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

Philip Washbourne, Peter M. Thompson, Mario Carta, Edmar T. Costa, James R. Mathews, Guillermina Lopez-Benditó, Zoltán Molnár, Mark W. Becher, C. Fernando Valenzuela, L. Donald Partridge, Michael C. Wilson
Nat Neurosci. 2001-12-19; 5(1): 19-26
DOI: 10.1038/nn783

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1. Nat Neurosci. 2002 Jan;5(1):19-26.

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

Washbourne P(1), Thompson PM, Carta M, Costa ET, Mathews JR, Lopez-Benditó G,
Molnár Z, Becher MW, Valenzuela CF, Partridge LD, Wilson MC.

Author information:
(1)Department of Neurosciences, University of New Mexico Health Science Center,
Albuquerque, New Mexico 87131, USA.

Comment in
Nat Neurosci. 2002 Jan;5(1):4-6.

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

DOI: 10.1038/nn783
PMID: 11753414 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus