 |
 | Home | Contact Us | FAQ | Search & Site Map | Link to Us |
 | Sign In | Join | Other 45 Sites in Network |
Medical Forum / General / Vision / July 2005Photoreceptors and sensitivity
Dear forum, can someone explain me the reason why the rods and cones in our eyes do differ in their sensitivity to light ? Is this due to chemical differences in the visual purple that they contain or does the shape and size of their outer segment play a role as well ? Any input is very welcome ! Johannes You are probably correct. I just know that they were "designed" for different functions, so their structure, chemistry and neural connections were optimized for their intended function: cones for fine detail and color perception, rods for low level light detection and motion. For the precise differences, I'm sure some of the more technically oriented scientists will help you out there, or you can consult a textbook on retina structure and function. w.stacy, o.d. ohannes wrote: > Dear forum, > [quoted text clipped - 5 lines] > Any input is very welcome ! > Johannes Well I'm no expert on this topic, but since I'm doing a Physiology Specialist, I know a little bit about this ... Light absorbing pigment is embedded within the sensory membranes of cones and rods. This pigment is composed of retinal and opsin (a protein). The protein opsin differs for each type of photoreceptor (i.e., differences in amino acid sequences) and determines light absorption. In rods, the pigment is Rhodopsin. In cones, there are three different types of pigments. Each pigment absorbs a different band of the visual spectrum (S cones, blue, ~420 nm; M cones, green, ~525 - 545 nm; L cones, red, ~ 552 - 557 nm). Really, each cone type has it's own absorption curve (responds to a range of wavelengths - some more than others). Any colour we see is a varying mixture of these primary colours ... but yeah, I won't go into the details of colour vision ... Hope that was clear enough ... > In cones, there are > three different types of pigments. Each pigment absorbs [quoted text clipped - 5 lines] > mixture of these primary colours ... but yeah, I won't go > into the details of colour vision ... I don't need details but is there anything that can be done so I don't need to use a magic marker on the tags of my pants -- "Navy Blue", "Black", "dark Green"? I didn't need this when younger. -Quick > I don't need details but is there anything that can be > done so I don't need to use a magic marker on the > tags of my pants -- "Navy Blue", "Black", "dark Green"? > I didn't need this when younger. Brighter light in the closet. :) -MT >> I don't need details but is there anything that can be >> done so I don't need to use a magic marker on the >> tags of my pants -- "Navy Blue", "Black", "dark Green"? >> I didn't need this when younger. > > Brighter light in the closet. :) yes... small nuclear reactor. I can still differentiate slight color differences in bright sunlight. -Quick > yes... small nuclear reactor. I can still differentiate slight > color differences in bright sunlight. Sounds like either the magic marker or a live-in fashion consultant are in order... w.stacy, o.d. Many thanks for yout input, but I have a follow-up : What happens to the signalling chain of the rods if they are light adapted ? Their rhodopsin is still beeing bleached and they should be hyperpolarized so that the following cells in the retina are not beeing inhibited. How does the retina know that it shouldn´t pay any more attention to that signal but listen to the cones instead ? Johannes > How does the retina know that it shouldn´t pay any > more attention to that signal but listen to the cones instead ? The rods are saturated and never recover in bright light. With rhodopsin exhausted, they can't stimulate depolarization and don't even contribute noise. I'm also curious how rods and cones are made sensitive over two such widely different ranges. There's great information at (http://www.psych.ndsu.nodak.edu/mccourt/Psy460/Sensitivity%20Regulation/sensitiv ity%20regulation.html). If the link doesn't work, google "rod cone intensity regulation" without the quotes. -MT I'm not sure how detailed an answer you want, so I'm going to write this with the assumption that you have some working knowledge of the neuron and also some basic physiological/biochemical principles (you may even know most of this already ;). In the absence of light: 1. Retinal binds to a binding site in opsin. 2. Resting levels of cGMP are (relatively) high, causing cGMP-gated sodium channels to open. Potassium channels are also open. Sodium influx is greater than potassium efflux, so the rod remains depolarized (average membrane potential: - 40 mV). Glutamate (neurotransmitter) is tonically released while the neuron is at rest. Because of the sensitivity of Rhodopsin, it can be activated by as little as a single proton. When this occurs ... 