群馬大学神経科学グループ 脳研究統合フォーラム
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未来先端研究機構国際セミナー 3rd June GIAR seminar(6/3)のお知らせ

皆様のご参加をお待ちしております。

【日時/Dates】 6月3日 11:00~12:00  3rd June. 11:00 ~12:00

【場所/Venue】 重粒⼦線医学センター カンファレンス室

【参加費/Fee】 無料/free

【言語Language】英語English

【事前申込Registration】不要Not required

Regulation of a synaptic pathway in Autism spectrum disorders.

Reiko T. Roppongi PhD
Research Associate,
Kleysen Institute of Advanced Medicine
Department of Physiology and Pathophysiology
Health Sciences Centre and University of Manitoba
Manitoba, Canada.

 

Development of precise connections, known as synapses, between nerve cells is
required for proper brain development and function. Synapse are the basic
functional units of the nervous system and are the main conduits for information
transfer between nerve cells. Specialized proteins at synapses known as synapse
organizing proteins initiate the development of synapses and are also required for
their maintenance and function. Mutations in the genes for the synapse
organizing proteins can predispose individuals to a variety of neurodevelopmental
and psychiatric disorders such as autism, schizophrenia and intellectual disability.
Therefore, it is critical to understand how synapse organizing proteins function.
Though a large number of synapse organizing proteins have been discovered, how
their functions are controlled is poorly understood. The leucine rich repeat
transmembrane (LRRTM4) and Neurexin (NRXN1-3) are strongly associated
with non-syndromic autism spectrum disorders (ASD). We have discovered that
neurexins are modified with HS sugar chains. LRRTM4 binds to the HS chains of
neurexins and mediates presynaptic differentiation through neurexins. LRRTM4
is among the most potent excitatory synapse organizers. Mice expressing a
mutant form of LRRTM4 that cannot bind to neurexin show structural and
functional deficits at dentate gyrus excitatory synapses. These findings
underscore the neurexin-HS-LRRTM4 trans-synaptic complex regulates
excitatory synapse development and function in the mammalian brain and that
altering the HS modification on neurexins may alter synaptic pathways
associated with ASD.
Contact:GIAR support office Kanazawa (Ext. 8028)
お問合せ先:未来先端研究支援係 金澤

掲載:2019/05/31

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