what are retinal ganglion cells (RGC) ?
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The other answers are okay as far as they go.  However, the unique feature of the retinal ganglion cells is that they are the only cells (i.e. defined as the cells) that project out of the retina to the brain.  The other cells in the retina make their connections within the retina.
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1 cornea\n2 anterior chamber and aqueous humor in anterior cavity\n3 pupil hole in iris\n4 posterior chamber of anterior cavity with more aqueous humor\n5 lense (which must be able to focus properly inc suspensory ligaments, ciliary body-muscle mechanism, but light not THRU here per se)\n6 posterior cavity with vitreos humor\n7 retina (hopefully lands on macula lutea, highest cones)and not the blindspot) retina cones-rods sends impulse to\n8 the sensory neurons which lead to \n9 optic nerve,then to\n10 occipital lobe of brain. Brain must work or you can't see even if all the parts of eye listed above work. \n\nNo pictures...sorry. Easy to find online pics
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Jardon B, Bonaventure N. \nCentre de Neurochimie du C.N.R.S. Strasbourg, France.\n\nThe frog horizontal monocular optokinetic nystagmus (OKN) is asymmetrical, the temporal-nasal (T-N) stimulation being the sole stimulation efficient to evoke the reflex, the nasal-temporal (N-T) component being almost absent. Coil recordings showed that, in adult animals, prolonged monocular visual deprivation by unilateral eyelid suture provoked the appearance of the N-T component. The OKN became symmetrical, reacting for both directions of stimulation. Microinjection of either gamma-aminobutyric acid (GABAA) agonist 4,5,6,7-tetrahydroisoxazolo (5,4-C) Pyridin-3-ol (THIP) or muscarinic cholinergic antagonist atropine into the nucleus lentiformis mesencephali, the pretectal mesencephalic structure involved in OKN, transiently abolished the presence of N-T component. This result suggests that the phenomenon of visual plasticity, occurring after a week of monocular deprivation, can be due, at least partially, to reduction in pretectal GABAergic inhibition, and to concomitant activation of cholinergic muscarinic receptors.\n\nPMID: 1584460 [PubMed - indexed for MEDLINE]
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The retina in the back of the eye is a thin and transparent sensitive film.\n\nIt contains two types of receptor cells, rods and cones.\n\nCones handle day and color vision.\n\nRods are responsible for night vision. They are concentrated more at the sides of\nthe eye’s back wall. Therefore, objects are best seen at the sides, or ‘corners’ of our eyes, where rods are there.\n\nRods  are super sensitive than cones.  That is they respond to very small power of light.\n\nBut they take some 30 to 40 minutes to reach their maximum effectiveness.\n\nThey do not react to colors but react to the brightness.
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Basically, light passes through the front of the eye, the pupil, and the crystalline lens.  It hits the retina (the back of the eye), which has special cells that transform the light energy into a signal that the brain can understand.  The brain then interprets the image.  Of course, there are many other things that come into play, like how the eyes work together and how strong the eyes are.
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On the back inner surface of each eye is a unique tissue called the "retina." All images entering the eye fall on the retina - just as images entering a camera fall on the film. The human retina contains two types of light-sensing cells: \n\nThe "cones" are specialized cells which fill the central part of the retina. The cones sense and discriminate colors. They also see most clearly, giving us our sharp, clear, fully colored, daytime vision. The cones, however, see only ahead but not to the sides (no peripheral vision), and they do not sense very dim light. The cones function with and complement the functions of other retinal cells called the "rods." \nThe "rods" are specialized cells which fill the peripheral or the off-center portions of the retina. The rods see only in black, white and gray. They do not discriminate colors. The rods give us side or peripheral vision, in bright daylight, in very dim light, and in mixed lighting conditions such as being on a dark road at night with bright oncoming headlights shining into one’s eyes. In very dim light, with no bright lights visible, a person is probably seeing with his rods, only. This is confirmed if everything appears in black, white and gray – without colors. In a dim-light environment, with one or two bright pinpoint lights, the person sees with both the cones (for the bright light) and the rods (for the dim light). Unfortunately, prolonged viewing of a bright light in a dim field causes the wide pupils to close to smaller sizes and may also desensitize the rods - temporarily reducing the person's ability to see in dim light. Thus, nighttime drivers want oncoming cars to lower their headlight beams, to prevent their being blinded. Once the bright light is gone, the pupils open up again and the rod cells resensitize, thus restoring good night vision. Most aircraft and some autos use red lights to illuminate the panel instruments because this color does not contract the pupils or overload the rods. \nCategory 1 – Blurred Vision in Dim Light … with sharp vision in moderate to bright light. These people see clearly in daylight but with blurred vision at night or in semi-darkness. They usually do not complain of "too little" ambient light and they do not complain of glare. People with this problem are the most numerous of all the people with night vision impairments and are often in their 40's or 50's. MOST CAN BE HELPED EFFECTIVELY with a pair of prescription glasses prescribed especially for night driving or outdoors night vision at distance.