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The transduction of light in the eye is an incredibly complex process. Let's start by considering the base level of the eye in the dark. For simplicity, let's only consider rods in our discussion.
Without stimulation, there are two channels that are active in terms of generating membrane potential. The standard potassium channels are open as they are in many other locations in the body, and some nonstandard sodium channels are open, as well. These nonstandard channels use cyclic GMP (cGMP) to keep them open. Therefore, the default state for these cells is to be depolarized, leading to the dark current.
When the eye is stimulated by light, a few changes happen based on lights interaction with a molecule of rhodopsin, which is a combination of 11 cis-retinal and opsin. First, a photon converts 11 cis-retinal to trans-retinal. This change dislodges retinal from its pocket in opsin, causing opsin to undergo a conformational change and causing the loss of rhodopsin's purple color and making the location in the eye colorless (bleaching). Opsin, now called metarhodopsin II, then activates phosphodiesterase 6 (PDE6) through a cascade involving a G-protein. PDE6 degrades cGMP, closing the aforementioned sodium channels and hyperpolarizing the membrane to different degrees depending on how much PDE6 is activated, which is based on the intensity of incoming light (more photons, more retinal isomerization, more PDE6 activation, more cGMP degradation, greater hyperpolarization). This hyperpolarization then decreases the amount of neurotransmitter released, allowing transmission of the brightness signal.
I hope this helps!
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