Axonally transported proteins associated with axon growth in rabbit central and peripheral nervous systems.

dc.contributor.author

Skene, JH

dc.contributor.author

Willard, M

dc.date.accessioned

2021-01-02T07:06:55Z

dc.date.available

2021-01-02T07:06:55Z

dc.date.issued

1981-04

dc.date.updated

2021-01-02T07:06:53Z

dc.description.abstract

In an effort to determine whether the "growth state" and the "mature state" of a neuron are differentiated by different programs of gene expression, we have compared the rapidly transported (group I) proteins in growing and nongrowing axons in rabbits. We observed two polypeptides (GAP-23 and GAP-43) which were of particular interest because of their apparent association with axon growth. GAP-43 was rapidly transported in the central nervous system (CNS) (retinal ganglion cell) axons of neonatal animals, but its relative amount declined precipitously with subsequent development. It could not be reinduced by axotomy of the adult optic nerves, which do not regenerate; however, it was induced after axotomy of an adult peripheral nervous system nerve (the hypoglossal nerve, which does regenerate) which transported only very low levels of GAP-43 before axotomy. The second polypeptide, GAP-23 followed the same pattern of growth-associated transport, except that it was transported at significant levels in uninjured adult hypoglossal nerves and not further induced by axotomy. These observations are consistent with the "GAP hypothesis" that the neuronal growth state can be defined as an altered program of gene expression exemplified in part by the expression of GAP genes whose products are involved in critical growth-specific functions. When interpreted in terms of GAP hypothesis, they lead to the following conclusions: (a) the growth state can be subdivided into a "synaptogenic state" characterized by the transport of GAP-23 but not GAP-43, and an "axon elongation state" requiring both GAPs; (b) with respect to the expression of GAP genes, regeneration involves a recapitulation of a neonatal state of the neuron; and (c) the failure of mammalian CNS neurons to express the GAP genes may underly the failure of CNS axons to regenerate after axon injury.

dc.identifier.issn

0021-9525

dc.identifier.issn

1540-8140

dc.identifier.uri

https://hdl.handle.net/10161/21969

dc.language

eng

dc.publisher

Rockefeller University Press

dc.relation.ispartof

The Journal of cell biology

dc.relation.isversionof

10.1083/jcb.89.1.96

dc.subject

Axons

dc.subject

Vagus Nerve

dc.subject

Hypoglossal Nerve

dc.subject

Optic Nerve

dc.subject

Retina

dc.subject

Animals

dc.subject

Rabbits

dc.subject

Nerve Tissue Proteins

dc.subject

Electrophoresis, Polyacrylamide Gel

dc.subject

Axonal Transport

dc.subject

Molecular Weight

dc.title

Axonally transported proteins associated with axon growth in rabbit central and peripheral nervous systems.

dc.type

Journal article

duke.contributor.orcid

Skene, JH|0000-0003-3205-0697

pubs.begin-page

96

pubs.end-page

103

pubs.issue

1

pubs.organisational-group

School of Medicine

pubs.organisational-group

Neurobiology

pubs.organisational-group

Duke Science & Society

pubs.organisational-group

Duke Institute for Brain Sciences

pubs.organisational-group

Duke

pubs.organisational-group

Basic Science Departments

pubs.organisational-group

Initiatives

pubs.organisational-group

Institutes and Provost's Academic Units

pubs.organisational-group

University Institutes and Centers

pubs.publication-status

Published

pubs.volume

89

Files

Original bundle

Now showing 1 - 1 of 1
Loading...
Thumbnail Image
Name:
Axonally transported proteins associated with axon growth in rabbit central and peripheral nervous systems.pdf
Size:
1.56 MB
Format:
Adobe Portable Document Format
Description:
Published version