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PreprintCC BY-NC-NDbioRxiv

Activity-dependent myelination in prefrontal circuits signals the offset of infantile amnesia

4 more authors
  1. 1Hospital for Sick Children

Abstract

Human and non-human infants can form memories for events, but these memories are not successfully consolidated into remote memory. While the neurobiological basis of this phenomenon-known as infantile amnesia-remains unclear, it is hypothesized that the neural circuits required for successful consolidation are insufficiently mature. Here we find that heightened activity in the prelimbic cortex of developing mice triggers a sequalae of maturational steps that culminates in adult-like memory persistence: Activity-dependent increases in brain-derived neurotrophic factor (BDNF) promote myelination of prelimbic circuits via activation of tyrosine kinase receptor B (TrkB) receptors on oligodendrocyte precursor cells (OPCs). Inhibiting any of these steps within a critical developmental window delays the offset of infantile amnesia, whereas promoting this sequalae results in the precocial emergence of memory persistence. Similar to critical periods in sensory cortices, our results indicate that developmental myelination is required for proper circuit maturation and emergence of adult-like memory function.

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BibTeX
@misc{golbabaei2026activitydependent,
  title = {{Activity-dependent myelination in prefrontal circuits signals the offset of infantile amnesia}},
  author = {A. Golbabaei and A. I. Ramsaran and A. Rashid and M. L. De Snoo and D. Karamboulas and J. Wo and B. Shahrbandi and Y. Li and B. S. Wang and A. Willis and M. Fukuchi and S. Kida and D. R. Kaplan and F. D. Miller and S. A. Josselyn and P. W. Frankland},
  howpublished = {bioRxiv},
  year = {2026},
  month = sep,
  doi = {10.64898/2026.09.03.749197},
  url = {https://www.biorxiv.org/content/10.64898/2026.09.03.749197v1},
  note = {CC BY-NC-ND},
}
RIS
TY  - UNPB
TI  - Activity-dependent myelination in prefrontal circuits signals the offset of infantile amnesia
AU  - A. Golbabaei
AU  - A. I. Ramsaran
AU  - A. Rashid
AU  - M. L. De Snoo
AU  - D. Karamboulas
AU  - J. Wo
AU  - B. Shahrbandi
AU  - Y. Li
AU  - B. S. Wang
AU  - A. Willis
AU  - M. Fukuchi
AU  - S. Kida
AU  - D. R. Kaplan
AU  - F. D. Miller
AU  - S. A. Josselyn
AU  - P. W. Frankland
PY  - 2026
DA  - 2026/09/03
PB  - bioRxiv
DO  - 10.64898/2026.09.03.749197
UR  - https://www.biorxiv.org/content/10.64898/2026.09.03.749197v1
AB  - Human and non-human infants can form memories for events, but these memories are not successfully consolidated into remote memory. While the neurobiological basis of this phenomenon-known as infantile amnesia-remains unclear, it is hypothesized that the neural circuits required for successful consolidation are insufficiently mature. Here we find that heightened activity in the prelimbic cortex of developing mice triggers a sequalae of maturational steps that culminates in adult-like memory persistence: Activity-dependent increases in brain-derived neurotrophic factor (BDNF) promote myelination of prelimbic circuits via activation of tyrosine kinase receptor B (TrkB) receptors on oligodendrocyte precursor cells (OPCs). Inhibiting any of these steps within a critical developmental window delays the offset of infantile amnesia, whereas promoting this sequalae results in the precocial emergence of memory persistence. Similar to critical periods in sensory cortices, our results indicate that developmental myelination is required for proper circuit maturation and emergence of adult-like memory function.
ER  -