Age-related hearing loss (presbycusis) is a complex state that reflect
s pathologic changes along the entire auditory neuraxis. Loss of speec
h understanding, decreased ability to localize sounds, and a decreased
ability to detect and extract signals in noise are characteristic pro
blems encountered by the elderly. Central (neural) presbycusis frequen
tly results in a dramatic loss in speech understanding without a paral
lel change in pure-tone thresholds. In spite of evidence that suggests
these deficits cannot be fully explained by peripheral changes alone,
few studies have examined the neurochemical basis of central auditory
dysfunction in aging. Age-related alterations in neural circuits invo
lved in the processing of acoustic information could reflect changes i
n the synthesis, degradation, uptake, release, and receptor sensitivit
y of neurotransmitters, perhaps secondary to cell loss and/or progress
ive deafferentation. A series of studies designed to test this hypothe
sis has examined aging in the central auditory system of the F344 rat.
Age-related changes associated with GABA neurotransmitter function in
an important auditory midbrain structure, the inferior colliculus, ha
ve been investigated. These studies found: (1) decreased numbers of GA
BA immunoreactive neurons; (2) decreased basal levels (concentrations)
of GABA; (3) decreased GABA release; (4) decreased glutamic acid deca
rboxylase activity; (5) decreased GABA, receptor binding; (6) decrease
d numbers of presynaptic terminals; and (7) subtle GABA, receptor bind
ing changes. Collectively, these age-related changes suggest altered G
ABA neurotransmitter function in the IC. Identification of specific ne
urotransmitter changes in structures important in speech processing co
uld eventually lead to the development of pharmacotherapy for selectiv
e types of age-related hearing loss.