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9.13神経生化学セミナーのご案内/Neurochemistry Seminar Announcement

Title: Calcium Channels and Synaptic Plasticity
Lecturer: William A. Catterall&s_comma; PhD
Professor and Chairman&s_comma; Department of Pharmacology&s_comma; University of Washington at

Time: September 13&s_comma; 2007 (Thu) 17:00~18:00
Place: Room 1304B (Seminar Room 7)&s_comma;13th floor&s_comma; New Medical Research Building
Host: Haruhiko Bito&s_comma; Department of Neurochemistry (hbito@m.u-tokyo.ac.jp)
Supported by Neuroscience Lecture Series&s_comma; Center for Integrated Brain Medical
Science&s_comma; a 21st Century COE Program from MEXT.

P/Q-type Ca current through Cav2.1 channels initiate synaptic transmission and
are regulated by calmodulin (CaM) at a site in the C-terminal containing an
IQ-like motif and a CaM binding domain (CBD). Brief&s_comma; local increases in Ca2+
support high affinity binding of the C-terminal lobe of CaM to the IQ-like
domain&s_comma; which causes facilitation. Sustained increases in Ca support binding of
the N-terminal lobe of CaM to the CBD&s_comma; which causes inactivation. The neuronal
calcium sensor protein CaBP1 binds to the Cav2.1 channel&s_comma; displaces CaM&s_comma; and
enhances inactivation&s_comma; whereas VILIP-2 slows Ca2+/CaM-dependent inactivation and
enhances facilitation. To examine the role of this regulation in synaptic
plasticity&s_comma; we expressed Cav2.1 channels in sympathetic neurons. Synaptic
transmission initiated by wild-type Cav2.1 channels showed facilitation&s_comma;
augmentation&s_comma; and depression&s_comma; but this short-term synaptic plasticity was lost
in mutant channels lacking the IQ-like domain and CBD. Evidently&s_comma; regulation of
Cav2.1 channels through interaction with calcium sensor proteins is responsible
for short-term synaptic plasticity at this model synapse.


脳神経医学専攻 神経生化学分野
〒113-0033 東京都文京区本郷7-3-1
e-mail: hbito@m.u-tokyo.ac.jp
Tel: 03-5841-3559 Fax: 03-3814-8154