\n\nMOSTLY AFFECTED are people whose ages range from the mid-40's to the mid-50's who are starting to become presbyopic due to aging. Typically, the person has some slight refractive error that does not affect visual acuity in bright light … but does reduce the person’s visual acuity in dim light. This results in the “blurred night vision” complaints. In most cases, both eyes are affected equally. People whose two eyes react differently should refer to additional information below.\n\nTHE CAUSE of "impaired night vision" in these cases is, most often, variation in the "depth-of-focus" of each eye with exposure to bright or dim light - and the resulting closing or opening of the eye's iris. In bright light, with the iris closed and the pupil of the eye small or even “pinpoint,” there is great depth-of-focus so that objects near and far remain in sharp focus. This conceals minor refractive errors such as common myopia (nearsightedness) and/or astigmatism (non-uniform corneal curvature distortions). A person attempts to drive at night in an area that has little or no ambient artificial lighting. The pupils become large as the iris opens. More light comes into each eye so that there is no complaint of being "night blind." However, with the large pupils, the depth-of-focus is reduced and the distant scene or road, sidewa
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I've known only two people with retinitis pigmentosa, and at that time (10 years ago), they did not know of a way to slow the progression of the tunnel vision. I don't know if anything has been discovered since then, however.\n\nGood luck.
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Your eye works in a similar way to a camera - light passes through the lens of your eye and is 'recorded' on the back of your eye (the retina).\n\nThe retina is like a movie screen which shows the picture you are seeing. The retina has two lots of cells called 'rods' and 'cones' [because that is what they look like.] Rods can 'see' black and white.  Cones can 'see' colors. They turn the picture into an electrical message for the brain.
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Glaucoma is not one disorder but a range of conditions in which the pressure inside the eye becomes too high. This results in damage to the optic nerve at the back of the eye which can lead to loss of vision if left untreated. Glaucoma is one of the most common causes of blindness worldwide.\n\nHow does glaucoma develop?\n\nThere is a constant flow of fluid through the eye. The flow into and out of the eye is carefully monitored in order to ensure that the eye maintains its round shape and does not become too hard or too soft. \n\nThis fluid is called the aqueous humour. It is secreted into the eye from an area behind the iris (the coloured part of the eye) and flows around through the pupil and drains out of the eye through several microscopic channels. \n\nGlaucoma usually develops when this flow of fluid becomes obstructed and there is a build-up of pressure within the eye.\n\nThere are two main sub-groups of glaucoma: \n\n\nprimary open angle glaucoma (formerly known as chronic simple glaucoma) is a slowly progressive condition which occurs when the tiny microscopic drainage channels gradually become blocked.\n\n\nprimary angle closure glaucoma (also known as closed angle or acute glaucoma) occurs much more rapidly when the flow of fluid inside the eye cannot pass through the pupil, causing a rapid rise in pressure inside the eye. \n\n\nThere are other types of glaucoma which are much rarer and can be caused by a variety of reasons:\n\n\ninflammation inside the eye (uveitis or iritis).\n\n\nthe growth of new vessels inside the eye, which may occur in connection with diabetes or after blood vessel blockage at the back of the eye.\n\n\ntreatment with certain medicines (eg corticosteroids). \n\n\nfollowing an eye injury.\n\n\nother rare abnormalities affecting the structure of the eye. \n\n\nCongenital glaucoma\n\nIt is very rare for children to be born with glaucoma but it is a recognised condition. There is a tendency for this to run in families, although it may occur in children with no family history of glaucoma at all.\n\nWhat are the symptoms of glaucoma?\n\n\nPrimary open angle glaucoma\n\nThe build up in pressure in this condition is very slow. Therefore visual loss is gradual and patients often do not notice any problem until there is evidence of severe visual impairment. \n\nThe peripheral (or side) vision is affected first and therefore the eyesight is not obviously affected. These peripheral areas of visual field loss increase until eventually the central vision is damaged leading to blindness.