Ectopic synaptogenesis in the mammalian retina caused by rod photoreceptor-specific mutations
Ectopic synaptogenesis in the mammalian retina caused by rod photoreceptor-specific mutations
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DOI：
10.1038/80639
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发表时间：
2000-11-01
影响因子：
25
通讯作者：
Wong, F
中科院分区：
文献类型：
--
作者：
Peng, YW;Hao, Y;Wong, F
除了视杆光感受器丧失之外，视杆光感受器特异性基因中的许多突变引起其他神经元类型的变性。识别由视杆细胞特异性突变启动并影响其他视网膜细胞的细胞-细胞相互作用机制对于理解视网膜变性的发病机制和进展非常重要。在这里，我们表明，在视杆细胞和视锥细胞变性，由于基因编码视紫红质和cGMP磷酸二酯酶β亚基（PDE-β）分别突变，视杆双极细胞接受异位突触视锥细胞在没有杆。因此，突触可塑性将某些视杆细胞特异性突变与涉及不同类型神经元的视网膜范围内的结构改变联系起来。
In addition to rod photoreceptor loss, many mutations in rod photoreceptor-specific genes cause degeneration of other neuronal types. Identifying mechanisms of cell-cell interactions initiated by rod-specific mutations and affecting other retinal cells is important for understanding the pathogenesis and progression of retinal degeneration. Here we show in animals with rod and cone degeneration due to mutations in the genes encoding rhodopsin and cGMP phosphodiesterase beta -subunit (PDE-beta) respectively, that rod bipolar cells received ectopic synapses from cones in the absence of rods. Thus, synaptic plasticity links certain rod-specific mutations to retina-wide structural alterations that involve different types of neurons.