Trimethyltin disrupts loudness recruitment and auditory threshold sensitivity in guinea pigs.

Trimethyltin (TMT) impairs auditory thresholds within minutes of systemic administration. However, there are no data which relate to the output of the auditory nerve at sound levels above threshold. In this experiment, we evaluated the functional effects of TMT on the auditory threshold by identifying the sound level which just produced a detectable compound action potential (CAP). We also assessed outer hair cell function by measuring the cochlear microphonic (CM), a nonpropagated ac potential which is phase-locked to the stimulus. Finally, we measured the growth of the N1 amplitude as a function of stimulus intensity at levels above threshold and of the summating potential (SP), a dc potential which has multiple generators. To isolate cochlear from systemic effects of TMT, the agent was applied directly to the round window, a structure separating the middle and inner ear, of anaesthetized guinea pigs. We show that TMT applied to the round window membrane can disrupt the function of the cochlea. Measurements of auditory function at supra-threshold levels showed clearly that TMT reduced the amplitude of N1 while having no measurable effect on the SP. These findings indicate that TMT blocks the recruitment of neuronal elements by loud sound. This pattern of impairment differs from that observed with aminoglycoside antibiotics, hypothermia, and presbycusis in which loudness recruitment has been reported.