title: [Dislocated neurons and neural network: hodological study of the motor cortex of the reeler mutant mouse].
abstract: Reeler, an autosomal recessive mutation in mice, causes cytoarchitectonic abnormalities of cerebral cortex, which are characterized by malposition of neurons. We examined hodological systems of the reeler motor cortex. The results are described as follows. (1) In normal controls, corticospinal tract neurons retrogradely labeled after the injection of HRP ioto the lumbar cord were situated only in layer V (layer of large pyramids: LP). In the reeler, by contrast, the labeled corticospinal tract neurons were scattered diffusely throughout all levels of the corresponding area. (2) In the normal controls, callosal commissural neurons retrogradely labeled after the HRP injection into the motor cortex were distributed in a bilaminar pattern such that the largest number of cells were located in the supragranular layers II (layer of small pyramids; SP) and III (layer of medium pyramids; MP), and in the infragranular layer V (LP). In the reeler mutant mice, callosal commissural neurons were found in all cortical layers, but two-thirds were situated in the lower half of the cortex. (3) In the normal controls, most of the thalamocortical neurons labeled after HRP injection into the motor cortex were located in the ventrolateral nucleus, the lateral division of the ventrobasal nucleus, the central lateral, paracentral and central intralaminar nuclei, and the medial division of the posterior complex. In the reeler mutant mice, retrogradely labeled neurons were again found in the nuclei referred to above, and the distribution pattern and morphology of HRP-filled neurons were also similar to those of normal controls. In the reeler, thalamocortical fibers took an abnormal course within the motor cortex: they ascended obliquely from the white matter to the pial surface and then descended obliquely to the deeper layers. These results strongly suggest that dislocated neurons project correctly to normally-situated and/or abnormally situated target(s).
authors.affiliation: Department of Anatomy, Hokkaido University School of Medicine, Sapporo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Terashima
authors.forename: K
authors.initials: K
authors.lastname: Inoue
authors.forename: Y
authors.initials: Y
authors.lastname: Inoue
mesh_terms: D000818:Animals; D019204:GTP-Binding Proteins / Q000378:metabolism / Q000502:physiology; D051379:Mice; D008818:Mice, Neurologic Mutants / Q000502:physiology*; D009044:Motor Cortex / Q000002:abnormalities* / Q000166:cytology; D009415:Nerve Net / Q000002:abnormalities*; D009474:Neurons / Q000378:metabolism; D013788:Thalamus / Q000002:abnormalities
chemical_list: D019204:GTP-Binding Proteins