Thesis of Matsuda Assistant Professor is now Accept the Neuron。Congrats。

AMPA receptor is responsible for the fast neurotransmitter in our brain、We have to control the memory and learning process。AMPA receptors are usually transported to the postsynaptic (dendrites)、Do not go to the presynaptic (axons)。The mechanism of this "polar transport" It was long a mystery、We、AP-4 of the adapter protein that controls the vesicular transport membrane proteins、Was the first time revealed that responsible for this polarity transport。further、Since AMPA receptors that are erroneously transported to the axon is decomposed captured by autophagosomes transchromosomic internally axon、AP-4 is to be involved in autophagy activity has been suggested。

This work is the result of joint research with Hokkaido University Miura, Watanabe teacher。

Baby girl first child was born in Kakegawa Assistant Professor。It is auction-chan。Congrats!!

Kakegawa Assistant Professor of paper is now Accept the Journal of Neuroscience。

Delta 2 receptors、It is essential for synapse formation in the cerebellum、At the same time synaptic plasticity phenomena underlying course of motor learning (long-term depression：Controls LTD)。In other words、Delta receptor is a unique molecule that controls the functional synaptic plasticity and morphological synaptic plasticity。By our lab work so far、Delta 2 receptors、Although it belongs to ionotropic glutamate receptor family、It does not bind to glutamate、And it has been reported that does not function as an ion channel。

In this study the intracellular site of delta 2 receptors (C-terminal) is、It is essential for functional synaptic plasticity features such as LTD and motor learning (eyeblink conditioning)、On the other hand、The morphological synapse formation was the first time revealed that the C-terminus is not essential。In other words、Delta 2 receptors、Through the C-terminal controls the functional synaptic plasticity、Other sites、Probably involved in morphological synapse formation through the extracellular domain (N-terminal)、It is thought that each driving a separate signaling system。

Graduate students of Nishiyama Mr. of paper is now Accept the Autophagy magazine。Congrats。

The relationship between the nerve cell death and autophagy has been attracting attention。For example,、In lurcher mutant mice、When the Delta 2 receptor is constantly activated、Neurodegenerative be seen along with the enhancement of autophagy in Purkinje cells。This molecular mechanism has been conducting research in our laboratory。

In this research、The Atg5 gene is essential for autophagy pathway has been created and studied the Purkinje cell-specific defects are not mice。Prior to denaturation of the Purkinje cells Interestingly、Swelling of the axons is observed、Image intracellular membrane structure is accumulation was observed in tumor most。It is considered an important finding in considering the origin and role of the auto phagocytosis transchromosomic in nerve cells。(Is a joint research with Ken Watanabe Medicine and Dentistry of Ken Mizushima Hokkaido University。）

Journal of Physiology paper is Assistant Professor Kakegawa (London)Now Accept to。Congrats。

Delta 2 receptors、Although it belongs to ionotropic glutamate receptor family、Whether it is unknown still what is functioning as an ion channel。In this paper、The channel domain was mutated to "channel dead" delta 2 receptor、By expressing the delta receptor null mutant mice、It was the challenge of this problem。

Surprisingly、"Channel dead" delta 2 receptors、As with normal delta 2 receptor、From to restore the cerebellum LTD failure、Delta 2 receptor is now for the first time clear that does not function as an ion channel。

Koda lecturer of paper is Publish to Eur J Neurosci、It was on the cover。Congrats。

Although the delta receptor is a molecule that controls the long-term depression (LTD) which is a basis course of motor learning in the cerebellum、It was so far unknown how the function to。In this paper、To deficient cerebellum the delta 2 receptor、By introducing a delta receptor with a viral vector、The LTD succeeded to be restored。

Interestingly、When the deficient C-terminus of the intracellular domain of Delta 2 receptor、That the LTD induction function of the delta 2 receptor is lost it was found。As a result、Delta 2 receptors、Rather than ionotropic glutamate receptor、Function as metabotropic receptors that transmit signals through the intracellular domain was suggested。

Iijima an assistant of the marriage celebration was conducted by Alice Garden。You happy!!

Joint research with RIKEN BSI FuruichiKen is now Accept the Journal of Neuroscience magazine。Kakegawa Assistant Professor has electrophysiological analysis of parallel fibers over Purkinje cells neurotransmission another Lobule of the cerebellum。

A paper by Associate Kakegawa J Physiol (London)Now in press in。Congrats。

This paper、By L7 promoter、By mating transgenic mice and delta 2 receptor null mutant mice expressing specific delta receptor in Purkinje cells、The recovery degree of various phenotypes of null mutant mouse thing was electrophysiological and morphological study。

Surprisingly、Not only normal delta 2 receptor、Delta 2 receptor mutated Q / R site to determine the Ca permeability in the channel pore also、It found that to recover most of the phenotype。From this it、Delta 2 receptor is now clear that the amino acid sequence does not function as a Ca channel but is expected to form a Ca ion transmission channel pore of。

Work on the function of Cbln family molecules of special research assistant Iijima、Eur J Neurosciにin pressに。Congrats。

Kameyama-kun of self-directed learning announcement of medical students was awarded the Excellence Award。Congrats。Kono's Hongo-kun of the research report also was very great。

To in press in the new book "The Glutamate Receptors" in the Review of Yuzusaki about the delta receptor The Humana Press。