| First Author | Li HP | Year | 2005 |
| Journal | Eur J Neurosci | Volume | 22 |
| Issue | 11 | Pages | 2689-96 |
| PubMed ID | 16324103 | Mgi Jnum | J:104312 |
| Mgi Id | MGI:3611655 | Doi | 10.1111/j.1460-9568.2005.04491.x |
| Citation | Li HP, et al. (2005) Aberrant trajectory of thalamocortical axons associated with abnormal localization of neurocan immunoreactivity in the cerebral neocortex of reeler mutant mice. Eur J Neurosci 22(11):2689-96 |
| abstractText | We examined the molecular mechanisms underlying the formation of the thalamocortical pathway in the cerebral neocortex of normal and reeler mutant mice. During normal development of the mouse neocortex, thalamic axons immunoreactive for the neural cell adhesion molecule L1 rarely invaded the cortical plate and ran centered in the subplate which is immunoreactive for neurocan, a brain-specific chondroitin sulfate proteoglycan. On the other hand, in homozygous reeler mutant mice, thalamic axons took an aberrant course to run obliquely through the cortical plate. Injection of bromodeoxyuridine at embryonic day 11 specifically labeled subplate neurons in normal mice, whilst in the reeler neocortex it labeled cells scattered in the cortical plate as well as in the superficial layer (superplate). Neurocan immunoreactivity was associated with the bromodeoxyuridine-positive cells in the superplate, as well as being present in oblique bands within the cortical plate, along which L1-bearing thalamic axons preferentially ran. The present results support our previous hypothesis proposed for normal rats that a heterophilic molecular interaction between L1 and neurocan is involved in determining the thalamocortical pathway within the neocortical anlage [T. Fukuda et al. (1997) Journal of Comparative Neurology, 382, 141-152]. |
