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

Journal article

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.

Authors: Washbourne, P; Thompson, P; Carta, M; Costa, E; Mathews, JR

• Publication status: Published
• Journal: Nature neuroscience
• Volume: 5
• Issue: 1
• Pages: 19-26
• Publication date: 2002-01-01
• DOI: 10.1038/nn783
• EISSN: 1546-1726
• ISSN: 1097-6256
• Language: English
• Keywords: Animals; Embryonic and Fetal Development; Mice; Immunohistochemistry; Embryo, Mammalian; Membrane Proteins; Diaphragm; Synaptic Transmission; Vesicular Transport Proteins; Neuromuscular Junction; Patch-Clamp Techniques; Exocytosis; SNARE Proteins; Neurons; Muscle, Skeletal; Synaptosomal-Associated Protein 25; Dermis; Cells, Cultured; Brain; Nerve Tissue Proteins; Mice, Knockout