GAP-43 as a 'calmodulin sponge' and some implications for calcium signalling in axon terminals

Published

Journal Article

In most neurons, the maturation of axonal growth cones to become stable synaptic terminals is accompanied by a dramatic decline in the abundance of a major growth cone component, GAP-43. Accumulation of GAP-43 persists, however, in a minority of mature synaptic terminals. What properties of axons and their terminals are affected by these changes in GAP-43 expression? Storm and colleagues first noted that the membrane- and calmodulin-binding properties of GAP-43 (a.k.a. P-57 or neuromodulin) could allow it to sequester a large fraction of calmodulin to the submembranous regions, and to release free calmodulin in response to protein kinase C activation. Analysis of evolutionarily conserved sequences in GAP-43 indicates that these properties are central to the biological effects of the protein. If GAP-43 is presumed to inactivate bound calmodulin, the network of GAP-43 in an axon terminal could be considered a regulatable calmodulin buffer, or 'calmodulin sponge', absorbing free calmodulin and releasing it in response to activation of protein kinase C. Such a calmodulin sponge has properties that could be useful in modulating the responses of membrane and cytoskeletal assembly events to calcium signals in growth cones, and in mediating long-term potentiation of neurotransmitter release from some pre-synaptic terminals. © 1990.

Full Text

Duke Authors

Cited Authors

  • Skene, JHP

Published Date

  • January 1, 1990

Published In

Volume / Issue

  • 13 / C

International Standard Serial Number (ISSN)

  • 0921-8696

Digital Object Identifier (DOI)

  • 10.1016/0921-8696(90)90040-A

Citation Source

  • Scopus