I wrote this answer for a similar question that someone else asked a couple of months ago:
The back of the retina contains so-called rod and cone cells. Rod cells contain rhodopsin which is a visual pigment with an absorption maximum at 498 nm. The cone cells contain one of three different cone-opsins with absorption maxima at 564, 533, and 437 nm, corresponding to the three primary colors that our eye sees: red, green, and blue (they are referred to as red, green, and blue, but if you look at a visible spectrum, it is more like yellow, green, and violet).
Rod cells are more sensitive than cone cells, so are responsible for vision at night. Cone cells are responsible for color vision. For example, if a bunch of red cone cells in one area of the retina are activated, you will see a red spot there. If a bunch of red cone cells and blue cone cells are activated in one part of the retina, you will see a purple spot there.
Anyway, let's say a light photon hits a rhodopsin molecule in a rod cell (one photon is all that is required for a rod cell--that's how sensitive it is). The rhodopsin molecule changes its conformation into a shape that can activate the G-protein transducin. Transducin then turns on another protein called cGMP phosphodiesterase. This is an enzyme that breaks down cGMP to 5'-GMP. cGMP is necessary for activation of sodium channels in the cell membrane. So when the concentration of cGMP goes down, the cGMP-gated sodium channels will close. The overall result of closing the sodium channels in the rod cell is to *hyperpolarize* it.
It seems counterintuitive--when light hits the photoreceptor cell, it becomes *inactivated*. The reason this makes sense is that the photoreceptor cells actually inhibit the next layer of cells in the pathway (on-center bipolar cells)--it's kind of a double negative. So by turning off the photoreceptor cell, you are essentially turning on the next cell in the pathway.
I'm simplifying this a bit. In reality, although photoreceptor cells inhibit the on-center bipolar cells, they also *activate* neighboring off-center bipolar cells. This leads to a much more complex discussion about image processing by the retina however, so I'm not going to go any further with that.
2007-03-22 11:25:24
·
answer #1
·
answered by grimmyTea 6
·
0⤊
0⤋
Vaguely complicated question; but essentially it goes like this
1) Photon hits hits retinal contained within rhodopsin receptor.
2) Retinal converts to all trans-retinal, activating the rhodoopsin, into meta-rhodopsin II.
3) Meta-rhodopsin II activates transductin, a small protein which then activates the phosphodiesterase enzyme, which then breaks down cGMP.
4) cGMP normally opens Na+ channels in rods, which depolarizes rods. The light-induced lack of cGMP stops this and the rods become hyperpolarized.
5) In their hyperpolarized state, rods do not release as much neurotransmitter
6) Glutamate hyperpolarizes on-center bipolar cells, and depolarizies off center bipolar cells.
7) Bipolar and horizontal cells then modulate the synaptic information out to amacrine and ganglion cells, which the transmit to the fibres of the optic nerve.
2007-03-22 11:33:07
·
answer #2
·
answered by Bill C 3
·
0⤊
0⤋