  A theoretical model was developed to investigate the rod phototransduction
process in the mouse. In particular, we explored the biochemical reactions of
several chemical components that contribute to the signaling process
into/around the membranous disks in the outer segments of the rod cells. We
constructed a rate equation model incorporating the molecular crowding effects
of rhodopsin according to experimental results, which may hinder the diffusion
of molecules on the disk mem- brane. The present model could effectively
reproduce and explain the mechanisms of the following phenomena observed in
experiments. First, the activations and relaxation of the wild-type mouse rod
cell progressed more slowly than those of mutant cells containing half the
amount of rhodopsin on the disk membrane. Second, the strong photoactivated
state of the cell was sustained for a longer period when the light stimuli were
strong. Finally, the lifetime of photoactivation exhibited a logarithmic
increase with increasing light strength given exposure to strong light stimuli.
