The pupillary light reflex induced by red and blue light stimulations, and melanopsin photoreception of the rabbit.

1998年发现了一种新的光敏色素--黑视素。后来，发现了含有黑视素的视网膜神经节细胞（mRGCs），并揭示了mRGCs在没有来自光感受器的输入的情况下会去极化，这意味着这些细胞是光敏的。mRGC介导瞳孔对光反射。我们研究了视网膜光感受器细胞的光感受机制，并使用对照、神经传递药物阻断（PB）模型和视网膜变性（Tg）转基因兔模型来评估瞳孔光反应的相对贡献。虽然在PB和Tg模型中杆和锥光感受器消失，但在蓝光（470 nm）照射期间仍然诱导缩瞳。我们的研究还表明，一些组织学鉴定的RGCs与mRGC的特征和结构一致。在具有外部视网膜损伤的眼睛中，瞳孔对蓝光的更大持续收缩反映了mRGC激活。

Recently, a new photosensitive pigment, melanopsin, was found in 1998. Later, melanopsin-containing retinal ganglion cells (mRGCs) were discovered and revealed that mRGCs would depolarize without input from the photoreceptors, meaning that these cells were photosensitive. The mRGCs mediate the pupillary light reflex. We investigated the mechanisms of photoreception by retinal photoreceptor cells, and to evaluate the relative contribution of pupil light response using the control, pharmacological blockade of neurotransmission (PB) model and a transgenic model of retinal degeneration (Tg) rabbit. Although rod and cone photoreceptors were disappeared in the PB and Tg model, miosis was still induced during exposure to blue light (470nm). Our study also indicated that some histologically-identified RGCs were consistent with the characteristics and structures of mRGC. The greater sustained constriction of pupils to blue light in eyes with outer retinal damage reflects mRGC activation.