Chapter 15
The Special Senses
563
15
Vitamin A supplements restore function if they are adminis-
tered early.
In countries where nutrition isn’t a problem,
retinitis
pigmentosa
—a group of degenerative retinal diseases that destroy
rods—are the most common causes of night blindness. Retinitis
pigmentosa results from pigment epithelial cells that are unable to
recycle the tips of the rods as they get sloughed off.
Check Your Understanding
7.
For each of the following, indicate whether it applies to
rods or cones: vision in bright light; only one type of visual
pigment; most abundant in the periphery of the retina; many
feed into one ganglion cell; color vision; higher sensitivity;
higher acuity.
8.
What does bleaching of the pigment mean and when does it
happen?
For answers, see Appendix H.
Visual Pathways and Processing
Trace the visual pathway to the visual cortex, and briefly
describe the steps in visual processing.
The Visual Pathway to the Brain
As we described earlier, the axons of the retinal ganglion cells
exit the eye in the
optic nerves
(Figure 15.19)
. At the X-shaped
optic chiasma
(
chiasm
5
cross), fibers from the medial aspect
of each eye cross over to the opposite side and then continue on
via the
optic tracts
. As a result, each optic tract
Contains fibers from the lateral (temporal) aspect of the eye
on the same side and fibers from the medial (nasal) aspect of
the opposite eye
Carries all the information from the same half of the visual
field
Notice that, because the lens system of each eye reverses all
images, the medial half of each retina receives light rays from
the
temporal
(lateralmost) part of the visual field (that is, from
the far leF or far right rather than from straight ahead), and the
lateral half of each retina receives an image of the nasal (central)
part of the visual field. Consequently, the leF optic tract carries
(and sends on) a complete representation of the right half of the
visual field, and the opposite is true for the right optic tract.
Te paired optic tracts sweep posteriorly around the hypo-
thalamus and send most of their axons to synapse with neurons
in the
lateral geniculate nuclei
(contained within the lateral
geniculate bodies) of the thalamus. Te lateral geniculate nuclei
maintain the fiber separation established at the chiasma, but
they balance and combine the retinal input for delivery to the
visual cortex. Axons of these thalamic neurons project through
the internal capsule to form the
optic radiation
of fibers in the
cerebral white matter (±igure 15.19). Tese fibers project to the
primary visual cortex
in the occipital lobes, where conscious
perception of visual images (seeing) occurs.
Some nerve fibers in the optic tracts send branches to the
midbrain. One set of these fibers ends in the
superior colliculi
,
Light and Dark Adaptation
Rhodopsin is amazingly sensitive. Even starlight bleaches some
of its molecules. As long as the light is low intensity, relatively
little rhodopsin bleaches and the retina continues to respond to
light stimuli. However, in high-intensity light, there is wholesale
bleaching of the pigment, and rhodopsin bleaches as fast as it is
re-formed. At this point, the rods are nonfunctional, but cones
still respond. Hence, retinal sensitivity automatically adjusts to
the amount of light present.
Light Adaptation
Light adaptation
occurs when we move
from darkness into bright light, as when leaving a movie
matinee. We are momentarily dazzled—all we see is white
light—because the sensitivity of the retina is still “set” for dim
light. Both rods and cones are strongly stimulated, and large
amounts of the visual pigments break down almost instan-
taneously, producing a flood of signals that accounts for the
glare.
Under such conditions, compensations occur. Te rod sys-
tem turns off—all of the transducins “pack up and move” to
the inner segment, uncoupling rhodopsin from the rest of the
transduction cascade. Without transducin in the outer segment,
light hitting rhodopsin cannot produce a signal. At the same
time, the less sensitive cone system and other retinal neurons
rapidly adapt, and retinal sensitivity decreases dramatically.
Within about 60 seconds, the cones, initially overexcited by the
bright light, are sufficiently desensitized to take over. Visual acu-
ity and color vision continue to improve over the next 5–10
minutes. Tus, during light adaptation, we lose retinal sensitiv-
ity (rod function) but gain visual acuity.
Dark Adaptation
Dark adaptation
, essentially the reverse of
light adaptation, occurs when we go from a well-lit area into a
dark one. Initially, we see nothing but velvety blackness because
(1) our cones stop functioning in low-intensity light, and (2) the
bright light bleached our rod pigments, and the rods are still
turned off.
But once we are in the dark, rhodopsin accumulates, trans-
ducin returns to the outer segment, and retinal sensitivity in-
creases. Dark adaptation is much slower than light adaptation
and can go on for hours. However, there is usually enough
rhodopsin within 20–30 minutes to allow adequate dim-light
vision.
During both light and dark adaptation, reflexive changes
occur in pupil size. Bright light shining in one or both eyes
constricts both pupils (elicits the
pupillary
and
consensual light
reflexes
). Tese pupillary reflexes are mediated by the pretectal
nucleus of the midbrain and by parasympathetic fibers. In dim
light, the pupils dilate, allowing more light to enter the eye.
Homeostatic Imbalance
15.10
Night blindness
, or
nyctalopia
(nic
0
tă-lo
9
pe-uh), is a condition
in which rod function is seriously hampered, impairing one’s
ability to drive safely at night. In countries where malnutrition
is common, the most common cause of night blindness is pro-
longed vitamin A deficiency, which leads to rod degeneration.
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