Rod photoreceptor cells initiate scotopic vision when the light receptor rhodopsin absorbs a photon of light to initiate phototransduction. These photoreceptor cells are exquisitely sensitive and have adaptive mechanisms in place to maintain optimal function and to overcome dysfunctional states. One adaptation rod photoreceptor cells exhibit is in the packing properties of rhodopsin within the membrane. The mechanism underlying these adaptations is unclear. Mouse models of congenital stationary night blindness with different molecular causes were investigated to determine which signals are important for adaptations in rod photoreceptor cells. Night blindness in these mice is caused by dysfunction in either rod photoreceptor cell signaling or bipolar cell signaling. Changes in the packing of rhodopsin within photoreceptor cell membranes were examined by atomic force microscopy. Mice expressing constitutively active rhodopsin did not exhibit any adaptations, even under constant dark conditions. Mice with disrupted bipolar cell signaling exhibited adaptations, however, they were distinct from those in mice with disrupted phototransduction. These differential adaptations demonstrate that although multiple molecular defects can lead to a similar primary defect causing disease (i.e., night blindness), they can cause different secondary effects (i.e., adaptations). The lighting environment or signaling defects present from birth and during early rearing can condition mice and affect the adaptations occurring in more mature animals. A comparison of effects in wild-type mice, mice with defective phototransduction, and mice with defective bipolar cell signaling, indicated that bipolar cell signaling plays a role in this conditioning but is not required for adaptations in more mature animals.

当光受体视紫质吸收光子以启动光转导时，视杆细胞启动暗视觉。这些感光细胞非常敏感，并具有适当的适应性机制来维持最佳功能和克服功能障碍状态。视紫红质在膜内的堆积特性是一种适应棒状光感受器细胞表现出的特性。这些适应的机制尚不清楚。研究了具有不同分子原因的先天性静止性夜盲小鼠模型，以确定哪些信号对视杆细胞的适应很重要。这些小鼠的夜盲症是由视杆细胞信号传导或双极细胞信号传导功能障碍引起的。通过原子力显微镜检查视紫质在感光细胞膜内的堆积变化。即使在恒定的黑暗条件下，表达组成型活性视紫红质的小鼠也没有表现出任何适应性。双极细胞信号被破坏的小鼠表现出适应性，然而，它们与光转导被破坏的小鼠不同。这些不同的适应表明，虽然多个分子缺陷会导致类似的主要缺陷导致疾病（即夜盲症），但它们会导致不同的次要影响（即适应）。出生和早期饲养期间存在的光照环境或信号缺陷可以调节小鼠并影响更成熟动物发生的适应。对野生型小鼠、光转导缺陷小鼠、