Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 12

Vision 191

the membrane (Figure 12–13) and is attached to a lysine resi-
due at position 296 in the seventh transmembrane domain.
In the dark, the retinene
1
in rhodopsin is in the 11-
cis
con-
figuration. 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 concentra-
tion 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 photorecep-
tors; 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, replen-
ishing the rhodopsin supply. Some 11-cis retinene is also syn-
thesized from vitamin A. All of these reactions, except the
formation of the all-trans isomer of retinene 1 , are indepen-
dent of the light intensity, proceeding equally well in light or

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.

K+

Na+

Na+

Dark

K+

Na+

Light

CLINICAL BOX 12–5

Vitamin Deficiencies

In view of the importance of vitamin A in the synthesis of

retinene 1 , it is not surprising that a deficiency in this vita-

min produces visual abnormalities. Among these, one of

the earliest to appear is night blindness (nyctalopia). Vita-

min 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 func-

tion, but concomitant cone degeneration occurs as vitamin

A deficiency develops. Vitamin A deficiency is due to inade-

quate intake of foods high in vitamin A (liver, kidney, whole

eggs, milk, cream, and cheese) or beta-carotene, a precur-

sor of vitamin A, found in dark green leafy vegetables and

yellow or orange fruits and vegetables. Vitamin A defi-

ciency is rare in the United States, but it is still a major pub-

lic health problem in the developing world. Annually,

about 80,000 individuals worldwide (mostly children in un-

derdeveloped countries) lose their sight from severe vita-

min A deficiency. Prolonged deficiency is associated with

anatomic changes in the rods and cones followed by de-

generation 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.

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.

Rod disk

membrane

Cytoplasmic

surface

Intradiskal

surface

R

N

C

OHOH

OH

OH

OH

OH