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  • Title: [Developmental plasticity of corticospinal projections in the spinal cord gray matter of normal and hemicortectomized rat].
    Author: Aotani H, Ono K, Uematsu J, Shimada M.
    Journal: No To Shinkei; 1998 Apr; 50(4):339-45. PubMed ID: 9592823.
    Abstract:
    In the previous study we demonstrated in rats that aberrant ipsilateral CST fibers were increased when the cerebral cortex was surgically ablated unilaterally during the neonatal period. Origin of these aberrant fibers was confirmed to involve collateral axons, ramified from their parent axons. In this study, possible plastic change and the critical period for the outgrowth of CST fibers into the spinal cord gray matter in the rat after unilateral (right side) cortical damage at different ages measured in days were examined using anterograde horseradish peroxidase (HRP). HRP was injected into the left sensorimotor cortex in both normal and experimental rats. In the normal control rats, the outgrowth of HRP positive axons into the spinal gray matter was first noticed at 7 day of age in the vicinity of the right dorsal funiculus, and then reached maximal density and extension at 10 and 14 days of age, respectively. From 21 days onwards, the density and extension of HRP positive axons in the gray matter decreased rapidly except in the medial part close to the dorsal funiculus. In rats whose right cerebral cortex were damaged at day 1 of age, the pattern of the outgrowth of HRP positive axons into the right gray matter was much the same as that in age-matched controls. However, significantly different from the control, many HRP positive axons were noted even in the contralateral gray matter. HRP-positive axons in the contralateral left gray matter were also abundant in the rats who sustained cortical damage at 7 and 14 days, but were decreased considerably when the cerebral cortex was damaged at 28 days of age. When damage occurred at 56 days of age, HRP-positive axons did not increase in the left gray matter, indicating that the critical period of axonal plasticity after localized damage was before 4 weeks of age in rats.
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