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

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

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Brain / cytology
  • Brain / embryology
  • Brain / metabolism
  • Cells, Cultured
  • Dermis / cytology
  • Dermis / metabolism
  • Diaphragm / metabolism
  • Embryo, Mammalian / physiology
  • Embryonic and Fetal Development
  • Exocytosis / physiology*
  • Immunohistochemistry
  • In Vitro Techniques
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mice
  • Mice, Knockout
  • Muscle, Skeletal / cytology
  • Muscle, Skeletal / metabolism
  • Nerve Tissue Proteins / genetics
  • Nerve Tissue Proteins / metabolism*
  • Neuromuscular Junction / physiology
  • Neurons / physiology*
  • Neurons / ultrastructure
  • Patch-Clamp Techniques
  • SNARE Proteins
  • Synaptic Transmission / physiology*
  • Synaptosomal-Associated Protein 25
  • Vesicular Transport Proteins*

Substances

  • Membrane Proteins
  • Nerve Tissue Proteins
  • SNARE Proteins
  • Snap25 protein, mouse
  • Synaptosomal-Associated Protein 25
  • Vesicular Transport Proteins