論文 - 詳細
| RRC ID | 88280 |
|---|---|
| 著者 | Nishibe M, Katsuyama Y, Yamashita T. |
| タイトル | Developmental abnormality contributes to cortex-dependent motor impairments and higher intracortical current requirement in the reeler homozygous mutants. |
| ジャーナル | Brain Struct Funct |
| Abstract |
The motor deficit of the reeler mutants has largely been considered cerebellum related, and the developmental consequences of the cortex on reeler motor behavior have not been examined. We herein showed that there is a behavioral consequence to reeler mutation in models examined at cortex-dependent bimanual tasks that require forepaw dexterity. Using intracortical microstimulation, we found the forelimb representation in the motor cortex was significantly reduced in the reeler. The reeler cortex required a significantly higher current to evoke skeletal muscle movements, suggesting the cortical trans-synaptic propagation is disrupted. When the higher current was applied, the reeler motor representation was found preserved. To elucidate the influence of cerebellum atrophy and ataxia on the obtained results, the behavioral and neurophysiological findings in reeler mice were reproduced using the Disabled-1 (Dab1) cKO mice, in which the Reelin-Dab1 signal deficiency is confined to the cerebral cortex. The Dab1 cKO mice were further assessed at the single-pellet reach and retrieval task, displaying a lower number of successfully retrieved pellets. It suggests the abnormality confined to the cortex still reduced the dexterous motor performance. Although possible muscular dysfunction was reported in REELIN-deficient humans, the function of the reeler forelimb muscle examined by electromyography, morphology of neuromuscular junction and the expression level of choline acetyltransferase were normal. Our results suggest that the mammalian laminar structure is necessary for the forepaw skill performance and for trans-synaptic efficacy in the cortical output. |
| 巻・号 | 223(6) |
| ページ | 2575-2587 |
| 公開日 | 2018-7-1 |
| DOI | 10.1007/s00429-018-1647-8 |
| PII | 10.1007/s00429-018-1647-8 |
| PMID | 29536172 |
| MeSH | Animals Cell Adhesion Molecules, Neuronal / genetics* Deep Brain Stimulation / methods* Developmental Disabilities / complications* Developmental Disabilities / genetics* Electromyography Extracellular Matrix Proteins / genetics* Female Forelimb / physiopathology Functional Laterality / genetics Male Mice Mice, Neurologic Mutants Movement Disorders / etiology* Movement Disorders / pathology Movement Disorders / therapy* Mutation / genetics* Nerve Tissue Proteins / genetics* Nerve Tissue Proteins / metabolism Neuromuscular Junction / genetics Neuromuscular Junction / physiopathology Receptors, Cholinergic / metabolism Reelin Protein Serine Endopeptidases / genetics* |
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 1 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| 実験動物マウス | RBRC00045 |