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Sci Rep. 2016 Sep 28;6:34196. doi: 10.1038/srep34196.

The decline in synaptic GluN2B and rise in inhibitory neurotransmission determine the end of a critical period.

Scientific reports

Noriko Isoo, Takae Ohno, Mutsumi Isowaki, Satoshi Fukuda, Naoyuki Murabe, Hiroaki Mizukami, Keiya Ozawa, Masayoshi Mishina, Masaki Sakurai

Affiliations

  1. Department of Physiology, Teikyo University School of Medicine, 2-11-1 Kaga, Itabashi-ku, Tokyo 173-8605, Japan.
  2. Division of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical University, 3311-1 Yakushiji, Shimono, Tochigi 329-0498, Japan.
  3. Division of Genetic Therapeutics, the Institute of Medical Science, the University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
  4. Department of Molecular Neurobiology &Pharmacology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
  5. Brain Science Laboratory, The Research Organization of Science and Technology, Ritsumeikan University, 1-1-1 Nojihigashi, Kusatsu, Shiga 525-8577, Japan.

PMID: 27677249 PMCID: PMC5039748 DOI: 10.1038/srep34196

Abstract

Neuronal plasticity is especially active in the young, during short windows of time termed critical periods, and loss of a critical period leads to functional limitations in the adults. The mechanism that governs the length of critical periods remains unknown. Here we show that levels of the NMDA receptor GluN2B subunit, which functions as a Ca

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