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The Journal of Neuroscience, March 5, 2008, 28(10):2366-2374; doi:10.1523/JNEUROSCI.3828-07.2008

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Development/Plasticity/Repair
Neurite Outgrowth and In Vivo Sensory Innervation Mediated by a Ca_V2.2–Laminin β2 Stop Signal

Sharon B. Sann,¹ Lin Xu,¹ Hiroshi Nishimune,^2,3 Joshua R. Sanes,³ and Nicholas C. Spitzer¹

¹Neurobiology Section, University of California, San Diego, La Jolla, California 92093-0357, ²Department of Anatomy and Cell Biology, University of Kansas, Kansas City, Kansas 66160, and ³Department of Molecular and Cellular Biology and Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138

Correspondence should be addressed to Sharon B. Sann, Neurobiology Section, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0357. Email: ssann{at}ucsd.edu

Axons and dendrites of developing neurons establish distributed innervation patterns enabling precise discrimination in sensory systems. We describe the role of the extracellular matrix molecule, laminin β2, interacting with the Ca_V2.2 calcium channel in establishing appropriate sensory innervation. In vivo, Ca_V2.2 is expressed on the growth cones of Xenopus laevis sensory neurites and laminin β2 is expressed in the skin. Culturing neurons on a laminin β2 substrate inhibits neurite outgrowth in a specific and calcium-dependent manner. Blocking signaling between laminin β2 and Ca_V2.2 leads to increased numbers of sensory terminals in vivo. These findings suggest that interactions between extracellular matrix molecules and calcium channels regulate connectivity in the developing nervous system.

Key words: axon guidance; calcium channel; extracellular matrix; skin; growth cone; Xenopus

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Received Aug. 21, 2007; revised Dec. 19, 2007; accepted Jan. 16, 2008.

Correspondence should be addressed to Sharon B. Sann, Neurobiology Section, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0357. Email: ssann{at}ucsd.edu

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