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Sculpting the neuronal intracellular environment: from single molecule behavior to local signal integration
Sculpting the neuronal intracellular environment: from single molecule behavior to local signal integration

開催日 2014/9/12
時間 9:00 - 11:00
会場 Room B(501)
Chairperson(s) 合田 裕紀子 / Yukiko Goda (理化学研究所 脳科学総合研究センター シナプス可塑性・回路制御研究チーム / RIKEN, Brain Science Institute, Japan)
瀬藤 光利 / Mitsutoshi Setou (浜松医科大学 解剖学講座 細胞生物学分野 / Department of Cell Biology and Anatomy Hamamatsu University School of Medicine, Japan)

Imaging and controlling the biochemical reactions in single dendritic spines of hippocampal neuron by 2-photon excitation based technique

  • S2-B-1-4
  • 村越 秀治 / Hideji Murakoshi:1,2 
  • 1:生理学研究所 / National Institute for Physiological Sciences, Japan 2:科学技術振興機構さきがけ / PRESTO, JST, Saitama, Japan 

Ca2+/Calmodulin-dependent kinase II (CaMKII) is one of the most important signaling molecules for long-term potentiation and associated spine enlargement underlying learning and memory. Here, to understand the function of CaMKII for synaptic plasticity, we developed genetically encoded light-inducible CaMKII inhibitor and photo-activatable CaMKII by using LOV2 derived from phototropin1. We applied these newly developed optogenetic tools for the study of structural plasticity of single dendritic spines by using 2-photon fluorescence microscope and glutamate uncaging, and found that 1) ~60 s of CaMKII activation is sufficient for inducing transient and sustained spine enlargement, 2) CaMKII activation alone is sufficient for triggering structural plasticity. In addition, using 2-photon fluorescence lifetime imaging microscopy, we visualized the activity of CaMKII downstream molecules, Cdc42 and RhoA which are the regulator of actin polymerization, to understand the spatiotemporal dynamics of these molecules during structural plasticity. And, we found that Cdc42 and RhoA were rapidly activated in the stimulated spine, and were then followed by a phase of persistent activation lasting more than 30 min. Furthermore, the inhibition of the RhoA pathway preferentially inhibited the initial spine growth, whereas the inhibition of the Cdc42 pathway blocked the maintenance of sustained structural plasticity. Thus, RhoA and Cdc42 relay transient CaMKII activation to synapse-specific, long-term signaling required for spine structural plasticity.

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