\n\nBecause primary open angle glaucoma is not usually recognised until it is advanced, people are screened for the condition as part of the optician's routine examination when eye tests are carried out. \n\nThe optician will check the pressure, examine the nerve at the back of the eye and test the field of vision if this is indicated. As primary open angle glaucoma is rare in people under the age of 40, these screening tests are usually only carried out after this age. \n\nHow is primary open angle glaucoma treated?\n\nThere are a number of different types of eye drops which are available to treat primary open angle glaucoma:\n\n\nbeta-blockers \n\n\nprostaglandin analogues \n\n\nadrenaline type drops (sympathomimetics) \n\n\ncarbonic anhydrase inhibitors \n\n\nmiotics (parasympathomimetics).\n\n\nBeta-blockers\n\nThese drops are usually used twice a day. They reduce the amount of fluid being secreted into the eye. These drops may need to be avoided in people with asthma or heart disease as they can be absorbed into the circulation, thereby causing problems in these areas. Timolol (Timoptol) is an example of a beta-blocker.\n\n\nProstaglandin analogues\n\nThis drop is used once a day in the evening. It works by increasing the drainage of fluid out of the eye. The best recognised side effect of this drop is that it can change the colour of the eye. Latanoprost (Xalatan) is an example of a prostaglandin analogue.\n\n\nAdr
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the flash lights up the blood vessels in the retina
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cornea the surface of which is covered with a layer of cells called epithelium\n\nokay I may have misunderstood the question, I thought the question was what structures BEFORE the retina, not HOW the retina works, hence my answer.
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Not being to see well at night. For more info see http://www.retina-international.org/nightbld.htm
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dunnerzplant pretty much has it right.  To give a more basic explanation, the retina has an array of "rods and cones" laid out like pixels on a tv screen, and they are all connected to the visual cortex that has a similar array of perceptive neurons that can piece all fo the signals together as a picture.\n\nDifferent cells in the retina have different chemicals that are sensitive to different colors, or wavelengths of light.  When light of that color strike that cell, the chemical does a slight shape-shift that ignites a mechanism to change the cell's output of neuroreceptors, liek a switch.  Once the light disappears, the photochemical shifts back to its latent state, and the perception of that color also ceases.\n\nIt's pretty cool stuff, really.  Any good Molecular and Cellular Biology textbook will give a good description of how the whole thing works.  I think even a basic college Biology text will give a rudimentary treatment of the subject.
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behind the retina - farsighted (HYPEROPIA)
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There are two types of cells. Rod & cone cells. Rod cells are responsible for black & white vision, cone cells for color vision. at the yellow spot, there are only cone cells, at the other areas of the retina, there are rod cells. At the blind spot, there is neither.
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Supporting cell that surround neurons in the peripheral nervous system.
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The back of your eye is a multi-layered sheet of tissue called the Retina. The retina contains millions of special cells called photoreceptors. Photoreceptors contain a special molecule called Rhodopsin. Rhodopsin is broken by light into Opsin and Retinal, causing a chain of events resulting in a message to your nervous system. There are two major types of photoreceptors; rod cells and cone cells. The rhodopsin in Rod cells is most sensitive to low levels of (blue-green) light, and thus rod cells are responsible for your night vision. (notice that dark-red light doesn't leave an afterimage in the dark and destroy your night vision - it doesn't activate rod cells and use up their rhodopsin very much). Cone cells are responsible for color vision. Three types of cone cells exist, and each type contains modified rhodopsin that is most sensitive to red, blue or green light respectively. The information sent from the cone cells is sent to the fourth and third layers of the optic cortex in the back of your brain, where "Blob cells" are the first step towards integrating color information. A full-color picture is assembled from these seperately color-sensitive cells, just as the red-green-blue dots on a television screen merge into a full-color image. However, it is important to keep in mind that the separate photoreceptors are each sensitive to a RANGE of light-frequencies, of which red, blue and green are responded to best. \n     The retinas of color-blind animals do not contain all three cone cell types, if any at all. For this reason, animals rely more on motion than on fine detail to understand their visual environments. Humans can become colorblind as well, when mutations occur in any of the three varieties of rhodopsin used in cone cells. Some animals do have color vision (like birds) and others (like bees) can see light that we can't (i.e. ultraviolet). The necessary photoreceptor cells are found in the retinas of these animals.