Journal
CELL REPORTS
Volume 41, Issue 7, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2022.111643
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Funding
- Dana Foundation [R37 MH065635, R01 HD103641, T32-MH019524-27, T32-NS-86750-5, T32AG052909, RRRC: 00773]
- NIDA IRP Transgenic Rat Project
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Episodic memories formed in early childhood rapidly decay, but their latent traces remain stored long term. The maturation of parvalbumin interneurons (PVIs), a major mechanism of critical periods, contributes to memory development. Episodic infantile learning increases the levels of parvalbumin in the dorsal hippocampus (dHPC). These PVIs are required for infantile memory formation and are critical for memory development.
Episodic memories formed in early childhood rapidly decay, but their latent traces remain stored long term. These memories require the dorsal hippocampus (dHPC) and seem to undergo a developmental critical period. It remains to be determined whether the maturation of parvalbumin interneurons (PVIs), a major mechanism of critical periods, contributes to memory development. Here, we show that episodic infantile learning significantly increases the levels of parvalbumin in the dHPC 48 h after training. Chemogenetic inhibition of PVIs before learning indicated that these neurons are required for infantile memory formation. A bilateral dHPC injection of the gamma-aminobutyric acid type A receptor agonist diazepam after training elicited long-term memory expression in infant rats, although direct PVI chemogenetic activation had no effect. Finally, PVI activity was required for brain-derived neurotrophic factor (BDNF)-dependent maturation of memory competence, i.e., adult-like long-term memory expression. Thus, dHPC PVIs are critical for the formation of infantile memories and for memory development.
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