Cross-modal interactions of auditory and somatic inputs in the brainstem and midbrain and their imbalance in tinnitus and deafness.

Abstract

This review outlines the anatomical and functional bases of somatosensory influences on auditory processing in the normal brainstem and midbrain. It then explores how interactions between the auditory and somatosensory system are modified through deafness, and their impact on tinnitus is discussed. Literature review, tract tracing, immunohistochemistry, and in vivo electrophysiological recordings were used. Somatosensory input originates in the dorsal root ganglia and trigeminal ganglia, and is transmitted directly and indirectly through 2nd-order nuclei to the ventral cochlear nucleus, dorsal cochlear nucleus (DCN), and inferior colliculus. The glutamatergic somatosensory afferents can be segregated from auditory nerve inputs by the type of vesicular glutamate transporters present in their terminals. Electrical stimulation of the somatosensory input results in a complex combination of excitation and inhibition, and alters the rate and timing of responses to acoustic stimulation. Deafness increases the spontaneous rates of those neurons that receive excitatory somatosensory input and results in a greater sensitivity of DCN neurons to trigeminal stimulation. Auditory-somatosensory bimodal integration is already present in 1st-order auditory nuclei. The balance of excitation and inhibition elicited by somatosensory input is altered following deafness. The increase in somatosensory influence on auditory neurons when their auditory input is diminished could be due to cross-modal reinnervation or increased synaptic strength, and may contribute to mechanisms underlying somatic tinnitus.