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Journal of Neuroscience, Vol 15, 5275-5285, Copyright © 1995 by Society for Neuroscience
Expression and in vitro function of beta 1-integrin laminin receptors in the developing avian ciliary ganglion [published erratum appears in J Neurosci 1996 Nov 1;16(21):7097-8]
CD Weaver, CK Yoshida, I de Curtis and LF Reichardt
Department of Physiology, University of California at San Francisco 94143, USA.
In chick development, ciliary ganglion (CG) neurons go through a period of
axon extension from approximately embryonic day (E)4 to E8, followed by a
period of synaptogenesis and neuronal cell death. By examining the
immunohistochemical localization of laminin, in conjunction with Dil
labeling of the ciliary nerve projection, we have determined that the
pathway taken by these neurons is rich in laminin expression. Therefore,
laminins are good candidate molecules for mediating outgrowth of these
neurons in vivo. In vitro, the ability of CG neurons to extend neurites on
laminin-1 (EHS laminin, alpha 1 beta 1 gamma 1) is maximal up to E8, then
declines dramatically. CG neuron outgrowth on laminin-1 requires the
activity of beta 1-class integrins. We have used subunit-specific
antibodies to determine which of the five beta 1- containing heterodimers
known to be laminin receptors (alpha 1 beta 1, alpha 2 beta 1, alpha 6 beta
1, alpha 7 beta 1) are expressed, and which mediate neurite outgrowth.
While we could not detect expression of alpha 2 or alpha 7, we have found
that alpha 1, alpha 3 beta 1, and alpha 6 beta 1 are expressed on the
surface of ciliary ganglion neuron cell bodies and axons, both in vitro and
in vivo. Furthermore, antibodies against alpha 3 and alpha 6, but not alpha
1, interfered with CG neurite outgrowth on laminin-1 in vitro. Taken
together, these data suggest that interactions of cell surface alpha 3 beta
1 and alpha 6 beta 1 integrins with laminin-1 are likely to mediate growth
of CG neurons during pathfinding in vivo.
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