Our ability to identify different sound sources-to distinguish predators from prey, for example-rests upon the ear's ability to decompose complex sounds into their frequency components. Although the cochlear traveling wave initiates this process, individual hair cells are also tuned to specific frequencies both through hair-bundle mechanics and sometimes by electrical resonance. Not only the active process of hair cells, but even their synaptic transmission has been found to be frequency-selective.
Afferent axons of the eighth cranial nerve carry information from the cochlea into the auditory nuclei of the brainstem. These nerve fibers are excited by a neurotransmitter, glutamate, released by hair cells at specialized ribbon synapses. Unlike ordinary synapses, which respond to transient action potentials about 100 mV in amplitude, a ribbon synapse can release transmitter continuously and signal threshold stimuli only one thousandth as large. In addition, the ability of these synapses to encode phase information at frequencies up to 4 kHz helps us to localize sound sources in space by comparing the arrival times of signals at the two ears.
Hearing deficiency is widespread in industrialized countries, in which about 10% of the population is affected. Genetic deafness is relatively common, with at least 200 forms of syndromal hearing impairment and 100 non-syndromal types. Hearing can be damaged by loud sounds, for example in an industrial or military setting; by ototoxic drugs, including common antibiotics and anti-cancer agents; and by infections. Finally, in the phenomenon of presbyacusis, hearing deteriorates with age. In all of these cases, the dominant problem is the loss of hair cells. An important focus of contemporary research is therefore the potential restoration of human hearing through the reprogramming of progenitor cells in the ear.
