Rosen G D, Sherman G F, Richman J M, Stone L V, Galaburda A M
Dyslexia Research Laboratory, Beth Israel Hospital, Boston, MA 02215.
Brain Res Dev Brain Res. 1992 Jun 19;67(2):285-91. doi: 10.1016/0165-3806(92)90229-p.
Molecular layer ectopias spontaneously occur in immune-disordered mice, and the accompanying paper demonstrates that these ectopias are associated with a break in the external glial limiting membrane and with distortion of radial glial fibers at birth. It was hypothesized that injury to the developing neocortex is the main etiologic event for molecular layer ectopias. To test this hypothesis, puncture wounds were made on the surface of the cerebral cortex of newborn rats and mice. These wounds produced, in adulthood, molecular layer ectopias similar in appearance to those seen spontaneously in immune-disordered mice. Further, these ectopias show similar distortions of radial glial fibers during development, and of neurofilaments in adulthood. This work supports the notion that injury could be a factor in the production of molecular layer ectopias.
分子层异位在免疫功能紊乱的小鼠中自发出现，并且随附论文表明，这些异位与出生时外胶质界膜的破裂以及放射状胶质纤维的扭曲有关。据推测，发育中的新皮层损伤是分子层异位的主要病因。为了验证这一假设，在新生大鼠和小鼠的大脑皮层表面制造穿刺伤口。这些伤口在成年期产生了与免疫功能紊乱小鼠中自发出现的分子层异位外观相似的分子层异位。此外，这些异位在发育过程中显示出与放射状胶质纤维类似的扭曲，在成年期则显示出神经丝的类似扭曲。这项工作支持了损伤可能是分子层异位产生的一个因素这一观点。
