Rods and cones were named for the different appearance of the outer segment—the distal end next to the pigmented layer of each of these types of photoreceptors. The outer segments of rods are cylindrical or rod-shaped; those of cones are tapered or cone-shaped. Transduction of light energy into a receptor potential occurs in the outer segment of both rods and cones. The photo pigments are integral proteins in the plasma membrane of the outer segment.
In cones the plasma membrane is folded back and forth in a pleated fashion; in rods the pleats pinch off from the plasma membrane to form discs. The outer segment of each rod contains a stack of about 1000 discs, piled up like coins inside a wrapper. Photoreceptor outer segments are renewed at an astonishingly rapid pace. In rods, one to three new discs are added to the base of the outer segment every hour while old discs slough off at the tip and are phagocytized by pigment epithelial cells. The inner segment contains the cell nucleus, Golgi complex, and many mitochondria. At its proximal end, the photoreceptor expands into bulblike synaptic terminals ﬁlled with synaptic vesicles. The ﬁrst step in visual transduction is absorption of light by a photopigment, a colored protein that undergoes structural changes when it absorbs light, in the outer segment of a photoreceptor. Light absorption initiates the events that lead to the production of a receptor potential. The single type of photopigment in rods is rhodopsin. Three different cone photopigments are present in the retina, one in each of the three types of cones. Color vision results from different colors of light selectively activating the different cone photopigments. All photopigments associated with vision contain two parts: a glycoprotein known as opsin and a derivative of vitamin A called retinal. Vitamin A derivatives are formed from carotene, the plant pigment that gives carrots their orange color. Good vision depends on adequate dietary intake of carotene-rich vegetables such as carrots, spinach, broccoli, and yellow squash, or foods that contain vitamin A, such as liver. Retinal is the light-absorbing part of all visual photopigments. In the human retina, there are four different opsins, three in the cones and one in the rods (rhodopsin). Small variations in the amino acid sequences of the different opsins permit the rods and cones to absorb different colors (wavelengths) of incoming light. Photopigments respond to light in the following cyclical process.
- In darkness, retinal has a bent shape, called cis-retinal, which ﬁts snugly into the opsin portion of the photopigment. When cis-retinal absorbs a photon of light, it straightens out to a shape called trans-retinal. This cis-to-trans conversion is called isomerization and is the ﬁrst step in visual transduction. After retinal isomerizes, several unstable chemical intermediates form and disappear. These chemical changes lead to production of a receptor potential.
- In about a minute, trans-retinal completely separates from opsin. The ﬁnal products look colorless, so this part of the cycle is termed bleaching of photopigment.
- An enzyme called retinal isomerase converts trans-retinal back to cis-retinal.
- The cis-retinal then can bind to opsin, reforming a functional photopigment. This part of the cycle—resynthesis of a photopigment—is called regeneration.
The pigmented layer of the retina adjacent to the photoreceptors stores a large quantity of vitamin A and contributes to the regeneration process in rods. The extent of rhodopsin regeneration decreases drastically if the retina detaches from the pigmented layer. Cone photopigments regenerate much more quickly than the rhodopsin in rods and are less dependent on the pigmented layer. After complete bleaching, regeneration of half of the rhodopsin takes 5 minutes; half of the cone photopigments regenerate in only 90 seconds. Full regeneration of bleached rhodopsin takes 30 to 40 minutes.
ANATOMY OF ROD & CONE CELLS
CYCLIC REACTION FOR OPSIN OF RETINA
Light and Dark Adaptation
When you emerge from dark surroundings (say, a tunnel) into the sunshine, light adaptation occurs—your visual system adjusts in seconds to the brighter environment by decreasing its sensitivity. On the other hand, when you enter a darkened room such as a theater, your visual system undergoes dark adaptation—its sensitivity increases slowly over many minutes. The difference in the rates of bleaching and regeneration of the photopigments in the rods and cones accounts for some (but not all) of the sensitivity changes during light and dark adaptation. As the light level increases, more and more photopigment is bleached. While light is bleaching some photopigment molecules, however, others are being regenerated. In daylight, regeneration of rhodopsin cannot keep up with the bleaching process, so rods contribute little to daylight vision. In contrast, cone photopigments regenerate rapidly enough that some of the cis form is always present, even in very bright light. If the light level decreases abruptly, sensitivity increases rapidly at ﬁrst and then more slowly. In complete darkness, full regeneration of cone photopigments occurs during the ﬁrst 8 minutes of dark adaptation. During this time, a threshold (barely perceptible) light ﬂash is seen as having color. Rhodopsin regenerates more slowly, and our visual sensitivity increases until even a single photon (the smallest unit of light) can be detected. In that situation, although much dimmer light can be detected, threshold ﬂashes appear gray-white, regardless of their color. At very low light levels, such as starlight, objects appear as shades of gray because only the rods are functioning.
Release of Neurotransmitter by Photoreceptors
As mentioned previously, the absorption of light and isomerization of retinal initiates chemical changes in the photoreceptor outer segment that lead to production of a receptor potential. To understand how the receptor potential arises, however, we ﬁrst need to examine the operation of photoreceptors in the absence of light. In darkness, sodium ions ﬂow into photoreceptor outer segments through ligand-gated “Na” channels. The ligand that holds these channels open is cyclic GMP (guanosine monophosphate) or cGMP. The inﬂow of “Na”, called the “dark current,” partially depolarizes the photoreceptor. As a result, in darkness the membrane potential of a photoreceptor is about –30 mV. This is much closer to zero than a typical neuron’s resting membrane potential of –70 mV. The partial depolarization during darkness triggers continual release of neurotransmitter at the synaptic terminals.
The neurotransmitter in rods, and perhaps in cones, is the amino acid glutamate (glutamic acid). At synapses between rods and some bipolar cells, glutamate is an inhibitory neurotransmitter: It triggers inhibitory postsynaptic potentials (IPSPs) that hyperpolarize the bipolar cells and prevent them from sending signals on to the ganglion cells. When light strikes the retina and cis-retinal undergoes isomerization, enzymes are activated that break down cGMP. As a result, some cGMP-gated “Na” channels close, “Na” inﬂow decreases, and the membrane potential becomes more negative, approaching –70 mV. This sequence of events produces a hyperpolarizing receptor potential that decreases the release of glutamate. Dim lights cause small and brief receptor potentials that partially turn off glutamate release; brighter lights elicit larger and longer receptor potentials that more completely shut down neurotransmitter release. Thus, light excites the bipolar cells that synapse with rods by turning off the release of an inhibitory neurotransmitter! The excited bipolar cells subsequently stimulate the ganglion cells to form action potentials in their axons.
REACTION OF PHOTORECEPTOR IN LIGHT