1. Retinal is converted from its 11-cis isomer to its all-trans isomer. Because of this structural change, it cannot bind to opsin any longer***. This activated form of retinal (often denoted R*), activates the protein transducin (T*). 2. The activated transducin then activates a cGMP phosphodiesterase, which converts cGMP to GMP. 3. The above decrease in cGMP levels leads to the closure of sodium channels. Because there is less sodium influx, but continued potassium efflux, the inside of the cell is hyperpolarized (to about -70 mV). 4. The release of glutamate onto the bipolar cells decreases. Bright light will close all sodium channels, and stop all neurotransmitter release. Dimmer light will cause a response that is proportional to the light intensity. *** This active form of retinal is released from the pigment (this is what you referred to as "bleaching"). It diffuses out of the rod and into the pigment epithelium. There it reverts back to the trans configuration and moves back into the rod to again bind to the opsin. This regeneration allows a continued light sensitivity of photoreceptors. In fact, even in intense lighting conditions, a significant number of active photoreceptor molecules is maintained. Yes, so that was a crash course in the physiology of the retina ;) (a lot of things were left out, but they're not necessary for a basic understanding). Hope it helped! > Many thanks for yout input, but I have a follow-up : > What happens to the signalling chain of the rods if they are light [quoted text clipped - 6 lines] > > Johannes This is getting quite interesting for me (surely for others as well). Mike wrote :"The rods are saturated and never recover in bright light. With rhodopsin exhausted, they can't stimulate depolarization and don't even contribute noise." I can understand that very well because it explains the long recovery time of the rods that can be seen in the dark adaptation curve. More than that it answers my question about the the bipolar cells´ behavior in the light adapted state : It doesn´t have to listen to the rods any more because they don´t signal any more. Now silverblue001 wrote :"... In fact, even in intense lighting conditions, a significant number of active photoreceptor molecules is maintained." Do I have to understand that in opposition to the statement above and does it mean that the rods do maintain some sensitivity during intense lighting situations ? If so, I would think that they keep on producing some kind of signal. And that leads me back to my question : How does the bipolar cell know when to ignore the rods´ signal ? If I show some lack of understanding here, please help me fill it in ! Johannes > Now silverblue001 wrote :"... In fact, even in intense lighting > conditions, a significant number of active photoreceptor molecules is [quoted text clipped - 5 lines] > rods´ signal ? If I show some lack of understanding here, please help > me fill it in ! In high luminance conditions, vision is *primarily* a function of cones. That doesn't mean that ALL of the rods are inactive. Bipolar cells DO NOT ignore the signals. This is an extremely complicated topic. Unless some of the eyedocs here are also retinal electrophysiologists, you might not get complete answers to all your questions. I suggest doing a little googling and you will find some additional info most likely from journal references or website of university research groups. I will mention two important points that haven't already been made by others here that might help you understand the complexity of this topic 1. There are many different types of bipolar cells. Some receive input from only rods. Some receive input from only cones. And some receive input from a mixture of both. Thus there are parallel as well as mixed channel of neural input from photoreceptors into the bipolars. 2. Aside from receptor-level light adaptation processes (opsin regeneration, rhodopsin phosphorylation, etc) there are also postreceptor processes. There are other cells in the retina, for example horizontal cells, that feedback onto photoreceptors and also influence the bipolars. These cells can modify neural responsiveness to both high and low light levels. I know enough about this topic to know that I don't know very much! Good luck! |
Reply to this Message |
 Sign In
 Join
 My Latest Posts My Monitored Threads My Blog My Photo Gallery My Profile My Homepage Start New Thread Enable EMail Alerts Rate this Thread
|
©2008 Advenet LLC Privacy Policy - Terms of Use
This website includes both content owned or controlled by Advenet as well as content owned or controlled by third parties.