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首页> 外文期刊>Neuron >Failure to maintain eye-specific segregation in nob, a mutant with abnormally patterned retinal activity.
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Failure to maintain eye-specific segregation in nob, a mutant with abnormally patterned retinal activity.

机译：无法维持nob的眼睛特异性隔离，nob是具有异常模式的视网膜活性的突变体。

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摘要

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 wild-type 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.
机译：两只眼睛的轴突末端最初在背侧膝状核（dLGN）中重叠，但随后会精简以占据不重叠的区域。建立和维持这种隔离需要视网膜活动。我们显示，尽管存在视网膜活动，但当活动的结构发生变化时，分离的投影会分离。在发育早期，无b波（nob）小鼠中的自发性视网膜活性与野生型小鼠没有区别，并且眼睛特异性分离正常进行。但是，在睁大眼睛的周围，结节视网膜的自发性和视觉诱发的活动变得异常，这与无法保留精确的眼睛特定区域有关。暗养研究表明，改变视觉体验不负责任。转基因挽救nob视网膜中间神经元内的突变蛋白（nyctalopin），而无需挽救在dLGN中的视网膜投射神经元或其突触后靶标中的表达，可恢复自发的视网膜活性模式并防止分离。因此，正常结构的自发性视网膜活性可稳定新近提纯的成视网膜细胞。

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