Kefalov V J, Crouch R K, Cornwall M C
Department of Physiology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA.
Neuron. 2001 Mar;29(3):749-55. doi: 10.1016/s0896-6273(01)00249-5.
Regeneration of visual pigments of vertebrate rod and cone photoreceptors occurs by the initial noncovalent binding of 11-cis-retinal to opsin, followed by the formation of a covalent bond between the ligand and the protein. Here, we show that the noncovalent interaction between 11-cis-retinal and opsin affects the rate of dark adaptation. In rods, 11-cis-retinal produces a transient activation of the phototransduction cascade that precedes sensitivity recovery, thus slowing dark adaptation. In cones, 11-cis-retinal immediately deactivates phototransduction. Thus, the initial binding of the same ligand to two very similar G protein receptors, the rod and cone opsins, activates one and deactivates the other, contributing to the remarkable difference in the rates of rod and cone dark adaptation.
首先11-顺式视黄醛与视蛋白进行非共价结合，随后配体与蛋白质之间形成共价键。在此，我们表明11-顺式视黄醛与视蛋白之间的非共价相互作用会影响暗适应速率。在视杆细胞中，11-顺式视黄醛在敏感度恢复之前会引发光转导级联反应的短暂激活，从而减缓暗适应。在视锥细胞中，11-顺式视黄醛会立即使光转导失活。因此，同一配体与两种非常相似的G蛋白受体（视杆和视锥视蛋白）的初始结合，会激活一种受体而使另一种失活，这导致了视杆和视锥暗适应速率的显著差异。
