Histopathological study on cerebellar dysgenesis of shaking rat Kawasaki (SRK)

Fujii, Yasuko; Ohno, Masaki; Shimada, Morimi

doi:10.1016/0387-7604(94)90042-6

Cited by 6 publications

(9 citation statements)

References 26 publications

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“…This wide distribution pattern of CST neurons across the radial axis of the cortex is very similar to the distribution pattern of CST neurons of the reeler mouse (Terashima et al, 1983, Inoue et al, 1991Hoffarth et al, 1995). Previous histological studies (Aikawa et al, 1988;Fujii et al, 1994) also suggested similarities between the SRK rat and the reeler mouse on the basis of morphological aspects. First, the cerebral cortex of the SRK rat is characterized by the absence of layer I and faulty lamination of layers II-VI (Aikawa et al, 1988).…”

Section: Discussionsupporting

confidence: 80%

“…Furthermore, a recent report has suggested an additional function for reelin in guiding axonal extension in the developing hippocampus (Del Rio et al, 1997). From the similarity of phenotype between reeler and SRK indicated by the present and previous data (Aikawa et al, 1988;Fujii et al, 1994), it seems possible that the SRK phenotype might arise from disruption of the reelin gene in the rat. However, there is another mouse mutant, scrambler, which has a strikingly similar phenotype to the reeler, although the gene affected in this mutation is located on a different chromosome to that known to be mutated in the reeler (Gonzá lez, et al, 1996;Sweet, et al, 1996).…”

Section: Discussionsupporting

confidence: 64%

“…Histological analysis of the cerebral cortex of this mutant rat showed an absence of the molecular layer (layer I), faulty lamination of layers II-VI, and oblique bundles of myelinated fibers ascending from the white matter to the pial surface (Aikawa et al, 1988). In the cerebellum, Purkinje cells were scattered away from their normal location to the deep cerebellar mass (Aikawa et al, 1988;Fujii et al, 1994). These results indicate a very close resemblance between the phenotype of the SRK mutant rat and that of the reeler mouse.…”

mentioning

confidence: 67%

“…First, the cerebral cortex of the SRK rat is characterized by the absence of layer I and faulty lamination of layers II-VI (Aikawa et al, 1988). Second, in this mutant rat, the size of the cerebellum is much reduced, and ectopic Purkinje cells are embedded in the deep cerebellar mass (Aikawa et al, 1988;Fujii et al, 1994). Third, the highly organized laminar structure of the hippocampal formation is disrupted in the SRK rat (Aikawa et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…This suggests that the SRK mutant may provide another good animal model for the study of the mechanisms underlying the formation of the laminated structure of the mammalian CNS. At present, description of abnormalities have been largely confined to the cerebellum and cerebral cortex (Aikawa et al, 1988;Fujii et al, 1994), but it will be interesting to investigate other nonlaminated structures such as the inferior olivary complex, the motor and mesencephalic trigeminal nuclei, and the facial nucleus, all areas that have been shown to be disrupted in the reeler mouse (Goffinet, 1983(Goffinet, , 1984bTerashima et al, 1993Terashima et al, , 1994Terashima, 1996).…”

Section: Discussionmentioning

confidence: 99%

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Corticospinal tract neurons are radially malpositioned in the sensory‐motor cortex of the shaking rat Kawasaki

Ikeda¹,

Terashima²

1997

J. Comp. Neurol.

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Shaking rat Kawasaki (SRK) is an autosomal recessive mutant rat that exhibits tremor, dystonia, and ataxia and that is characterized by abnormal lamination of the cerebral and cerebellar cortices and the hippocampus. To examine whether or not layer V neurons in the mutant neocortex are malpositioned in accordance with the aberrant laminar cytoarchitecture, horseradish peroxidase (HRP) was injected into the lumbar spinal cord of SRK mutant and normal control rats to label cortical pyramids projecting through the corticospinal tract (CST). HRP-labeled CST neurons of both normal and SRK rats were found mainly in the hindlimb area of the sensory-motor cortex, indicating a normal tangential distribution of labeled CST neurons in the SRK mutant. In the radial axis, however, labeled CST neurons were spread throughout all layers of the mutant cortex, whereas those in normal rats were restricted to layer V. In the mutant, most labeled CST neurons located in the inner third of the cortex had a typical pyramidal form with an upright apical dendrite, but many of those located near the pial surface displayed abnormal shapes and could be subdivided into inverted pyramidal, horizontal, and bipolar neurons on the basis of their dendritic morphology. The abnormal distribution pattern of labeled CST neurons in the mutant was quantified using a standardized measure of their depth distribution, where 0% = the level of the white matter and 100% = the pial surface. The mean value for the SRK cortex of 47.0% was significantly greater than the figure of 40.5% for normal rats (P < 0.01, Student's t test), indicating a spread of CST neurons toward the pial surface in SRK, but even more striking was the size of the standard deviation: 30.4 in SRK compared with 7.1 in controls. The distribution pattern of CST neurons of the SRK rat was also statistically identical with that of the reeler mouse, which is a well-known mutant that also exhibits an abnormal lamination pattern in the cerebral cortex. These results indicate that neuronal components of the neocortex of the SRK mutant are intermingled along the radial axis, but not in the tangential axis, and provide further evidence for a strong similarity between this spontaneous rat mutation and the reeler malformation.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionsupporting

