Mechanisms underlying this plasticity.

In each sensory modality, receptor organ damage leads to an unmasking of normally silent inputs in the corresponding primary cortex. This probably causes loss of inhibition in the deprived sensory cortex and a modification in its organization (see, for example, Garraghty et al., 1991; Hendry and Jones, 1986). In the present study, a loss of inhibition may have occurred at the border between the damaged and undamaged areas, resulting in cortical over-representation at the cut-off frequency. However, Rajan (1998) demonstrated in animals that, even if such decreased inhibition does occur in case of steeply sloping high-frequency hearing loss, it is not accompanied by any cortical tonotopic map reorganization. Loss of inhibitory input may not be the only cause of plasticity. A second mechanism, such as axonal sprouting, may be involved in this plasticity.

Thus, although the perceptual changes in DLF performance induced by hearing-aid fitting may well reflect a central reorganization, the mechanisms of this plasticity remains unclear, since not all the parameters at work in such reorganization are yet known. Nevertheless it may be hypothesized that the process involves new masking of silent input responsible for inhibition in the primary auditory cortex.