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Title: The interaction of mammalian Class C Vps with nSec-1/Munc18-a and syntaxin 1A regulates pre-synaptic release

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [3];  [4];  [1];  [1]
  1. Department of Neurochemistry, National Institute of Neuroscience, NCNP, Kodaira, Tokyo 187-8502 (Japan)
  2. Department of Biochemistry and Cellular Biology, National Institute of Neuroscience, NCNP, Kodaira, Tokyo 187-8502 (Japan)
  3. Department of Cell Biology, Faculty of Bio-Science, Nagahama Institute of Bio-Science and Technology, Nagahama, Shiga 526-0829 (Japan)
  4. Department of Biochemistry, Juntendo University School of Medicine, Bunkyo-ku, Tokyo 113-8421 (Japan)

Membrane docking and fusion in neurons is a highly regulated process requiring the participation of a large number of SNAREs (soluble N-ethylmaleimide sensitive factor attachment protein receptors) and SNARE-interacting proteins. We found that mammalian Class C Vps protein complex associated specifically with nSec-1/Munc18-a, and syntaxin 1A both in vivo and in vitro. In contrast, VAMP2 and SNAP-25, other neuronal core complex proteins, did not interact. When co-transfected with the human growth hormone (hGH) reporter gene, mammalian Class C Vps proteins enhanced Ca{sup 2+}-dependent exocytosis, which was abolished by the Ca{sup 2+}-channel blocker nifedipine. In hippocampal primary cultures, the lentivirus-mediated overexpression of hVps18 increased asynchronous spontaneous synaptic release without changing mEPSCs. These results indicate that mammalian Class C Vps proteins are involved in the regulation of membrane docking and fusion through an interaction with neuronal specific SNARE molecules, nSec-1/Munc18-a and syntaxin 1A.

OSTI ID:
20854586
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 350, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2006.09.104; PII: S0006-291X(06)02152-8; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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