GAP-43: an intrinsic determinant of neuronal development and plasticity

Trends Neurosci. 1997 Feb;20(2):84-91. doi: 10.1016/s0166-2236(96)10072-2.


Several lines of investigation have helped clarify the role of GAP-43 (FI, B-50 or neuromodulin) in regulating the growth state of axon terminals. In transgenic mice, overexpression of GAP-43 leads to the spontaneous formation of new synapses and enhanced sprouting after injury. Null mutation of the GAP-43 gene disrupts axonal pathfinding and is generally lethal shortly after birth. Manipulations of GAP-43 expression likewise have profound effects on neurite outgrowth for cells in culture. GAP-43 appears to be involved in transducing intra- and extracellular signals to regulate cytoskeletal organization in the nerve ending. Phosphorylation by protein kinase C is particularly significant in this regard, and is linked with both nerve-terminal sprouting and long-term potentiation. In the brains of humans and other primates, high levels of GAP-43 persist in neocortical association areas and in the limbic system throughout life, where the protein might play an important role in mediating experience-dependent plasticity.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain / growth & development*
  • GAP-43 Protein
  • Membrane Glycoproteins / physiology*
  • Mice
  • Nerve Tissue Proteins / physiology*
  • Neuronal Plasticity / physiology*


  • GAP-43 Protein
  • Membrane Glycoproteins
  • Nerve Tissue Proteins