**3.8 The gerbil as a model of strial or metabolic presbyacusis**

The data discussed above describe a wide range of age-dependent pathologies of the gerbil cochlea. In summary, they suggest that loss of EP due to pathology of the SV and the lateral wall are the main factors that contribute to the threshold shifts observed in auditory nerve fibres and the CAP in old gerbils. This pattern resembles the category of strial atrophy in humans (Schuknecht & Gacek, 1993).

The loss of sensitivity was most pronounced at the tip of single-fibre tuning curves (Schmiedt et al., 1990) and in masked CAP tuning curves (Hellstrom & Schmiedt, 1996) of old gerbils and led to a decreased tip-to-tail ratio of the tuning curves. These changes are similar to the effects of a reduced EP on single-fibre tuning curves in cat (Sewell, 1984). Consequently, Hellstrom & Schmiedt (1996) proposed that "the quiet-aged gerbil can be used as a model for an intact hair-cell system coupled to a chronically lowered EP". This view was supported by a subsequent study where changes of cochlear function due to a reduction of the EP by chronic furosemide application to the round window in young gerbils resembled those found in quiet-aged, old gerbils (Lang et al., 2010). Schmiedt (1983) proposed the "dead battery theory" and reported that increasing the EP by current injection into scala media in an old animal with an initial EP of 41 mV was associated with increased CAP amplitude and a 20 dB reduction of CAP threshold.

In summary, cochlear sensitivity in quiet-aged gerbils declines on average with a high degree of inter-animal variability. The loss of EP due to degeneration of the SV appears to be the main reason for decreased sensitivity in old gerbils, while loss of hair cells and auditory nerve fibres appear less important. Consequently, gerbils are a useful model of human strial or metabolic cochlear presbyacusis.
