Hippocampus-dependent, event-related memories formed in early infancy in human and non-human animals are rapidly forgotten. Recently the authors reported that high levels of hippocampal neurogenesis contribute to accelerated rates of forgetting during infancy. Here, they ask whether these memories formed in infancy are permanently erased (i.e., storage failure) or become progressively inaccessible with time (i.e., retrieval failure). To do this, they developed an optogenetic strategy that permanently expressed channelrhodopsin-2 (ChR2) in neuronal ensembles that were activated during contextual fear encoding in infant mice. They then examined whether reactivation of ChR2-tagged ensembles in the dentate gyrus was sufficient for memory recovery in adulthood. They found that optogenetic stimulation of tagged dentate gyrus neurons recovered “lost” infant memories up to 3 months following training and that memory recovery was associated with broader reactivation of tagged hippocampal and cortical neuronal ensembles. Thus, infant memories may be recovered under specific conditions and are not permanently lost.
Guskjolen A, Kenney JW, de la Parra J, Yeung BA, Josselyn SA, Frankland PW: Recovery of “Lost” Infant Memories in Mice. Curr. Biol.pii: S0960-9822(18)30695-X. doi: 10.1016/j.cub.2018.05.059. [Epub ahead of print, June 26, 2018].