Olivocochlear projections contribute to superior intensity coding in cochlear nucleus small cells

Abstract

support-information-section).Adam Hockley received his PhD at the Institute of Hearing Research in Nottingham, UK, where he learned about auditory brainstem physiology while studying the role of nitric oxide in the cochlear nucleus in tinnitus. From here, he moved to the Shore Lab at the University of Michigan and began to focus on intensity coding within the small cell cap of the cochlear nucleus. He has found important intensity-coding abilities in this area and hopes to study these more in the future, assessing how brainstem circuits are altered by auditory pathologies. Calvin Wu received his PhD in biology from University of North Texas, where he studied cellular and network physiology in cultured cortical neurons. He is currently a Research Investigator at the Kresge Hearing Research Institute, University of Michigan, where he completed his postdoctoral work. His current research focuses on multisensory integration and plasticity in the auditory brainstem and their roles in auditory processing deficits or tinnitus.

Synaptic plasticity of inhibitory synapses onto medial olivocochlear efferent neurons

“…Functional evidence describing the complexity of synaptic inputs to MOC neurons corroborates existing histological evidence that multiple classes of neurons form synapses onto olivocochlear efferent neurons, indirectly influencing cochlear function. Recent work demonstrates that MOC neurons are excited by both ascending sound‐driven inputs from CN T‐stellate and small cell cap cells and descending excitation from the IC (Hockley et al., 2022; Romero & Trussell, 2021). MOC neurons are also inhibited by ascending sound‐driven pathways via MNTB neurons (Torres Cadenas et al., 2020).…”

“…The time course of decay of sustained MNTB–MOC inhibition is in the range of hundreds of milliseconds, which is too long to account for the spike latencies of MOC neuron sound responses. Therefore, activation of MOC neurons by both ascending excitatory drive from the CN (Hockley et al., 2022; Romero & Trussell, 2021) and descending, facilitating excitation from the IC (Romero & Trussell, 2021) likely overcomes inhibition to evoke action potentials in MOC neurons. This hypothesized interaction of excitation and inhibition in MOC neurons, combined with the low synaptic release probability and subsequent facilitation of MOC effects on cochlear OHCs (Ballestero et al., 2011), is consistent with the build‐up of ‘fast’ MOC effects as measured by distortion product otoacoustic emissions (∼100 ms; Guinan, 2011).…”

“…Many MOC neurons have zero to low rates of action potentials in vivo in the absence of sound (Brown, 1989;Maison et al, 2003;Robertson & Gummer, 1985). The presynaptic circuitry driving MOC neuron activity is incompletely known, but anatomical (Brown et al, 2003(Brown et al, , 2013Darrow et al, 2012;De Venecia et al, 2005) and recent functional (Romero & Trussell, 2021) work indicates that T-stellate cells of the ventral cochlear nucleus (VCN) are the primary sound-driven inputs to MOC neurons, with contributions from cells of the cochlear nucleus (CN) small shell cap (Hockley et al, 2022). MOC neurons are also strongly excited by descending projections from the inferior colliculus (IC) (Romero & Trussell, 2021).…”

Neural correlates of masked and unmasked tones: psychoacoustics and late auditory evoked potentials (LAEPs)

“…However, as the intensity JND is the same for the same target tone level regardless of the amount of masking release, our results indicate that the physical target tone level is encoded and preserved, in addition to the enhanced neural representation at thresholds as an internal signal-to-noise ratio (iSNR). For the intensity encoding at the level of CN, small cells showed preserved intensity encoding of the target tone in the presence of the noise (Hockley et al, 2022). These cells displayed a unique rate-level function where the spike rate increases without saturation with increasing levels up to 90 dB SPL (Hockley et al, 2022).…”

“…For the intensity encoding at the level of CN, small cells showed preserved intensity encoding of the target tone in the presence of the noise (Hockley et al, 2022). These cells displayed a unique rate-level function where the spike rate increases without saturation with increasing levels up to 90 dB SPL (Hockley et al, 2022). This could be a possible mechanism of the intensity coding in masking release conditions.…”