THE BEHAVIOR OF THE F(2)-F(1) ACOUSTIC DISTORTION-PRODUCT - LACK OF EFFECT OF BRAIN-STEM LESIONS IN ANESTHETIZED GUINEA-PIGS

Two tones of frequency f(1) and f(2) (the primary tones), when presented simultaneously to the ear, generate acoustic distortion products in the external ear canal. One of these distortion products, of frequency f(2)-f(1), has been shown to undergo a reversible change in amplitude when the primary tones generating distortion are presented continuously to the test (ipsilateral) ear (Brown, 1988; Kirk and Johnstone, 1993). The effect is apparent for low and moderate primary tone intensities and has been postulated to be caused by the action of a neural feedback loop via the superior olivary complex. We have carried out a series of studies of this phenomenon in anaesthetized guinea pigs, making brainstem lesions positioned so as to interrupt the known medial and/or lateral efferent projections to the cochlea from the superior olivary complex. We could not demonstrate any consistent change after lesioning, either in the baseline level of f(2)-f(1) or in the alteration of f(2)-f(1) caused by continuous monaural primary tones. These results are not consistent with the suggestion by others that a neural feedback loop involving either the medial (Brown, 1988) or lateral (Kirk and Johnstone, 1993) olivocochlear efferents may be responsible for the effect. We therefore conclude that either 1) the changes in f(2)-f(1) produced by continuous low-level primary tones reflect the operation of intrinsic hair cell mechanisms and do not involve efferent feedback via brainstem nuclei or 2) a neural feedback loop does play a role, but this loop involves an unknown pathway that was not interrupted by our lesions.