Ganong's Review of Medical Physiology, 23rd Edition

Na +
K +
Na +
Dark
FIGURE 12–12 Effect of light on current flow in visual
receptors. In the dark, Na + channels in the outer segment are held
open by cGMP. Light leads to increased conversion of cGMP to 5'-GMP,
and some of the channels close. This produces hyperpolarization of
the synaptic terminal of the photoreceptor.
the membrane (Figure 12–13) and is attached to a lysine residue
at position 296 in the seventh transmembrane domain.
In the dark, the retinene 1 in rhodopsin is in the 11-cis configuration.
The only action of light is to change the shape of
the retinene, converting it to the all-trans isomer. This, in
turn, alters the configuration of the opsin, and the opsin
change activates the associated heterotrimeric G protein,
which in this case is called transducin or Gt 1 . The G protein
exchanges GDP for GTP, and the α subunit separates. This
subunit remains active until its intrinsic GTPase activity
hydrolyzes the GTP. Termination of the activity of transducin
is also accelerated by its binding of β-arrestin.
The α subunit activates cGMP phosphodiesterase, which
converts cGMP to 5'-GMP (Figure 12–14). cGMP normally
acts directly on Na + channels to maintain them in the open
position, so the decline in the cytoplasmic cGMP concentration
causes some Na + channels to close. This produces the
hyperpolarizing potential. This cascade of reactions occurs
very rapidly and amplifies the light signal. The amplification
helps explain the remarkable sensitivity of rod photoreceptors;
these receptors are capable of producing a detectable
response to as little as one photon of light.
After retinene 1 is converted to the all-trans configuration, it
separates from the opsin (bleaching). Some of the all-trans
retinene is converted back to the 11-cis retinene by retinal
isomerase, and then again associates with scotopsin, replenishing
the rhodopsin supply. Some 11-cis retinene is also synthesized
from vitamin A. All of these reactions, except the
formation of the all-trans isomer of retinene 1 , are independent
of the light intensity, proceeding equally well in light or
K +
Na +
Light
CLINICAL BOX 12–5
Vitamin Deficiencies
CHAPTER 12 Vision 191
In view of the importance of vitamin A in the synthesis of
retinene 1 , it is not surprising that a deficiency in this vitamin
produces visual abnormalities. Among these, one of
the earliest to appear is night blindness (nyctalopia). Vitamin
A deficiency also contributes to blindness by causing
the eye to become very dry, which damages the cornea
(xerophthalmia) and retina. Vitamin A first alters rod function,
but concomitant cone degeneration occurs as vitamin
A deficiency develops. Vitamin A deficiency is due to inadequate
intake of foods high in vitamin A (liver, kidney, whole
eggs, milk, cream, and cheese) or beta-carotene, a precursor
of vitamin A, found in dark green leafy vegetables and
yellow or orange fruits and vegetables. Vitamin A deficiency
is rare in the United States, but it is still a major public
health problem in the developing world. Annually,
about 80,000 individuals worldwide (mostly children in underdeveloped
countries) lose their sight from severe vitamin
A deficiency. Prolonged deficiency is associated with
anatomic changes in the rods and cones followed by degeneration
of the neural layers of the retina. Treatment
with vitamin A can restore retinal function if given before
the receptors are destroyed. Other vitamins, especially
those of the B complex, are also necessary for the normal
functioning of the retina and other neural tissues.
R
C
OH
OH
OH
OH
OH
OH
Intradiskal
surface
Rod disk
membrane
Cytoplasmic
surface
FIGURE 12–13 Diagrammatic representation of the
structure of rhodopsin, showing the position of retinene 1 (R) in
the rod disk membrane. Retinene 1 is parallel to the surface of the
membrane and is attached to a lysine residue at position 296 in the
seventh transmembrane domain.
N