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色素沉着和白化大鼠视网膜中的蛋白激酶C免疫反应性。

Protein kinase C immunoreactivity in the pigmented and albino rat retina.

作者信息

Baker Gary E, Dovey Maria, Davda Priesh, Guibal Christophe, Jeffery Glen

机构信息

Department of Optometry & Visual Science, City University, Northampton Square, London EC1V 0HB, UK.

出版信息

Eur J Neurosci. 2005 Nov;22(10):2481-8. doi: 10.1111/j.1460-9568.2005.04453.x.

Abstract

The albino retina is abnormal. The central region is under-developed and some cell populations are reduced or increased in number. Not least of these anomalies is the deficit in the rod population in hypopigmented rodents and carnivores. Given this abnormality we have examined the distribution of rod bipolar cells in albino rats to determine whether this subsequent stage in the rod pathway is similarly disrupted. A monoclonal antibody to protein kinase C was used to determine the distribution of rod bipolar cells in juvenile and adult pigmented and albino rats. Immunoreactive rod bipolar cells and their processes were counted in transverse sections passing through both the central and peripheral retina. The mean densities of immunoreactive cells were significantly reduced in albino retinas at both juvenile (postnatal day 15) and adult stages, in the former by 14% and the latter by 9%. This was evident across the entire central-to-peripheral extent of the retina. The reduced rod photoreceptor population found in albinos appears therefore to be consequential for the magnitude of their major target population, rod bipolar cells. The decrease in the rod bipolar population indicates a change in retinal cytoarchitecture and implies a disruption of functional organization of the albino retina, especially that underlying the scotopic channel. This, coupled with observations that some other retinal interneuronal populations may be disrupted, implies disordered retinal processing in albinos and emphasizes the likelihood that abnormal visual function in albinos may be as much a result of anomalous retinal circuitry as of the known photoreceptor deficit or chiasmatic misrouting.

摘要

白化病患者的视网膜是异常的。其中心区域发育不全,一些细胞群的数量减少或增加。在色素沉着不足的啮齿动物和食肉动物中,视杆细胞数量的减少是这些异常情况中较为突出的一点。鉴于这种异常情况,我们研究了白化病大鼠中视杆双极细胞的分布,以确定视杆细胞通路的这一后续阶段是否同样受到破坏。使用一种针对蛋白激酶C的单克隆抗体来确定幼年和成年有色和白化病大鼠中视杆双极细胞的分布。在穿过视网膜中央和周边区域的横切面上对视免疫反应性视杆双极细胞及其突起进行计数。在幼年(出生后第15天)和成年阶段,白化病视网膜中免疫反应性细胞的平均密度均显著降低,前者降低了14%,后者降低了9%。这在视网膜从中央到周边的整个范围内都很明显。因此,白化病患者中视杆光感受器数量的减少似乎对其主要靶细胞群——视杆双极细胞的数量产生了影响。视杆双极细胞数量的减少表明视网膜细胞结构发生了变化,并意味着白化病视网膜的功能组织受到破坏,尤其是在暗视觉通道方面。这一点,再加上观察到其他一些视网膜中间神经元群可能受到破坏,意味着白化病患者的视网膜处理过程紊乱,并强调白化病患者异常视觉功能很可能既是已知的光感受器缺陷或视交叉错误布线的结果,也是视网膜电路异常的结果。

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