We aim to clarify the mechanism of postnatal brain development and find a solution for developmental disorders.
Aya Ito-Ishida, M.D., Ph.D.
Team Leader, Brain Development and Disorders
aya.ishida [at] riken.jp
- Research Overview
- Selected Publications
- Research Scientist or Postdoctoral Researcher Position (W21049)
Our lab aims to understand fundamental mechanisms of postnatal brain development and to clarify the origin of developmental disorders such as autism. Infants’ brains undergo dynamic functional and structural changes during the first year of life. We elucidate this process by studying the roles of synaptic proteins in the maturation of neural circuitry. We use multidisciplinary approaches that span molecular, synaptic, circuit, and behavioral levels. By applying these techniques to the mouse models of developmental disorders, we aim to find a solution that could provide a novel therapeutic strategy.
Main Research Field
- Complex systems
Related Research Fields
- Complex systems
- Biological sciences
- Medicine, dentistry, and pharmacy
- Neuroscience (Neurophysiology/General neuroscience)
- Animal physiology/ Animal behavior
Papers with an asterisk(*) are based on research conducted outside of RIKEN.
- * Ito-Ishida A*, Baker SA, Sillitoe RV, Sun Y, Zhou J, Ono Y, Iwakiri J, Yuzaki M, Zoghbi HY*. (* co-corresponding authors)
“MeCP2 Levels Regulate the 3D Structure of Heterochromatic Foci in Mouse Neurons.”
Journal of Neuroscience. 40(45), 8746-8766. (2020)
- * Ito-Ishida A, Yamalanchili HK, Shao Y, Baker SA, Heckman LD, Lavery LA, Kim J, Lombardi LM, Sun Y, Liu Z, Zoghbi HY.
“Genome Wide Distribution of Linker Histone H1.0 is Independent of MeCP2.”
Nature Neuroscience. 21(6), 794-798. (2018)
- * Lu H, Ash RT, He L, Kee SE, Wang W, Yu F, Hao S, Meng X, Ure K, Ito-Ishida A, Tang B, Sun Y, Ji D, Tang J, Arenkiel BR, Smirnakis SM, Zoghbi HY.
“Loss and gain of MeCP2 lead to similar hippocampal circuit abnormalities that are rescued by deep brain stimulation in a Rett syndrome mouse model.”
Neuron, 91(4), 739-747. (2016).
- * Ure K, Lu H, Wang W, Ito-Ishida A, Wu Z, He Y, Sztainberg Y, Tang J, Zoghbi HY.
“Restoration of Mecp2 expression in GABAergic neurons is sufficient to rescue multiple disease features in a mouse model of Rett Syndrome.”
eLife, Jun 21;5:e14198. (2016)
- * Ito-Ishida A, Ure K, Chen H, Swann JW, Zoghbi HY.
“Loss of MeCP2 in parvalbumin-and somatostatin-expressing neurons in mice leads to distinct Rett Syndrome-like phenotypes.”
Neuron. 88(4), 651-8. (2015).
- * Ito-Ishida A, Kakegawa W, Kohda K, Miura E, Okabe S, Yuzaki M.
“Cbln1 downregulates the formation and function of inhibitory synapses in mouse cerebellar Purkinje cells.”
European Journal of Neuroscience. 39(8), 1268-80. (2014)
- * Ito-Ishida, A, Miyazaki, T., Miura, E., Matsuda, K., Watanabe, M., Yuzaki, M. and Okabe, S.
“Presynaptically released Cbln1 induces dynamic axonal structural changes by interacting with GluD2 during cerebellar synapse formation.”
Neuron 76(3), 549-564. (2012)
- * Matsuda, K., Miura, E., Miyazaki, T., Kakegawa, W., Emi, K., Narumi, S., Fukazawa, Y., Ito-Ishida, A., Kondo, T., Shigemoto, R., Watanabe, M. and Yuzaki, M.
“Cbln1 is a ligand for an orphan glutamate receptor delta2, a bidirectional synapse organizer.”
Science 328(5976): 363-368. (2010)
- * Ito-Ishida, A, Miura, E., Emi, K., Matsuda, K., Iijima, T., Kondo, T., Kohda, K., Watanabe, M. and Yuzaki, M.
“Cbln1 regulates rapid formation and maintenance of excitatory synapses in mature cerebellar Purkinje cells in vitro and in vivo.”
Journal of Neuroscience. 28(23): 5920-5930. (2008)
- * Ito-Ishida, A., Kakegawa, W. and Yuzaki, M.
“ERK1/2 but not p38 MAP kinase is essential for the long-term depression in mouse cerebellar slices.”
European Journal of Neuroscience. 24(6): 1617-1622. (2006)