In congenital stationary night blindness due to rhodopsin mutations, which cellular mechanism causes rod dysfunction?

• A. Increased cone signaling to bipolar cells
• B. Decreased rhodopsin production
• C. Hyperactive phosphodiesterase termination
• D. Mutated rhodopsin continuously activates transducin

Answer: (D)

In rods, light-activated rhodopsin starts a cascade: it activates transducin, which then stimulates phosphodiesterase (PDE6) to lower cGMP levels, causing the cGMP-gated channels to close and the rod to hyperpolarize, reducing transmitter release to bipolar cells. If rhodopsin is mutated so it continuously activates transducin even without light, the cascade stays on. This keeps cGMP low and channels closed, so rods behave abnormally in darkness and fail to signal properly in low light, producing congenital stationary night blindness. The mutation effectively makes the system think it’s always “on,” which disrupts normal night-vision signaling.

Other options don’t fit this mechanism: signaling from cones would affect cone pathways rather than rods; simply having less rhodopsin would reduce light sensitivity but wouldn’t cause the ongoing, constitutive activation characteristic of this condition; and a hyperactive termination of the cascade would shorten signals rather than produce the persistent, inappropriate activation seen with the mutation.