confidence: 64%

mentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Corticospinal tract neurons are radially malpositioned in the sensory‐motor cortex of the shaking rat Kawasaki

Ikeda¹,

Terashima²

1997

J. Comp. Neurol.

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Missplicing resulting from a short deletion in the reelin gene causes reeler‐like neuronal disorders in the mutant shaking rat Kawasaki

Kikkawa

Yamamoto

Misaki

et al. 2003

J of Comparative Neurology

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The shaking rat Kawasaki (SRK) is an autosomal recessive mutant that exhibits reeler-like abnormal locomotor behaviors. The murine reeler mutants arise from several mutations in the specific gene called reelin, which result in defects of Reelin expression or secretion in the cerebral cortex and other regions of CNS. To address the issue of whether the SRK mutation also arises from a mutation in reelin, we analyzed the reelin gene in SRK. Northern analysis of reelin mRNA from normal rats showed that rat reelin was expressed as a approximately 12-kb transcript in both the cerebrum and the cerebellum, whereas reelin expression was markedly reduced in the SRK brains. In situ hybridization analysis showed that reelin mRNA in the SRK brains was expressed in Cajal-Retzius cells in the marginal zone of the cerebral cortex and outer granular cells in the cerebellar cortex in similar manners to normal controls, but its expression was considerably reduced. On Western blotting and immunohistochemical analyses using antibodies specific for the Reelin protein, no immunoproduct was recognized in the cerebral and cerebellar cortices. From the cDNA sequences, we found a 64-base heterologous sequence in SRK reelin, which contains a termination codon in the reading frame. Furthermore, genomic DNA analysis revealed that a 10-base deletion, which contains a predicted splice donor site, occurred in the SRK genomic reelin gene, resulting in "read through" into the following intron in SRK. Thus, the SRK mutation is another type of mutation that lacks expression of the functional Reelin protein and, therefore, causes the reeler phenotype.

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Branchiogenic motoneurons innervating facial, masticatory, and esophageal muscles show aberrant distribution in the reeler‐phenotype mutant rat, Shaking Rat Kawasaki

Setsu

Ikeda

Woodhams³

et al. 2001

J of Comparative Neurology

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Shaking Rat Kawasaki (SRK) is an autosomal recessive mutant rat that is characterized by cerebellar ataxia. Although previous studies indicated many points of similarity between this mutant rat and the reeler mouse, nonlaminated structures such as the facial nucleus have not been studied in this mutant rat. Nissl-stained sections through the brainstem showed that the cytoarchitecture of the facial, motor trigeminal, and ambiguus nuclei was abnormal in SRK, especially in the lateral cell group of the facial nucleus and the compact formation of the ambiguus nucleus. To examine whether orofacial motoneurons are also malpositioned in the SRK rat, horseradish peroxidase (HRP) was injected into the facial, masticatory, and abdominal esophageal muscles of the SRK rats and normal controls to label facial, trigeminal, and ambiguus motoneurons, respectively. HRP-labeled facial, trigeminal, and ambiguus motoneurons of the SRK rat were distributed more widely than those of their normal counterparts, as in the case of the reeler mouse, with the one exception that labeled facial motoneurons innervating the nasolabial muscle were distributed more widely in the ventrolateral-to-dorsomedial direction in comparison with those of the reeler mutant. These data demonstrate that nonlaminated structures in the brainstem of the SRK rat are affected severely, as is the case in the reeler mutant mouse.

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Histopathological study on cerebellar dysgenesis of shaking rat Kawasaki (SRK)

Cited by 6 publications

References 26 publications

Corticospinal tract neurons are radially malpositioned in the sensory‐motor cortex of the shaking rat Kawasaki

Corticospinal tract neurons are radially malpositioned in the sensory‐motor cortex of the shaking rat Kawasaki

Missplicing resulting from a short deletion in the reelin gene causes reeler‐like neuronal disorders in the mutant shaking rat Kawasaki

Branchiogenic motoneurons innervating facial, masticatory, and esophageal muscles show aberrant distribution in the reeler‐phenotype mutant rat, Shaking Rat Kawasaki

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