Synaptic transmission regulated by a presynaptic MALS/Liprin-alpha protein complex

Curr Opin Cell Biol. 2006 Apr;18(2):223-7. doi: 10.1016/ Epub 2006 Feb 28.


Neurotransmission requires proper organization of synaptic vesicle pools and rapid release of vesicle contents upon presynaptic depolarization. Genetic studies have begun to reveal a critical role for scaffolding proteins in such processes. Mutations in genes encoding components of the highly conserved MALS/CASK/Mint-1 complex cause presynaptic defects. In all three mutants, neurotransmitter release is reduced in a manner consistent with aberrant vesicle cycling to the readily releasable pool. Recently, liprin-alpha proteins, which define active zone size and morphology, were found to associate with MALS/CASK, suggesting that this complex links the presynaptic release machinery to the active zone, thereby regulating neurotransmitter release.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
  • Guanylate Kinases
  • Humans
  • Membrane Proteins / metabolism*
  • Models, Biological
  • Nerve Tissue Proteins / metabolism
  • Presynaptic Terminals / metabolism
  • Presynaptic Terminals / physiology*
  • Synaptic Transmission / physiology*


  • APBA1 protein, human
  • Adaptor Proteins, Signal Transducing
  • Membrane Proteins
  • Nerve Tissue Proteins
  • CASK kinases
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Guanylate Kinases