Defects in reciprocal projections between the thalamus and cerebral cortex in the early development of Fezl-deficient mice
Defects in reciprocal projections between the thalamus and cerebral cortex in the early development of Fezl-deficient mice
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DOI：
10.1002/cne.21401
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发表时间：
2007-07-20
影响因子：
2.5
通讯作者：
Kawano, Hitoshi
中科院分区：
文献类型：
--
作者：
Komuta, Yukari;Hibi, Masahiko;Kawano, Hitoshi
Fez-like (Fezl) 是前脑胚胎锌指样蛋白，是一种选择性表达于发育皮质深层的转录抑制蛋白。我们通过使用免疫组织化学和亲脂性染料 DiI 和 DiA 的轴突标记，检查了 Fezl 缺陷胎儿小鼠的丘脑皮质和离皮质通路，特别关注丘脑皮质和离皮质轴突之间的时空关系。在正常小鼠中，丘脑和皮质轴突在胚胎日 (E) 13.5 和 E14.5 之间在内囊中相遇，并在分别延伸到目标皮质和丘脑时彼此束动。在 Fezl 缺陷小鼠中，大多数丘脑和皮质轴突分别停在内囊和 E14.5 的大脑皮层-大脑皮层下边界处。这种异常是短暂的，丘脑和皮质轴突在 E15.5 时达到其目标，尽管皮质原基中丘脑轴突的数量显着减少。 DiI 和 DiA 的双重标记证明了 E15.5 后该突变体的大脑皮层下和大脑皮层以及外囊中丘脑和皮质轴突的紧密并置。由于Fezl缺陷小鼠中确定大脑皮层-大脑皮层下边界的基因和丘脑皮质轴突引导分子的表达没有表现出显着变化，因此该突变体中丘脑皮质通路的异常形成可能是由表达Fezl的皮质传出神经元轴突缺陷引起的。
Fez-like (Fezl), the forebrain embryonic zinc finger-like protein, is a transcriptional repressor selectively expressed in the deep layers of the developing cortex. We examined the thalamocortical and corticofugal pathways in Fezl-deficient fetal mice by using immunohistochemistry and by axonal labeling with the lipophilic dyes DiI and DiA, with special attention to the spatiotemporal relation between thalamocortical and corticofugal axons. In normal mice, thalamic and cortical axons meet in the internal capsule between embryonic day (E) 13.5 and E14.5 and fasciculate with each other as they extend to their targets, the cortex and thalamus, respectively. In Fezl-deficient mice, most of the thalamic and cortical axons stop in the internal capsule and at the pallial-subpallial boundary at E14.5, respectively. This abnormality is transient, and the thalamic and cortical axons reach their targets at E15.5, although the number of thalamic axons is remarkably reduced in the cortical anlage. Double labeling with DiI and DiA demonstrated close apposition of the thalamic and cortical axons in the subpallium and pallium as well as in the external capsule of this mutant after E15.5. Because the expression of genes that define the pallial-subpallial boundary and guidance molecules of thalamocortical axons did not show remarkable changes in Fezl-deficient mice, abnormal formation of thalamocortical pathway in this mutant may be caused by the defect of axons of cortical efferent neurons that express Fezl.