Ball Sherry L, Pardue Machelle T, McCall Maureen A, Gregg Ronald G, Peachey Neal S
Research Service, Cleveland VA Medical Center, Cleveland, OH 44106, USA.
Vis Neurosci. 2003 May-Jun;20(3):267-72. doi: 10.1017/s0952523803203059.
In the nob mouse, a mutation in nyctalopin results in a loss of signal transmission from photoreceptors to depolarizing bipolar cells (DBCs). We used immunohistochemical techniques to assess the expression pattern of proteins found at either the photoreceptor terminal or bipolar cell dendrites within the outer plexiform layer. We labeled normal and nob retinas with antibodies against mGluR6, PKC, G0alpha, bassoon, PSD-95, the alpha1F subunit of voltage-gated calcium channels, trkB, and dystrophin. All labeling patterns in nob and normal retinas were comparable to those previously reported in mouse retina. Our results indicate that the absence of nyctalopin does not disrupt the expression pattern of other proteins known to be required for synaptic transmission.
在夜盲小鼠中，视黄醛结合蛋白的突变导致从光感受器到去极化双极细胞（DBCs）的信号传递丧失。我们使用免疫组织化学技术来评估在外网状层内光感受器末端或双极细胞树突中发现的蛋白质的表达模式。我们用抗mGluR6、PKC、G0α、巴松管、PSD-95、电压门控钙通道的α1F亚基、trkB和肌营养不良蛋白的抗体标记正常和夜盲小鼠的视网膜。夜盲小鼠和正常小鼠视网膜中的所有标记模式与先前在小鼠视网膜中报道的模式相当。我们的结果表明，视黄醛结合蛋白的缺失不会破坏已知突触传递所需的其他蛋白质的表达模式。
