Human Physiology, 14th edition (2016)

Sensory Physiology 305

Figure 10.44 Convergence in the retina and light sensitivity. Because bipolar cells receive input from the convergence
of many rods ( a ) , and because a number of such bipolar cells converge on a single ganglion cell, rods maximize sensitivity to low levels
of light at the expense of visual acuity. By contrast, the 1:1:1 ratio of cones to bipolar cells to ganglion cells in the fovea ( b ) provides
high visual acuity, but sensitivity to light is reduced.

Ganglion

cells

Ganglion

cells

Bipolar

cells

Bipolar

cells

(a) Light (b) Light

Rods

Convergence

Cones in fovea

No convergence

Pigmented

epithelium

CLINICAL APPLICATION

Age-related macular degeneration ( AMD )—involving

degeneration of the macula lutea and its central fovea—

affects one in three people by the age of 75 and is the lead-

ing cause of blindness. People with macular degeneration

lose the clarity of vision provided by the fovea and 30% of

the vision in the central region of the visual field. The dam-

age is usually related to the loss of retinal pigment epithe-

lium. Pigment epithelial cells may become damaged by

oxidative stress (discussed in chapters 5 and 19) and per-

haps by activation of the innate immune system (chapter 15,

section 15.1), which promote their apoptosis (chapter 3,

section 3.5). In its early stages, macular degeneration

is detectable by the appearance of cream-colored fatty

deposits called drusen in the macula lutea. Drusen are usu-

ally located between the retinal pigment epithelium and

Bruch’s membrane, the collagenous basement membrane

under the pigment epithelium. Although drusen are found

in almost everyone over the age of 50, excess drusen may

cause damage to the pigment epithelium. People with this

dry AMD form of the disease have moderate vision loss;

they can usually read but have difficulty seeing well enough

to drive at night.

Behind Bruch’s membrane is the connective tissue

choroid, containing blood vessels. If macular degeneration

progresses to the more serious wet AMD, there is neovas-

cularization (growth of new blood vessels) in the choroid,

stimulated by a paracrine regulator called vascular endothelial

growth factor ( VEGF ). The vessels invade the retina from the

choroid and cause fluid leakage, edema, and the degenera-

tion of photoreceptors. The swelling that results can increase

the thickness of the macula and fovea up to three times nor-

mal and seriously disrupt vision. Wet AMD is responsible for

most cases of blindness in people with macular degeneration.

In addition to age, other risk factors include smoking, expo-

sure to light, and a genetic predisposition to this disease. Genes

predisposing people to macular degeneration have recently been

identified, but the disease is caused by complex interactions of

both genetic and environmental influences. The progression may

be slowed by cessation of smoking, wearing sunglasses, and

taking multivitamins with antioxidants, zinc, and perhaps lutein

(found in green leafy vegetables). Treatment of wet AMD cur-

rently involves injections into the eye of antibodies that bind to

VEGF and prevent its stimulation of neovascularization.