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演題詳細

Poster

学習・長期記憶
Learning and Long-term Memory

開催日 2014/9/11
時間 16:00 - 17:00
会場 Poster / Exhibition(Event Hall B)

異なるセルアンサンブルの光遺伝学的活性化による連合記憶の人工的創出
Artificial association of information residing in hippocampus and amygdala

  • P1-270
  • 大川 宜昭 / Noriaki Ohkawa:1,2 斎藤 喜人 / Yoshito Saitoh:1,2 鈴木 章円 / Akinobu Suzuki:1,2 辻村 周平 / Shuhei Tsujimura:1,2 村山 絵美 / Emi Murayama:1,2 西園 啓文 / Hirofumi Nishizono:3 松尾 美奈 / Mina Matsuo:3 高橋 由香里 / Yukari Takahashi:4 長瀬 将志 / Masashi Nagase:4 杉村 弥恵 / Yae K. Sugimura:4 渡部 文子 / Ayako M. Watabe:4,5 加藤 総夫 / Fusao Kato:4,5 井ノ口 馨 / Kaoru Inokuchi:1,2 
  • 1:富山大院・医学薬学(医学)・生化学 / Dept Biochem, Grad Sch Med Pharm Sci, Univ of Toyama 2:JST, CREST / CREST, JST 3:富山大・生命科学先端研究センター・動物実験施設 / Div of Animal Exp Lab, Life Sci Res Cen, Univ of Toyama 4:東京慈恵会医科大学・神経科学研究部 / Dept Neurosci, Jikei Univ Sch of Med 5:名古屋大院・医学・神経情報薬理学 / Nagoya Univ Grad Sch of Med 

Memory is assumed to be stored in the brain as a cellular ensemble consisting of a set of neurons that is activated during learning. Although optical stimulation of a cellular ensemble is known to trigger the retrieval of the corresponding memory, it is unclear how the association of distinct information occurs at the cell ensemble level. Here, we show in mice that activation of a cell ensemble corresponding to two distinct memory events generates an artificial association between initially non-related events. In the context pre-exposure and immediate shock (IS) paradigm, mice failed to associate the shock with the pre-exposed context when the IS was delivered to their foot in a different context. Cells activated during the context pre-exposure and the IS in hippocampal CA1 and the basolateral amygdala (BLA) were targeted with channelrhodopsin-2, a light-activated cation channel. These cells were later simultaneously activated by optical stimulation in the mice's home cage. The next day, these mice exhibited freezing behaviour, an indicator of a fear response, in the pre-exposed context that was not originally associated with the shock. Thus, the artificial activation of distinct cell ensembles, without any sensory input, is capable of generating an artificially associated memory. Furthermore, our finding suggests that the association of distinct units of information is achieved through the synchronous activity of distinct cell ensembles. This mechanism may underlie memory update by incorporating novel information into pre-existing networks to form qualitatively new memories.

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