Infantile amnesia reflects a developmental critical period for hippocampal learning (Nature Neuroscience 2016; doi:10.1038/nn.4348)

報告日期: 2016/11/25
報告時間: 3:10/4:00
報告學生: 蔡宗志
講評老師: 蕭雅心
附件下載: 下載[1578-1473666575-1.pdf] 

Infantile amnesia reflects a developmental critical period for hippocampal learning

Authors: Travaglia, A., Bisaz, R., Sweet, E.S., Blitzer, R.D. and Alberini, C.M.

Journal: Nat. Neurosci. 19, 1225-1233 (2016).

Speaker: Tsung-Chih Tsai (蔡宗志)


Commentator: Ya-Hsin Hsiao (蕭雅心)

Place: Room 602

Infantile amnesia (IA) is defined as inability of adults to recall memory before the age of 3. IA not only exists in humankind, but also in rodent. Interestingly, the loss of infantile memory may have some impacts on our brain functions and physiology through our whole life. There is clear evidence that using reminder can reinstate infantile memory and have been widely reported in rodents and human. According to these observations, it is generally believed that IA is a memory retrieval problem due to the existence of formed infantile memory, called latent infantile memory. Based on current concepts of plasticity and memory, N-methyl-D-aspartate (NMDA) receptor component transition and lower brain-derived neurotrophic factor (BDNF) may be the candidates involved in IA at developmental stage. However, the molecular mechanisms of this phenomenon remain to be unelucidated. To investigate the mechanisms of the critical period for infantile amnesia and reminder effect, the authors proposed that NMDA receptor GluN2B subunit switches to GluN2A and BDNF-trkB signaling pathway contribute to latent infantile memory. To examine this hypothesis, inhibitory avoidance (IA) paradigm and then gave a reminder to remind latent infantile memory were chosen in rat model. They found infant (P17) forgot easier and more rapid than juvenile (P24). Interestingly, they found no matter how long after learning, giving reminder can recall latent infantile memory. Both infant and juvenile rats dramatically increased p-trkB after learning. In contrast to juvenile, infant has significantly increased GluN2A: GluN2B ratio after learning. Finally, the authors found GluN2B and mGluR5 activation can completely switch GluN2B to GluN2A and may accelerates the closing the period of infantile amnesia. They conclude that lower BDNF level and GluN2A:GluN2B ratio lead to latent infantile memory formation in developmental state.


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