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I'm confused as to why, when exposed to bright light, rod cells cease to function.

I understand that exposure to bright light bleaches all of the rhodopsin, but...so what?

Why doesn't the bleached product (opsonin/retinal) simply get re-synthesised back into rhodopsin as it does in dim light, and therefore continue the cycle and enable impulses?

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up vote 3 down vote accepted

In rods, the pigment Rhodopsin can be thought of as a receptor protein with a pre-bound chemical agonist. The receptor protein is called Opsin, and the pre-bound agonist is called retinal. The absorption of light causes a change in the conformation of retinal so that it activates the opsin, causing bleaching (changing the wavelengths absorbed by rhodopsin). The bleaching of rhodopsin stimulates a G-protein called transducin in the membrane, which activates phosphodiesterase, which in turn breaks down cGMP that is normally present in the cytoplasm of the rod and is necessary for the continued operation of the sodium channel sending the neural signal.

In the dark, the channel is open and the Rods are active. In bright light, due to the amplification from cascade effects, all of the channels will be closed, stopping the Rods from sending their normal signals until cGMP levels are able to compensate.

My guess is that the bleaching ceases fairly quickly and the proteins return to their original conforms shortly, but it's the cGMP levels (remember, cGMP is destroyed, so any new cGMP replacing the old must be synthesized first) that take a long time to recover as the signal to destroy the cGMP initiates a cascade that results in strong amplifications.

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A good guess but you need some kind of a reference for it –  rwst Aug 16 '12 at 7:18
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