Genetic ablation of the t-SNARE SNAP-25 distinguishes mechanisms of neuroexocytosis
Top Cited Papers
- 19 December 2001
- journal article
- research article
- Published by Springer Nature in Nature Neuroscience
- Vol. 5 (1) , 19-26
- https://doi.org/10.1038/nn783
Abstract
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.Keywords
This publication has 49 references indexed in Scilit:
- Patterning of Muscle Acetylcholine Receptor Gene Expression in the Absence of Motor InnervationNeuron, 2001
- Synaptic Assembly of the Brain in the Absence of Neurotransmitter SecretionScience, 2000
- Defective Neuromuscular Synaptogenesis in Agrin-Deficient Mutant MiceCell, 1996
- Multiple palmitoylation of synaptotagmin and the t‐SNARE SNAP‐25FEBS Letters, 1996
- Syntaxin and synaptobrevin function downstream of vesicle docking in drosophilaNeuron, 1995
- Structure of the Chicken Gene for SNAP-25 Reveals Duplicated Exons Encoding Distinct Isoforms of the ProteinJournal of Molecular Biology, 1993
- SNAP receptors implicated in vesicle targeting and fusionNature, 1993
- Spontaneous release of transmitter from growth cones of embryonic neuronesNature, 1983
- Structural changes after transmitter release at the frog neuromuscular junction.The Journal of cell biology, 1981
- Ca2+-dependent recycling of synaptic vesicles at the frog neuromuscular junction.The Journal of cell biology, 1980