Section Days abstract book 2010.indd - RUB Research School ...

new learning after reactivation was less pronounced than after a 1-day-interval but still
present for the number of pictures that were recalled. The impairing effect of new learning
after memory reactivation disappeared when the interval between initial learning and
reactivation was 28 days.
Conclusion:
Our findings indicate that older memories are less susceptible to reconsolidation effects than
recent memories. The present pattern of results is consistent with findings from animal studies
showing that as the time interval after initial learning increases, memories become
increasingly resistant to post-reactivation interfering disruptions [6, 7, 12]. These findings
represent the first evidence of a temporal gradient in memory reconsolidation of humans.
Why are older memories less susceptible to the disruptive effects of new learning after
their reactivation than younger memories? Initial information encoding and storage depends
on the hippocampus. With the passage of time, these memories become consolidated in
neocortical structures and completely [3, 13] or partially [14] independent of the
hippocampus. Reactivation of recent, not completely consolidated memories may result in
reengagement of those neural circuits that are involved in encoding and short-term storage,
with the effect that “the initial memory is partially overwritten in the interest of storing more
recently acquired information” [15]. Older memories, however, are stored in neocortical brain
areas that are different from the encoding circuits and are therefore less readily modifiable.
In this study we showed that the temporal dynamics of memory reconsolidation in
humans are dependent on the age of the memories, such that older memories are less sensitive
to modifications after their retrieval (i.e. during reconsolidation) than recent memories. These
findings may have important implications for the potential use of reconsolidation
manipulations as a treatment for anxiety disorders, such as PTSD [5, 16]. They suggest that
the possibility for therapeutic interventions after the reactivation of a memory of a traumatic
event may be most promising within a short time window after this event has happened.
References:
[1] Sara, S.J., Retrieval and reconsolidation: Toward a neurobiology of remembering.
Learning & Memory, 2000. 7: p. 73-84.
[2] Nader, K., Memory traces unbound. Trends in Neuroscience, 2003. 26(2): p. 65-72.
[3] Dudai, Y., The neurobiology of consolidation, or, how stable is the engram? Annual
Review of Psychology, 2004. 55: p. 51-86.
[4] Kindt, M., M. Soeter, and B. Vervliet, Beyond extinction: Erasing human fear responses
and preventing the return of fear. Nature Neuroscience, 2009. 12(3): p. 256-258.
[5] Schiller, D., et al., Preventing the return of fear in humans using reconsolidation update
mechanisms. Nature, 2009. 463: p. 49-53.
[6] Milekic, M.H. and C.M. Alberini, Temporally graded requirement for protein synthesis
following memory reactivation. Neuron, 2002. 36: p. 521-525.
[7] Suzuki, A., et al., Memory reconsolidation and extinction have distinct temporal and
biochemical signatures. The Journal of Neuroscience, 2004. 24: p. 4787-4795.
[8] Debiec, J., J.E. LeDoux, and K. Nader, Cellular and systems reconsolidation in the
hippocampus. Neuron, 2002. 36: p. 527-538.
[9] Lee, J.L.C., et al., Disrupting reconsolidation of drug memories reduces cocaine-seeking
behavior. Neuron, 2005. 47: p. 795-801.