sensitivity of the basilar membrane, making it more sensitive to low-
volume sounds. The outer hair cells contain a protein called prestin
(named after the musical notation presto) that elongates and con-
tracts as a function of membrane potential changes. This change in
shape affects the shape of the entire cell, which then pushes against
the basilar membrane, changing its stiffness and sensitivity—simply
amazing!
In the cerebral cortex, as with the visual system, multiple areas are
involved in the analysis of auditory information. The spatial mapping
of frequency that began at the basilar membrane is preserved all the
way through the pathways to A1. In addition, a great deal of neural
manipulation has taken place between the cochlea and the cortex, and
exactly what happens is still far from understood. Some of the tempo-
ral lobe auditory areas, such as Wernicke’s area, are very involved with
the perception of speech—more on this in Chapter 18.
Loss of hearing is a topic of significant interest and clinical concern.
Among possible causes of hearing loss are infections of the inner ear
that cause irreversible damage to hair cells. Other causes of hearing
loss are genetic anomalies that result in malfunctions of the cochlea.
Individuals possessing such anomalies may be born with impaired
hearing or even complete deafness. One such anomaly involves a gene
coding for a connexon ion channel protein, of the same type as those
forming electrical synapses between neurons and glia (see Chapter 6).
Connexon channels maintain ion flow between various chambers of
the cochlea. A mutation in the gene coding for a particular channel in
the cochlea, known as connexin 26, produces abnormal ion balances
within the cochlea. As a result, the hair cells cannot function, and the
person is deaf.
Perhaps the most common cause of hearing loss is acoustic trauma