■Full access to motor learning dimension parallel lines ni は Shin inner plastic su LTD But, But, it must be da ni は Memory Full sustain Do (Front Neural Circuits)2013.11.18

Emi K, Kakegawa W, Miura E, Ito-Ishida A, Kohda K, Yuzaki M. Reevaluation of the role of parallel fiber synapses in delay eyeblink conditioning in mice using Cbln1 as a tool. Front Neural Circuits. Epub.

http://www.frontiersin.org/neural_circuits/10.3389/fncir.2013.00180/abstract

Cerebellum is essential for learning and memory associated with the movement。The Marr-Albus-Ito、Long-term depression is one of synaptic plasticity (LTD; Long-Term Depression）が、Cerebellar parallel fiber - what happens in the Purkinje cell synapse has been considered to be the entity。However, in recent years、Instead LTD、Long-term potentiation is a phenomenon of the reverse(LTP; Long-Term Potentiation)But it reports that responsible for motor learning have been made。The LTD and LTP does not know may be how to participate in any step of the acquisition, maintenance, and recall of motor learning。Cbln1 gene-deficient mice(Cbln1 KO)In parallel fiber - Purkinje cell synapse formation shows the markedly impaired in cerebellar ataxia。Injection of recombinant Cbln1 the cerebellum of Cbln1 KO mouse、2Parallel fibers within days - that the Purkinje cell synapse is to normalize knew so far。Therefore, in this paper、To Cbln1 KO mouse performs a Madokame conditional learning (motor learning)、By injecting recombinant Cbln1 at various time points after learning induction、Parallel fibers in the various times of learning - we examined the involvement of the functions of the Purkinje cell synapse。In Cbln1 KO mouse is failure motor learning、Parallel fibers - does not occur LTD in Purkinje cell synapse、LTP was found to be induced in normal。But by recombination Cbln1 administration LTD was also able to induce motor learning and to normalize、Normal parallel fibers over the Purkinje cells in the maintenance of motor learning was found to be unnecessary。This work is the job of the center Emi's graduate student OB (now SONY)。

■Cause long-term depression by dephosphorylation of Stargazin by neural activity to promote the binding of the adapter protein (Nature Communications)2013.11.12

Matsuda S, Kakegawa W, Budisantoso T, Nomura T, Kohda K, Yuzaki M. Stargazin regulates AMPA receptor trafficking through adaptor protein complexes during long–term depression. Nat Commun. Epub.

http://www.nature.com/ncomms/index.html

Long-term depression is one of synaptic plasticity (LTD; Long-Term Depression）は、By the number of AMPA receptors in dendrites decreases、Efficiency of information transfer in the synapse is the phenomenon to be reduced in the long term。But we do not know well whether the number of AMPA receptors is controlled by any mechanism。Elucidation of the mechanism is not only a better understanding of brain function、It is expected to lead to the development of the understanding and treatment of a variety of brain diseases。It will be transported to the cell membrane (cell surface) after present in the cell membrane "membrane protein" that is synthesized in the cell。Membrane protein receives information extracellular、It plays a function of transmitting to the cell。For example AMPA receptors will excite the nerve cells by binding to the glutamate。The amount of membrane protein present on the cell surface、Transport and from within the cell to the cell membrane、It has been precisely controlled by a balance of speed to take from the cell membrane into the cell。This latter process is generally controlled by AP-2 or AP-3A adapter protein。But whether the transport into the cell of the AMPA receptor is controlled how by the adapter protein was a mystery until this。In this paper、AMPA is a receptor tightly bound to proteins Stargazin is、We found that it binds strongly when it is dephosphorylated with the enhancement of neural activity in the AP-2 and AP-3A。as a result、AMPA receptor -Stargazin complexes efficiently incorporate into cells、The number of AMPA receptors on the cell surface over a long period of time is reduced。Through this research、So far of the AMPA receptor that is directly linked to memory and learning was a mystery intracellular transport mechanism is now revealed for the first time。Nature CommunicationsIt became the online published in。

