Chapter 15
The Special Senses
559
15
How do we see other colors besides blue, green, and red?
Cones’ absorption spectra overlap, and our perception of inter-
mediate hues, such as yellow, orange, and purple, results from
differential activation of more than one type of cone at the same
time. For example, yellow light stimulates both red and green
cone receptors, but if the red cones are stimulated more than the
green cones, we see orange instead of yellow. When all cones are
stimulated equally, we see white.
Homeostatic Imbalance
15.9
Color blindness
is due to a congenital lack of one or more cone
pigments. Inherited as an X-linked condition, it is far more
common in males than in females. As many as 8–10% of males
have some form of color blindness.
Te most common type is red-green color blindness, result-
ing from a deficit or absolute absence of either red or green cone
pigments. Red and green are seen as the same color—either red
or green, depending on the cone pigment present. Many color-
blind people are unaware of their condition because they have
learned to rely on other cues—such as different intensities of the
same color—to distinguish something green from something
red, such as traffic signals.
Retinal is chemically related to vitamin A and is made from
it. Te cells of the pigmented layer of the retina absorb vitamin
A from the blood and serve as the local vitamin A depot for rods
and cones.
Retinal can assume a variety of distinct three-dimensional
forms, each form called an isomer. When bound to opsin, reti-
nal has a bent, or kinked, shape called
11-
cis
-retinal
, as shown
at the top of
Figure 15.16
. However, when the pigment is struck
by light and absorbs a photon, retinal twists and snaps into a
new configuration,
all-
trans
-retinal
, shown at the bottom of
Figure 15.16. Tis change, in turn, causes opsin to change shape
and assume its activated form.
Te capture of light by visual pigments is the
only
light-
dependent stage, and this simple photochemical event initiates
a whole chain of chemical and electrical reactions in rods and
cones that ultimately causes electrical impulses to be transmitted
Photoreceptor cells are highly vulnerable to damage and im-
mediately begin to degenerate if the retina becomes detached.
Tey are also destroyed by intense light, the very energy they
detect. How is it, then, that we do not all gradually go blind? Te
answer lies in the photoreceptors’ unique system for renewing
their light-trapping outer segment. Every 24 hours, new com-
ponents are synthesized in the cell body and added to the base
of the outer segment. As new discs are made, the discs at the tip
of the outer segment continually fragment off and pigment cells
phagocytize them.
Comparing Rod and Cone Vision
Rods and cones have different thresholds for activation. Rods,
for example, are very sensitive (they respond to very dim light—
a single photon), making them best suited for night vision and
peripheral vision. Cones, on the other hand, need bright light
for activation (have low sensitivity), but react more rapidly.
Cones have one of three different pigments that furnish a viv-
idly colored view of the world, but rods contain a single kind of
visual pigment so their inputs are perceived only in gray tones.
Rods and cones are also “wired” differently to other retinal
neurons. Rods participate in converging pathways, and as many
as 100 rods may ultimately feed into each ganglion cell. As a
result, rod effects are summated and considered collectively, re-
sulting in vision that is fuzzy and indistinct. (Te visual cortex
has no way of knowing exactly
which
rods of the large number
influencing a particular ganglion cell are actually activated.)
In contrast, each cone in the fovea (or at most a few) has a
straight-through pathway via its “own personal bipolar cell” to a
ganglion cell (see Figure 15.6b). Essentially, each foveal cone has
its own “labeled line” to the higher visual centers—permitting
detailed, high-acuity (high-resolution) views of very small areas
of the visual field.
Because rods are absent from the foveae and cones do not
respond to low-intensity light, we see dimly lit objects best
when we do not look at them directly, and we recognize them
best when they move. If you doubt this, go out into your back-
yard on a moonlit evening and see how much you can actually
discriminate.
Table 15.1
summarizes the differences between rods and
cones.
The Chemistry of Visual Pigments
How do photoreceptors translate incoming light into electri-
cal signals? Te key is a light-absorbing molecule called
retinal
that combines with proteins called
opsins
to form four types
of visual pigments. Depending on the type of opsin to which
it is bound, retinal absorbs different wavelengths of the visible
spectrum.
Te cone opsins differ both from the opsin of the rods and
from one another. Te naming of cones reflects the colors (that
is, wavelengths) of light that each cone variety absorbs best. Blue
cones respond maximally to wavelengths around 420 nm, green
cones to wavelengths of 530 nm, and red cones to wavelengths
at or close to 560 nm (see Figure 15.10b).
Table 15.1
Comparison of Rods and Cones
RODS
CONES
Noncolor vision (one visual
pigment)
Color vision (three visual
pigments)
High sensitivity; function in dim
light
Low sensitivity; function in
bright light
Low acuity (many rods
converge onto one ganglion
cell)
High acuity (one cone per
ganglion cell in fovea)
More numerous (20 rods for
every cone)
Less numerous
Mostly in peripheral retina
Mostly in central retina
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