| First Author | Michele M | Year | 2009 |
| Journal | Mol Cell Neurosci | Volume | 41 |
| Issue | 4 | Pages | 397-408 |
| PubMed ID | 19394429 | Mgi Jnum | J:154255 |
| Mgi Id | MGI:4367537 | Doi | 10.1016/j.mcn.2009.04.004 |
| Citation | Michele M, et al. (2009) Tenascin-C stimulates contactin-dependent neurite outgrowth via activation of phospholipase C. Mol Cell Neurosci 41(4):397-408 |
| abstractText | Tenascin-C (Tnc) is transiently expressed during neural development. Within its alternatively spliced fibronectin type III (TNfn) -motifs the TNfnD domain is crucial for a neurite outgrowth-promoting region that is recognized by the GPI-linked adhesion molecule of the Ig-superfamily contactin. In order to understand the downstream signaling mechanisms, embryonic day E18 rat hippocampal neurons were cultivated on TNfnBD-containing and control substrates in the presence of various inhibitors. As predicted, axon outgrowth promotion could be suppressed by antibodies to the TNfnD domain, to contactin, or to the beta1-integrin subunit. The chelators BAPTA/AM or EGTA as well as blockade of membrane-based calcium channels or of the release of calcium from intracellular stores reduced axon growth to control levels. The inhibition of phospholipase C and its downstream targets protein kinase C or calmodulin kinase likewise blocked outgrowth promotion. We propose that TNfnBD stimulates the outgrowth of hippocampal neurons by activating calcium- and phospholipase C-depending pathways. Digital video microscopy studies revealed that increase of fiber length was caused by an augmentation of growth cone velocity. |
