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Article
Nature Neuroscience  5, 19 - 26 (2002)
Published online: 19 December 2001; | doi:10.1038/nn783

Genetic ablation of the t-SNARE SNAP-25 distinguishes mechanisms of neuroexocytosis

Philip Washbourne1, 4, 7, Peter M. Thompson1, 5, 7, Mario Carta1, Edmar T. Costa1, 6, James R. Mathews1, Guillermina Lopez-Benditó3, Zoltán Molnár3, Mark W. Becher2, C. Fernando Valenzuela1, L. Donald Partridge1 & Michael C. Wilson1

1  Department of Neurosciences, University of New Mexico Health Science Center, Albuquerque, New Mexico 87131, USA

2  Department of Pathology, University of New Mexico Health Science Center, Albuquerque, New Mexico 87131, USA

3  Department of Human Anatomy and Genetics, University of Oxford, South Parks Road OX1 3QX, UK

4  Present address: Center for Neuroscience, University of California, Davis, California 95616, USA

5  Present address: Department of Psychiatry, University of Texas Health Sciences Center, San Antonio, Texas 78284, USA

6  Present address: Department of Physiology, Federal University of Pará, 66075-900 Belém, Pará, Brazil

7  The first two authors contributed equally to this work

Correspondence should be addressed to Michael C. Wilson
mwilson@salud.unm.edu
Axon outgrowth during development and neurotransmitter release depends on exocytotic mechanisms, although what protein machinery is common to or differentiates these processes remains unclear. Here we show that the neural t-SNARE (target-membrane-associated−soluble N-ethylmaleimide fusion protein attachment protein (SNAP) receptor) SNAP-25 is not required for nerve growth or stimulus-independent neurotransmitter release, but is essential for evoked synaptic transmission at neuromuscular junctions and central synapses. These results demonstrate that the development of neurotransmission requires the recruitment of a specialized SNARE core complex to meet the demands of regulated exocytosis.

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Nature Neuroscience
ISSN: 1097-6256
EISSN: 1546-1726
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