Visual response properties of retinal ganglion cells in the royal college of surgeons dystrophic rat
Visual response properties of retinal ganglion cells in the royal college of surgeons dystrophic rat
复制标题
皇家外科学院营养不良大鼠视网膜神经节细胞的视觉反应特性。
DOI：
10.1167/iovs.05-1450
复制
发表时间：
2006-08-01
影响因子：
4.4
通讯作者：
Zhang, Hong
中科院分区：
文献类型：
--
作者：
Pu, Mingliang;Xu, Liang;Zhang, Hong
目的
对营养不良的皇家外科学院(以下简称RCS)大鼠出生后100天的视网膜神经节细胞反应模式的变化进行了描述，作为视网膜抢救和视力恢复策略的基线。这种方法能够评估退化视网膜中的受体后神经元属性推断光感受器功能下降的程度。
方法
从年龄匹配的营养不良RCS(RCS-rdy(-))和同源RCS-p(+)(以下简称野生型或wt)大鼠体外视觉对照下记录大视网膜神经节细胞的单位反应。用常规的空间和通量刺激调制对细胞进行分析。
结果
在营养不良的RCS大鼠的感光细胞退化过程中，神经节细胞的单个单位和群体属性改变缓慢，在出生第一个月时检测到的表观感受野大小、对比敏感度和阈值敏感度显著降低。空间频率调谐和对比反应在出生后第76天(P)非常弱，同时信噪比(S-N)逐渐下降，到出生后(P)107时基本一致。这种下降只是简单的响应性丧失，因为背景激发频率随着时间的推移而大幅增加。WT视网膜以中心细胞为主(15/23个细胞)，营养不良动物以偏心细胞为主(24/27个细胞)。
结论
营养不良的RCS大鼠退变的第一个明确迹象是神经节细胞阈值敏感度和接受野大小平行下降，随后是空间总和的恶化。可以说，这些变化可以定性地解释为光感受器信号丢失。然而，在p90的b波消失很久之前，神经节细胞群体特征从开到离中心的明显转变表明，在视杆细胞和视锥细胞死亡之前的光感受器应激的早期阶段，发生了一种反应机制，如双极细胞重新布线和/或神经元表型的转变。
PURPOSE
Alterations in retinal ganglion cell response patterns were profiled in dystrophic Royal College of Surgeons (hereafter RCS) rats over the first 100 postnatal days as a baseline for retinal rescue and vision restoration strategies. This method enabled the evaluation of the extent to which postreceptoral neuronal attributes in degenerating retinas mirror inferred declines in photoreceptor function.
METHODS
Single-unit responses from large retinal ganglion cells were recorded from age-matched dystrophic RCS (RCS-rdy(-)) and congenic RCS-p(+) (hereafter wild-type or wt) rats were recorded in vitro under visual control. Cells were profiled with conventional spatial and flux stimulus modulations.
RESULTS
Ganglion cell single unit and population attributes alter slowly over the course of photoreceptor degeneration in dystrophic RCS rats, with significant decreases in apparent receptive field size, contrast sensitivity, and threshold sensitivity detected by the first month of life. Spatial frequency tuning and contrast responses were extremely weak by postnatal day (P)76, paralleled by a progressive decline in signal-to-noise (S-N) ratio to roughly unity by postnatal day (P)107. This decline was only a simple loss of responsivity, as background firing rates increased substantially over time. Whereas wt retinas were dominated by ON-center cells (15/23 cells), dystrophic animals were dominated by OFF-center cells by P47 (24/27 cells).
CONCLUSIONS
The first definitive signs of degeneration in dystrophic RCS rats are parallel decreases in ganglion cell threshold sensitivity and receptive field size, followed by deterioration in spatial summation. Arguably, these changes can be qualitatively explained as photoreceptor signaling losses. However, the apparent shift in population profile from ON- to OFF-center ganglion cells long before loss of the b-wave at P90 implies that a reactive mechanism such as bipolar cell rewiring and/or transformation of neuronal phenotypes occur during the early phase of photoreceptor stress, before rod and cone death.