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.
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ANATOMY OF ROD & CONE CELLS |
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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.
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REACTION OF PHOTORECEPTOR IN DARKNESS |
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REACTION OF PHOTORECEPTOR IN LIGHT |
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