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東京大学遺伝子実験施設セミナーのご案内

アメフラシやマウス、ラットを用いた記憶の研究で幅広い成果を上げておられる韓国ソウル大学のBong-Kiun Kaang教授が来日される機会にセミナーをお願いしましたのでご案内いたします。

タイトル:Role of A Nucleolar Protein ApLLP in Synaptic Plasticity and Memory
演者:Bong-Kiun Kaang (School of Biological Sciences&s_comma; College of Natural
Sciences&s_comma; Seoul National University)
日時:平成16年9月4日(月)11:00~12:30
場所:東京大学理学部1号館2階233号講義室
http://www.u-tokyo.ac.jp/campusmap/cam01_06_01_j.html

講演要旨:
Synaptic plasticity is a key feature of long-term memory formation in various organisms. Previously&s_comma; we cloned a LAPS18-like protein in Aplysia (ApLLP) and showed that ApLLP is localized in the nucleus&s_comma; mainly in the nucleolus&s_comma; and its localization is mediated by N- and C-terminal nuclear localization signals (NLSs) (Kim et al.&s_comma; 2003). In Limax marginatus&s_comma; the ApLLP homologue Learning Associative Protein of Slug 18 kD (LAPS18) is induced by odor-taste associative learning&s_comma; which evokes odor avoidance by association of conditioned stimulus (carrot juice smell) and unconditioned stimulus (quinidine sulfate solution) (Nakaya et al.&s_comma; 2001). These results suggested that LAPS18 might be involved in the synthesis of RNA or protein&s_comma; which is required for long-term synaptic plasticity. Therefore&s_comma; we hypothesized that ApLLP may be induced by a memory-related signal and participates in the synthesis of new RNA or protein required for long-term synaptic plasticity. We used the Aplysia culture system to examine the effect of depolarization on ApLLP and the ability of ApLLP to increase synaptic strength. Here&s_comma; we demonstrate that ApLLP&s_comma; a novel nucleolus protein is critically involved in both long-term facilitation (LTF) and behavioral sensitization. Membrane depolarization induced ApLLP expression&s_comma; which activated ApC/EBP expression through a direct binding to CRE. LTF was produced by a single pulse of 5-HT 30 min after the membrane depolarization. This LTF was blocked when either ApLLP or ApC/EBP were blocked by specific antibodies. In contrast&s_comma; ApLLP overexpression induced LTF in response to a single 5-HT treatment. Simultaneously&s_comma; a siphon noxious stimulus (SNS) to intact Aplysia induced ApLLP and ApC/EBP expression&s_comma; and single tail shock 30 min after SNS transformed short-term sensitization to long-term sensitization of siphon withdrawal reflex. These results suggest that ApLLP is an activity-dependent transcriptional activator that switches short-term facilitation to long-term facilitation.

Reference: Kim H et al. "A Nucleolar Protein ApLLP Induces ApC/EBP Expression Required for Long-Term Synaptic Facilitation in Aplysia Neurons." Neuron. 2006&s_comma; 49(5):707-718.



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