Unmyelinated type II afferent neurons report cochlear damage

• DOI: 10.1073/pnas.1515228112
• Publication Date: 2015-11-10T04:14:28Z
• Authors: Chang Liu; Elisabeth Glowatzki; Paul Albert Fuchs
• Keywords: Ions; 0301 basic medicine; Nerve Fibers, Unmyelinated; KCNQ Potassium Channels; Cochlea; Rats, Sprague-Dawley; Hair Cells, Auditory, Outer; 03 medical and health sciences; Adenosine Triphosphate; Receptors, Glutamate; Receptors, Purinergic P2Y; Potassium; Animals; Neurons, Afferent; Ion Channel Gating

Significance Painfully loud sound causes protective or withdrawal responses, rather than continued listening. This differential behavior invites comparison with somatic pain responses driven by the anatomically distinct subset of small-diameter, unmyelinated afferents—C fibers. Like somatic C fibers, unmyelinated type II cochlear afferents differ in size, number, and innervation pattern from type I afferents that encode sound. Here, we show that type II afferents are excited during cochlear tissue damage in part by the algogenic cytoplasmic metabolite adenosine triphosphate (ATP). This finding, together with previous evidence that type II afferents respond weakly to synaptic transmission from cochlear hair cells, and normally are insensitive to sound, supports the identification of type II afferents as cochlear nociceptors, mediating the sensation of painfully loud sound.