An early development defect in the cerebral cortex of the reeler mouse. A morphological study leading to a hypothesis concerning the action of the mutant gene.
Brains of reeler and normal mouse embryos have been studied on semi-thin sections and with Golgi impregnations. No change can be seen in the neuroepithelium or in the primary cortical organization. The first evidence of a morphological abnormality appears at E 14, in the cortical plate. Instead of being closely packed and radially oriented, nerve cells are loosely arranged and show quite variable orientations of their long axis and apical dendrite. The axons run obliquely through the cortical plate and do not display the characteristic angular course seen in the normal animal. It is suggested that the primary defect in reeler mice may be in the plasma membrane of cortical plate cells, resulting in a loss of their capacity for mutual recognition and binding. This could account for the cytoarchitectonic disorganization in this mutant, especially the absence of a molecular layer and the inversion of the histogenetic gradient in the developing cerebral cortex.
D000818:Animals; D001369:Axons / Q000648:ultrastructure; D002462:Cell Membrane / Q000648:ultrastructure; D002540:Cerebral Cortex / Q000473:pathology*; D003712:Dendrites / Q000648:ultrastructure; D051379:Mice; D008818:Mice, Neurologic Mutants / Q000502:physiology*; D009474:Neurons / Q000648:ultrastructure; D013997:Time Factors