■Rab8a と は b Prev Full apical membrane transport ni da But, it must be formed ni は Fiber Hair Do (J Cell Sci)2013.11.11

Sato T, Iwano T, Kunii M, Matsuda S, Mizoguchi R, Jung Y, Hagiwara H, Yoshihara Y, Yuzaki M, Harada R, Harada A. Rab8a and Rab8b are essential for multiple apical transport pathways but insufficient for ciliogenesis. J Cell Sci. Epub.

http://www.ncbi.nlm.nih.gov/pubmed/24213529

It is a joint research with Osaka University Harada teacher。Matsuda lecturer was examined for the presence or absence of transport abnormalities to the basolateral membrane in the Purkinje cell。

■To control the Golgi structure and transport of dense-core vesicle CAPS1 is (J Neurosci)2013.11.7

Sadakata T, Kakegawa W, Shinoda Y, Hosono M, Katoh-Semba R, Sekine Y, Sato Y, Tanaka M, Iwasato T, Itohara S, Furuyama K, Kawaguchi Y, Ishizaki Y, Yuzaki M, Furuichi T. CAPS1 Deficiency Perturbs Dense-Core Vesicle Trafficking and Golgi Structure and Reduces Presynaptic Release Probability in the Mouse Brain. J Neurosci. 33:17326-34, 2013

http://www.ncbi.nlm.nih.gov/pubmed/24174665

Gunma University Sadakata teacher、It is a joint research with Tokyo University of Science Furuichi teacher。Kakegawa instructor was responsible for electrophysiology。

■World without delta - patient family lacking 2 receptor delta (Neurology)2013.10.1

Hills LB, Masri A, Konno K, Kakegawa W, Lam A-TN, Lim-Melia E, Chandy N, Hill RS, Panlow JN, Al-Saff M, Nasir R, Chairs JM, Barkovich AJ, Watanabe M, Yuzaki M, GH Mochisa. Deletions in GRID2 lead to a recessive syndrome of cerebellar ataxia and tonic upgaze in humans. Neurology. published ahead of print September 27, 2013

http://www.ncbi.nlm.nih.gov/pubmed/?term=24078737

2 is a family tree of the report of the person lacking the delta 2 receptor。In one of the family、We have exactly the same exon 2 as that reported in mutation ho-15J of the mouse has been deleted。It is characterized by proceeding to the cerebellar atrophy progressive Unlike the mouse in humans。It will be considered to find a similar family future。This study is a joint research with Harvard University Ganesh Mochida teacher and Hokkaido University Watanabe laboratory。

■δ2 receptor LTD gatekeeper to determine whether or not happen (Commun Integr Biol)2013.9.27

Kohda K, Kakegawa W, Yuzaki, M. Unlocking the secrets of the delta2 glutamate receptor: a gatekeeper for synaptic plasticity in the cerebellum. Commun Integr Biol. Epub.

https://www.landesbioscience.com/journals/cib/article/26466/

Consideration could not write to the following PNAS paper is also a short review, including。

■LTD or not？―長期抑圧（LTD)Delta receptor master key to determine whether the happening (PNAS)2013.2.20

Kohda K, Kakegawa W, Matsuda S, Yamamoto T, Hirano H, Yuzaki M. The d2 glutamate receptor gates long-term depression by coordinating interactions between two AMPA receptor phosphorylation sites. Proc Natl Acad Sci USA. 110:E948-57, 2013

http://www.pnas.org/content/early/2013/02/15/1218380110

Movement memory in the cerebellum、Cerebellar granule cells - long-term depression is synaptic plasticity between Purkinje cells (LTD)It is believed that it is essential。It does not occur LTD in mice lacking the delta type 2 glutamate receptor。However, the causes and mechanism had been left remains a mystery。Finally succeeded in solving this mystery in this paper。Delta 2 receptor has been found to be acting as a so-called master key to determine whether or not occur or LTD occurs。This work is co-first author paper of Koda lecturer Kakegawa lecturer。