I-CAN-DO Program in Liaison Laboratory
Date:May 12, 2010
Global COE Mini Symposium

Organizer: Kenichi Yamamura, Minoru Kawakami
Venue: IMEG 1F Conference room
Invited Speakers: Nobuki Nakanishi / Yuichi Iino


Global COE Mini Symposium
gAnalysis of nervous system functions in model organisms and its potential research applicationsh

y Date z Wednesday, May 12, 2010 13:00 - 16:10

y Venue z Conference Room, IMEG 1F

y Invited Speaker z Nobuki Nakanishi, PhD. (Sanford-Burnham Medical Research Institute)
@@@@@@@@@@@@@Yuichi Iino, PhD. ( Tokyo University of Tokyo )

y Program z

13:00-13:30 Daisuke Matsumaru Global COE Jr.RA Department of Organ Formation
@
gGenetic analysis of Hedgehog signaling for the ventral body wall development and the onset of omphalocele formation.h

13:30-14:00 Minoru Kawakami Assistant Professor Department of Phylogeny
@
gEffects of cyclosporin A administration on gene expression in rat brain.

14:00-15:00 Nobuki Nakanishi Associate Professor Center for Neuroscience, Aging and Stem Cells Sanford-Burnham Medical Research Institute
@
gGenetic analysis of mice lacking the NR3A subunit of NMDA receptorsh
k Summary l
Glutamate is the major excitatory neurotransmitter in mammalian brain. NMDA-type glutamate receptors (NMDARs) are thought to act as integrators of coincident synaptic signals, while their hyperactivation causes neurodegeneration. The conventional NMDAR requires two distinct subunits,
NR1 and NR2, to form functional channels. We and others have identified a third family of NMDAR subunits, designated NR3. Through the analyses of NR3A knockout (KO) and transgenic mice, we have shown that NR3A acts as an inhibitory subunit of NMDARs. Furthermore, we have identified a large gene family named takusan, whose expression is upregulated in NR3A KO
mice. Biochemical and cellular studies reveal that takusan plays a role in the organization of postsynaptic molecules. We currently explore whether takusan proteins can be exploited as therapeutic agents combating neurodegenerative diseases such as Alzheimer's.

15:00-15:10 Break

15:10-16:10 Yuichi Iino Professor Molecular Genetics Research Laboratory University of Tokyo
@gMolecular mechanisms of salt chemotaxis learning in C. elegans h
k Summary l
The nametode C. elegans has 302 neurons and its entire neural circuit is known. It also allows forward genetic screening to isolate behavioral mutants. The chemotaxis behavior of this animal is plastic. For example, C. elegans raised under standard conditions shows positive chemotaxis to NaCl. However, when it is kept with NaCl but without food, it now learns to avoid NaCl. Through analyses of mutants defective in this form of learning (salt chemotaxis learning), we found that the insulin/PI 3-kinase signaling pathway is essential for learning. The Gq/DAG/nPKC pathway was found to act antagonistically to the insulin pathway. Mutants in the homologue of calsyntenin, which is abundant in mammalian brain, was also found to be defective in learning. I will describe the molecular and neural mechanisms of learning along with the behavioral strategy of chemotaxis.

Organizer : Kenichi Yamamura, Minoru Kawakami, IMEG
Contact Information: Global COE Promotion Office Ikuko Yamaguchi (Ext.5006)



I-CAN-DO Program