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Synaptic Plasticity

開催日 2014/9/13
時間 17:10 - 18:10
会場 Room J(313+314)
Chairperson(s) 竹本 さやか / Sayaka Takemoto-Kimu (東京大学大学院医学系研究科 神経生化学教室 / Department of Neurochemistry, Graduate School of Medicine, University of Tokyo, Japan)
安部 健太郎 / Kentaro Abe (京都大学大学院医学研究科 生体情報科学講座 / Department of Biological Sciences, Graduate School of Medecine, Kyoto University, Japan)

Experience-dependent synaptic regulation requires postsynaptic mGluR-IP3 signaling in the mature barrel cortex

  • O3-J-5-3
  • 久保田 淳 / Jun Kubota:1 金丸 和典 / Kazunori Kanemaru:1 関谷 敬 / Hiroshi Sekiya:1 大久保 洋平 / Yohei Okubo:1 飯野 正光 / Masamitsu Iino:1 
  • 1:東京大院・医・薬理 / Dept Pharmacol, Univ of Tokyo, Tokyo, Japan 

Cortical synapses are modified by sensory experience, a process that is considered as a fundamental mechanism to support learning and long-term adaptation to an altered environment. This process occurs developmentally during a window of heightened plasticity called a critical period, but also takes place throughout life. However, the underlying molecular mechanisms remain unclear, especially in mature animals. Here we investigated the mechanism underlying whisker deprivation-induced synaptic weakening after the critical period. Whisker deprivation decreased the presynaptic glutamate release probability at layer 4 (L4)-layer 2/3 (L2/3) synapses in the barrel cortex of mice. As previously reported, type 1 cannabinoid receptor (CB1R)-dependent depression contributes to this weakening during the critical period, in which L2/3 synapses share around postnatal day 12-14. After this period, the involvement of CB1R was diminished and we surprisingly found that deprivation-induced weakening was restored by a positive allosteric modulator of the metabotropic glutamate receptor (mGluR). Furthermore, mGluR antagonists or chronic suppression of inositol 1,4,5-trisphosphate (IP3) signaling in the L2/3 postsynaptic neurons showed effects similar to those of whisker deprivation. These results suggest that experience-dependent mGluR-IP3 signaling in the postsynaptic neurons retrogradely regulates the presynaptic functions in the mature barrel cortex, providing a novel insight into deprivation-induced plasticity in the cerebral cortex.

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