Modulation of auditory processing by non-auditory brain areas: Effects of acoustic trauma

Abstract

Acoustic trauma (AT) induced hearing loss elicits plasticity in the form of altered spontaneous firing throughout the central auditory pathway, including at the level of the medial geniculate nucleus (MGN). Non-auditory areas such as the prefrontal cortex (PFC) and amygdala are thought to modulate auditory processing in the MGN, which may play a role in sensory gating. In our laboratory, we investigated the functionality of inputs from the PFC and amygdala on MGN activity in different animal models (rat and guinea pig) both without and with AT. The effects of AT on auditory thresholds were investigated using auditory brainstem response (ABR) recordings or compound action potential recordings of the auditory nerve. To test circuitry functionality, we used single neuron recordings in the MGN combined with electrical stimulation of the PFC or amygdala. Our data showed, first, that electrical stimulation of either the PFC or amygdala resulted in a variety of effects within the MGN (facilitation, inhibition, or no effect) and, second, that AT and subsequent hearing loss significantly increased the magnitude of inhibition. This change in inhibition may represent a compensatory mechanism in response to the increased spontaneous activity in the central auditory pathway known to occur following hearing loss.