|  Help  |  About  |  Contact Us

Publication : Cortical layer development and orientation is modulated by relative contributions of reelin-negative and -positive neurons in mouse chimeras.

First Author  Hammond VE Year  2010
Journal  Cereb Cortex Volume  20
Issue  9 Pages  2017-26
PubMed ID  20053715 Mgi Jnum  J:175099
Mgi Id  MGI:5142365 Doi  10.1093/cercor/bhp287
Citation  Hammond VE, et al. (2010) Cortical layer development and orientation is modulated by relative contributions of reelin-negative and -positive neurons in mouse chimeras. Cereb Cortex 20(9):2017-26
abstractText  Reelin is an important protein that is indispensable for cortical lamination. In the absence of Reelin, cortical layers fail to form due to inappropriate neuron migration and positioning. The inversion of cortical layers is attributed to failure of neurons to migrate past earlier-generated neurons although how Reelin-insufficiency causes this is unclear. The issue is complicated by recent studies showing that very little Reelin is required for cortical layering. To test how variation in the number of Reelin-producing cells is linked to cortical lamination, we have employed Reelin(+/+) <--> Reelin(-/-) chimeras in which the number of Reelin-expressing neurons is adjusted. We found that the Reeler phenotype was rescued in chimeras with a large contribution of Reelin(+/+) neurons; conversely in chimeras with a weak contribution by Reelin(+/+) neurons, the mutant phenotype remained. However, increasing the number of Reelin(+/+) neurons beyond an unknown threshold resulted in partial rescue, with the formation of a correctly layered secondary cortex lying on top of an inverted mutant cortex. Therefore, the development of cortical layers in the correct order requires a minimal level of Reelin protein to be present although paradoxically, this is insufficient to prevent the simultaneous formation of inverted cortical layers in the same hemisphere.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

6 Bio Entities

Trail: Publication

0 Expression