Bhide P G, Frost D O
Department of Neurology, Massachusetts General Hospital, Boston 02129.
Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):11847-51. doi: 10.1073/pnas.89.24.11847.
Insights into the mechanisms of normal and pathological neural development may be gained by studying the reorganization of developing neural connections, caused experimentally or by disease. Many reorganized connections are assumed to arise by the anomalous stabilization of transient connections that occur during normal development. We report that, although the retina projects transiently to the somatosensory system in normal developing hamsters, the permanent retinal projections to the somatosensory system that arise as a consequence of early brain lesions are not formed by the stabilization of the normally transient projection. Instead, the transient retinal axons are replaced by retinal axons that do not normally project to the somatosensory system. The distinction between anomalous stabilization and substitution is significant for determining the cellular mechanisms underlying the development of neural connectivity.
通过研究由实验或疾病引起的发育中神经连接的重组，可能会深入了解正常和病理性神经发育的机制。许多重组连接被认为是由正常发育过程中出现的短暂连接的异常稳定所产生的。我们报告称，尽管在正常发育的仓鼠中视网膜会短暂投射到体感系统，但早期脑损伤导致的视网膜向体感系统的永久性投射并非由正常短暂投射的稳定形成。相反，短暂的视网膜轴突被通常不会投射到体感系统的视网膜轴突所取代。异常稳定和替代之间的区别对于确定神经连接发育的细胞机制具有重要意义。
