Iijima-kun (now Univ Basel studying in Scheiffele Research) and Miura's co-authored papers have been published in the European Journal of Neuroscience magazine。
http://www3.interscience.wiley.com/journal/123389540/abstract

We used to go the expression and biochemical analysis of C1ql family molecules in the brain。C1q family molecules having a structure similar to that of Cbln1 is specifically expressed in a completely different brain regions and Cbln1、It was found to be secreted as multimeric。Possibility of C1ql family molecules also involved in synaptic function in these brain regions are suggested。

Assistant Professor Matsuda's paperScience Notes (April 16 号).。Hokkaido University of Ken Watanabe、It is a joint research with Ken Shigemoto of NIPS。

Cbln1 receptor delta 2 receptors on the postsynaptic (GluD2)It is、Cbln1-CluD2 complex was discovered for the first time that you have to control the maturation of presynaptic and postsynaptic to the bidirectional。

This paperScience STKEIt was selected as Editor's Choice in。Also it was featured in newspapers and Nikkei Sangyo newspaper Kyodo News system。JST's press releaseClick here. 。

Autophagy is a graduate student journal articles Kun Katsumata(IF:5.48)Now Accept to。This paper referred to as "auto-phagocytosis transchromosomic in nerve axons is retrograde transport to the activity-dependent by dynein"。It is a joint research with Mizushima teacher of Tokyo Medical and Dental University。
http://www.landesbioscience.com/journals/autophagy/article/11262/

Accumulation of swelling and autophagosomal of nerve cell axons have been known in a variety of neurodegenerative diseases and ischemic brain。But not little is known about the physiological significance and the dynamics of the auto phagocytosis transchromosomic in axon。Using live imaging techniques in this paper、Autophagosomes transchromosomic is being transported to the cell body by dynein motor from axon、The number of auto-phagocytosis transchromosomic in axon by glutamate stimulation was revealed for the first time that the increase。

Autophagy is a graduate student journal articles Kun Katsumata(IF:5.48)Now Accept to。This paper referred to as "auto-phagocytosis transchromosomic in nerve axons is retrograde transport to the activity-dependent by dynein"。It is a joint research with Mizushima teacher of Tokyo Medical and Dental University。
http://www.landesbioscience.com/journals/autophagy/article/11262/

Accumulation of swelling and autophagosomal of nerve cell axons have been known in a variety of neurodegenerative diseases and ischemic brain。But not little is known about the physiological significance and the dynamics of the auto phagocytosis transchromosomic in axon。Using live imaging techniques in this paper、Autophagosomes transchromosomic is being transported to the cell body by dynein motor from axon、The number of auto-phagocytosis transchromosomic in axon by glutamate stimulation was revealed for the first time that the increase。

Coverage of the classroom took a "half-science half Professor" column of the Keio University School in the magazine "School"。
http://www.keio.ac.jp/ja/contents/seminar/2010/265_2.html

Thesis of Nishiyama Assistant Professor is now Accept the Journal of Neuroscience。Re-evaluation of neurodegeneration in "error char mouse：Sustained ion influx is not the cell death by autophagy、Is the paper that cause cell death accompanied by autophagy "。It is a joint research with Mizushima teacher of Tokyo Medical and Dental University。
http://www.jneurosci.org/cgi/content/abstract/30/6/2177

A phenomenon that neuronal cell death caused by glutamate receptors hyperexcitability、It has been known as the "excitable cell death"。Error char mouse、The point mutations δ2 type glutamate receptor、Cerebellar Purkinje cells by modifying be a mutant mice that cause cerebellar ataxia、It has been used as a model of excitable cells death for a long time。In the error char mouse、Or cells to die by hyperactivity of the "autophagy" the Purkinje cells engulf yourself、Or die by other causes was a long time unknown。In this paper、Autophagy is a phenomenon to be associated with cell death、It was revealed for the first time that it is not the cause。

Strategic Creative Research Promotion Department in FY 2009 the citrus fruit (CREST)Research area in：It was selected as the new adoption research leader in the "creation of elucidation and control technology of the formation and operation principle of the brain circuit."。

Under the theme of "Elucidation and control of synapse formation mechanism in the mature brain."、Hokkaido University Watanabe laboratory、Efforts will for five years along with the Niigata Sakimura Kenji laboratory。For details please
http://www.jst.go.jp/pr/info/info670/index.html



A paper by Kakegawa has been published in Journal of NeuroscienceIt became Accept to。Under the title "top N-terminal region of δ2 receptors rapidly induce cerebellar parallel fiber synapses in in vivo"、It is a joint research with Miyazaki Watanabe teacher of Hokkaido University。「It has been featured in "This Week in The Journal." "As was featured in this week's attention paper。

The last paper (J. Neurosci. 28:1460-1468, 2008)so、Delta 2 receptors controls the LTD signal transduction system via intracellular domain (C-terminal)、From that had been proposed to control the morphological synapse formation via a separate extracellular domain (N-terminal)。We found that it is actually induced synapse formation delta 2 receptor in just one day after when expressed in the cerebellum of the mature animal using a viral vector in this paper。We also see that the N-terminal domain is necessary and sufficient for this action。

Assistant Professor Iijima's paperJournal of NeuroscienceIt became Accept to。"Cbln1 is expressed suppressed by neural activity - homeostatic control in the development stage and mature stage" is the title of。

We、We previously reported that the new secreted factor Cbln1 is essential to maintain and synapse formation between cerebellar granule cells and Purkinje cells。In this paper、When neural activity in granule cells continuously increased to Cbln1 expression is decreased、As a result, we found that the synapse is out。With such a mechanism、Or maintaining the homeostasis prevent over-excitement、Possibility of motor learning related to that and go synaptic modification is suggested。

Invited review of Yuzusaki became in press in the cerebellum special issue of Neuroscience magazine。The title of "synaptic morphology and plasticity of the control mechanism by the two new molecules delta 2 receptor and Cbln1- old."。

Paperback review where the citrus fruit "Handbook of Neurochemistry & Now and in press in the Molecular Neurobiology "。It is titled "glutamate receptor -NMDA receptor and delta receptor"。

Matsuda (Megumi) thesis of Assistant Professor Kondo visiting researcher co-author is now Accept the European Journal of Neuroscience。
The Matsuda (Megumi) Assistant Professor and Miura Hokkaido University、Now Accept the joint research also European Journal of Neuroscience of the Watanabe teacher。

In the two papers is a new secretory synapse formation factor Cbln1 is、It is what was revealed for the first time to specifically bind to the postsynaptic membrane between cerebellar granule cells and Purkinje cells。That specific receptor has clearly indicated the presence at this site。
Despite using a completely different approach、This is where the fun was arrived at a common conclusion。

Graduate students of Ishida was appointed as Society for the Promotion of Science Research Fellow -SPD from the next fiscal year。Congrats!