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Scientists at the Allen Institute for Brain Science have taken an important step in identifying how the brain organizes itself during development.
The findings, published in the Journal of Comparative Neurology, describe in more detail than ever before the consequences of the loss of this key molecule needed in establishing proper brain architecture during brain development.
The study questions the current textbook explanation of abnormal brain development. Using a well-studied strain of mouse known as reeler, named for its abnormal "reeling" gait, an integral understanding has grown of how neurons migrate to their correct locations during brain development.
The reeler cortex has been described for many years as being "inverted" compared to a normal neocortex. However, the new research finds that this abnormal layering is far more complex, more closely resembling a mirror-image inversion of normal cortical layering.
Furthermore, the degree of disorganization is different for different cell types in different parts of the brain. This suggests that the correct patterning of the brain involves a complex set of processes selected by specific cell types.
This study combines high-throughput histology with highly specific cell markers (identifying genes with expression patterns in the Allen Mouse Brain Atlas), compared to a genome-wide map of gene expression of the adult mouse brain. The authors used a novel approach to identify features of cortical disorganization in the male reeler mouse that were unidentifiable with less specific methods previously available.
"To our surprise, we observed unexpected cellular patterning that is difficult to explain by current models of neocortical development," said Ed Lein, Senior Director, Neuroscience at the Allen Institute for Brain Science and senior author of the study.
"These findings have major implications ... These patterns suggest that there are a number of additional mechanisms beyond Reelin involved in the proper migration of newly generated neurons to their correct locations, and that different cell types use different cues in that process."
The reeler mouse has a spontaneous mutation in a gene called Reelin that has been implicated in autism. Studies of these mice, which are deficient in Reelin, have revealed the involvement of Reelin and its signaling pathway in the organization of the central nervous system during development. Particularly noted was its function in cortical layering, where newly generated neurons migrate from their birthplace to their proper positions in the developing cortex.
In the normal cortex this process results in a highly ordered architecture with different neuronal cell types restricted to specific cortical layers. With Reelin deficiency as seen in reeler mice, the migration process of newly generated neurons into the cortex is highly disrupted.
Using a technique that allows for precise localization of specific genes, Lein and collaborators were able to follow developmental expression patterns through several stages to describe precise effects of Reelin deficiency in several brain areas during neurodevelopment in reeler mice.
Using vivid images of cortical lamination, the authors illustrate the precise disorganization that occurs in reeler neurodevelopment compared to wild type mice. The paper includes 25 compelling full-color, cellular-resolution images, one of which is featured on the journal's cover for this issue.
Other authors on the paper include Maureen Boyle, Amy Bernard, Carol Thompson, Lydia Ng, Andrew Boe, Marty Mortrud, Michael Hawrylycz and Allan Jones from the Allen Institute for Brain Science and Robert Hevner from the University of Washington, Seattle Children's Hospital Research Institute.
About the Allen Institute for Brain Science
Original article: http://www.eurekalert.org/pub_releases/2011-08/aifb-nab080111.php