Experimental schizencephaly induced by Kilham strain of mumps virus: pathogenesis of cleft formation.
Experimental schizencephaly induced by Kilham strain of mumps virus: pathogenesis of cleft formation.
复制标题
腮腺炎病毒 Kilham 株诱导的实验性脑裂畸形:裂口形成的发病机制。
DOI:
10.1097/00001756-199910190-00005
复制
发表时间:
1999
期刊:
影响因子:
1.7
通讯作者:
Morimi Shimada
中科院分区:
文献类型:
--
作者:
Tomoyuki Takano;S. Takikita;Morimi Shimada
The pathogenesis of cleft formation in schizencephaly was analyzed by examining the brain lesions produced by the infection of the Kilham strain of mumps virus during the period of neuronal migration in hamsters. Mumps virus antigen was detected in the neuroepithelial cells within the ventricular zone, the choroid plexus in the lateral ventricles, and vimentin-immunoreactive radial glial fibers. The main pathological findings were cerebral hemorrhage, neuronal necrosis, microsulci on the cerebral cortex and cleft formation through the entire thickness of the cerebral mantle. The clefts seen in these experiments were lined by embryonal elements such as neuroepithelial cells and germinal cells. Based on these results and the original definition by Yakovlev and Wadsworth, the following two conclusions were suggested. First, the mumps virus localized to the neuroepithelial cells within the ventricular zone and the radial glial fibers may induce a destructive process and subsequent anomalous neuronal migration, resulting in cleft formation. Second, the formation of the ventricular cleft extending to the pial surface, which should be complete before the cortical infolding appears, is necessary in order to produce the characteristic cleft in schizencephaly which is associated with the pial-ependymal seam.