Hippocampal Neurogenesis Regulates Forgetting During Adulthood and Infancy

TLDR

Hippocampal neurogenesis continuously adds new neurons, remodeling circuits and, according to models, can degrade established memories—a process that may underlie infantile amnesia and varies across species. In adult mice, boosting neurogenesis after memory formation caused forgetting, whereas in infant mice and in species with low postnatal neurogenesis (guinea pigs, degus) reducing neurogenesis prevented forgetting and increasing it induced infantile amnesia.

Abstract

Throughout life, new neurons are continuously added to the dentate gyrus. As this continuous addition remodels hippocampal circuits, computational models predict that neurogenesis leads to degradation or forgetting of established memories. Consistent with this, increasing neurogenesis after the formation of a memory was sufficient to induce forgetting in adult mice. By contrast, during infancy, when hippocampal neurogenesis levels are high and freshly generated memories tend to be rapidly forgotten (infantile amnesia), decreasing neurogenesis after memory formation mitigated forgetting. In precocial species, including guinea pigs and degus, most granule cells are generated prenatally. Consistent with reduced levels of postnatal hippocampal neurogenesis, infant guinea pigs and degus did not exhibit forgetting. However, increasing neurogenesis after memory formation induced infantile amnesia in these species.