Failure to maintain eye-specific segregation in nob, a mutant with abnormally patterned retinal activity
Failure to maintain eye-specific segregation in nob, a mutant with abnormally patterned retinal activity
复制标题
DOI：
10.1016/j.neuron.2006.03.033
复制
发表时间：
2006-04-20
期刊：
影响因子：
16.2
通讯作者：
Guido, W
中科院分区：
文献类型：
--
作者：
Demas, J;Sagdullaev, BT;Guido, W
从两个眼睛轴突终端最初重叠的背外侧膝状体核（dLGN），但随后细化占据不重叠的领土。视网膜活动需要建立和维持这种分离。我们发现，尽管存在视网膜活动，分离的预测desegregate活动的结构时，被改变。在发育的早期，无b波（nob）小鼠的自发视网膜活动与野生型小鼠没有区别，眼特异性分离正常进行。但是，在睁开眼睛时，诺布视网膜的自发和视觉诱发活动变得异常，同时未能保留精确的眼睛特定区域。黑暗饲养研究表明，改变视觉经验是不负责。在nob视网膜中间神经元内的突变蛋白（nyctalopin）的转基因拯救，而不拯救在视网膜投射神经元或其在dLGN中的突触后靶点中的表达，恢复自发视网膜活动模式并防止去分离。因此，正常结构的自发视网膜活动稳定了新完善的视网膜神经回路。
Axon terminals from the two eyes initially overlap in the dorsal-lateral geniculate nucleus (dLGN) but subsequently refine to occupy nonoverlapping territories. Retinal activity is required to establish and maintain this segregation. We show that despite the presence of retinal activity, segregated projections desegregate when the structure of activity is altered. Early in development, spontaneous retinal activity in the no b-wave (nob) mouse is indistinguishable from that of wildtype mice, and eye-specific segregation proceeds normally. But, around eye-opening, spontaneous and visually evoked activity in nob retinas become abnormal, coincident with a failure to preserve precise eye-specific territories. Dark-rearing studies suggest that altered visual experience is not responsible. Transgenic rescue of the mutated protein (nyctalopin) within nob retinal interneurons, without rescuing expression in either retinal projection neurons or their postsynaptic targets in the dLGN, restores spontaneous retinal activity patterns and prevents desegregation. Thus, normally structured spontaneous retinal activity stabilizes newly refined retinogeniculate circuitry.