Auditory brainstem mechanisms likely compensate for self-imposed peripheral inhibition.

Feedback networks in the brain regulate downstream auditory function as peripheral as the cochlea. However, the upstream neural consequences of this peripheral regulation are less understood. For instance, the medial olivocochlear reflex (MOCR) in the brainstem causes putative attenuation of responses generated in the cochlea and cortex, but those generated in the brainstem are perplexingly unaffected. Based on known neural circuitry, we hypothesized that the inhibition of peripheral input is compensated for by positive feedback in the brainstem over time. We predicted that the inhibition could be captured at the brainstem with shorter (1.5 s) than previously employed long duration (240 s) stimuli where this inhibition is likely compensated for. Results from 16 normal-hearing human listeners support our hypothesis in that when the MOCR is activated, there is a robust reduction of responses generated at the periphery, brainstem, and cortex for short-duration stimuli. Such inhibition at the brainstem, however, diminishes for long-duration stimuli suggesting some compensatory mechanisms at play. Our findings provide a novel non-invasive window into potential gain compensation mechanisms in the brainstem that may have implications for auditory disorders such as tinnitus. Our methodology will be useful in the evaluation of efferent function in individuals with hearing loss.