue the memory deficit.

In parallel, we are trying to establish a complimentary line of research in human subjects, in collaboration with Dr Signy Sheldon at McGIll. In another collaboration with Dr Kris Onishi, we explore in children whether age correlates with susceptibility to interference and if reducing sensory stimulation can rescue possible deficits.