The cochlear nerve includes a small population of unmyelinated sensory fibers connecting outer hair cells to the brain. The functional role of these type-II afferent neurons is controversial, because neurophysiological data are sparse. A recent study reported that targeted deletion of peripherin, a type of neurofilament, eliminated type-II afferents and inactivated efferent feedback to the outer hair cells (Froud et al., 2015), thereby suggesting that type IIs were the sensory drive to this sound-evoked, negative-feedback reflex, the olivocochlear pathway. Here, we re-evaluated the cochlear phenotype in mice from the peripherin knockout line and show that 1) type-II afferent terminals are present in normal number and 2) olivocochlear suppression of cochlear responses is absent even when this efferent pathway is directly activated by shocks. We conclude that type-II neurons are not the sensory drive for the efferent reflex and that peripherin deletion likely causes dysfunction of synaptic transmission between olivocochlear terminals and their peripheral targets.
Significance Statement: Recent studies present opposing views on the role of unmyelinated sensory fibers in the auditory nerve: one suggests that type-II spiral ganglion neurons are nociceptors mediating auditory pain (Flores et al., 2015), and another suggests they comprise the sensory limb of the cochlear efferent reflex (Froud et al., 2015). Both cannot be correct, since nociceptors respond at traumatically high sound levels, whereas cochlear efferents respond near hearing threshold. Here, we re-examine the phenotype of the mutant mouse on which the latter case was based: we show that the type-II innervation is not missing in this mutant, as claimed, and that the loss of efferent feedback is due to a defect in efferent transmission, rather than a loss of sensory drive.
The authors have no relevant financial conflicts of interest to declare.
Research supported by grants from the NIDCD: R01 DC 0188 and P30 DC 05209.