periments (see Scharf, 1983) show that simple loudness adaptation does not depend on interaction between the two ears. For example, after loudness has adapted in one ear, the loudness of a new sound to the other ear is wholly unadapted. These results suggest a peripheral origin for simple adaptation. However, measurements of the cochlear action potential in the guinea pig show the same percentage decrease in the response of the eighth nerve after a 3-min exposure to a steady tone close to threshold as at higher levels ( T. Dumon, personal communication). This finding would seem to place loudness adaptation at a physiological level beyond the cochlea. However, recalling that the psychophysical loudness function is steeper near threshold, we cannot exclude the possibility that the translation from eighth-nerve response to "loudness" follows the same function (i.e., the neural responses beyond the eighth nerve change more rapidly below 30 dB SL than above). The same relative reduction in the neural response would then correspond to a greater decrease in loudness near threshold than at higher stimulus levels. These speculations are susceptible to empirical and theoretical tests. I end with them because they illustrate the relevance of ratio scaling not only in revealing how loudness changes as a function of such stimulus variables as duration and level, but also how these empirical relationships can be used to uncover the physiological mechanisms underlying subjective magnitude.
I thank Rhona Hellman for many helpful comments. Research was supported in part by a grant (2R01NS07270) from NIH and a grant (RR07143) under HEW's Biomedical Research Support Program.
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