Cognitive decline is a virtually universal aspect of the aging process. However, its neurophysiological basis remains poorly understood. We describe here more than 20 age-related cortical processing deficits in the primary auditory cortex of aging versus young rats that appear to be strongly contributed to by altered cortical inhibition. Consistent with these changes, we recorded in old rats a decrease in parvalbuminlabeled inhibitory cortical neurons. Furthermore, old rats were slower to master a simple behavior, with learning progressions marked by more false-positive responses. We then examined the effect of intensive auditory training on the primary auditory cortex in these aged rats by using an oddball discrimination task. Following training, we found a nearly complete reversal of the majority of previously observed functional and structural cortical impairments. These findings suggest that age-related cognitive decline is a tightly regulated plastic process, and demonstrate that most of these age-related changes are, by their fundamental nature, reversible. aging | cognitive decline | plasticity | inhibition | parvalbumin P erceptual and cognitive decline are near-universal aspects of normal aging (1, 2). Such deficits cannot be explained solely by a dysfunction of peripheral sensory organs and frequently translate to slowed perceptual processing and difficulty in accurately identifying stimuli under challenging (e.g., noisy, time-limited, attentionally demanding) conditions (3, 4). In the human auditory system, psychophysical and electroencephalography experiments have examined aspects of cognitive decline by using oddball detection paradigms, successive-signal masking studies, speech-in-noise studies, and compressed speech (5-7), among other strategies. These studies have shown that degraded signal salience, defective sensory adaptation and a slowing of sensory processing contribute to the deterioration of a wide range of perceptual and cognitive processes recorded in aged populations (3,(8)(9)(10). Animal models have been instrumental in defining the cellular and molecular basis of agerelated perceptual impairments. In rats, significant alterations in inhibitory function in various subcortical nuclei and the auditory cortex have been linked to abnormal temporal and spectral processing (11)(12)(13)(14). Interestingly, although these changes are often described as progressive plastic compensations secondary to a combination of slow peripheral deafferentation and chemical or molecular insults (11,15), the possibility that age-related changes might be by their plastic nature largely reversible has seldom been explored or proposed (16). Compelling evidence that these agerelated functional alterations can be prevented to some extent by sensory enrichment (9, 17) or even dietary improvements (15) certainly supports this concept. During adulthood, after the closure of developmental plasticity windows, attention-demanding intensive training strategies remain one of the most powerful means of directing plastic re...