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

Larry I. Benowitz*, Aryeh Routtenberg

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1135 Scopus citations


Several lines of investigation have helped clarify the role of GAP-43 (F1, 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.

Original languageEnglish (US)
Pages (from-to)84-91
Number of pages8
JournalTrends in Neurosciences
Issue number2
StatePublished - Feb 1 1997

ASJC Scopus subject areas

  • Neuroscience(all)


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