Abstract
The protective effect of the efferent system against acoustic trauma (AT) has been shown by several experimental approaches, including damage to one ear, sectioning of the olivocochlear bundle (OCB) in the floor of the IV ventricle, and knock-in mice overexpressing outer hair cell (OHC) cholinergic receptors, among others. Such effects have been related to changes in the regulation of the cholinergic efferent system and in cochlear amplification, which ultimately reverse upon protective hearing suppression. In addition to well-known circuits of the brainstem, the descending corticofugal pathway also regulates efferent neurons of the olivary complex. In this study, we applied our recently developed experimental paradigm of multiple sessions of electrical stimulation (ES) to activate the efferent system in combination with noise overstimulation. ABR thresholds increased 1 and 2 days after AT (8–16 kHz bandpass noise at 107 dB for 90 min) recovering at AT + 14 days. However, after multiple sessions of epidural anodal stimulation, no changes in thresholds were observed following AT. Although an inflammatory response was also observed 1 day after AT in both groups, the counts of reactive macrophages in both experimental conditions suggest decreased inflammation in the epidural stimulation group. Quantitative immunocytochemistry for choline acetyltransferase (ChAT) showed a significant decrease in the size and optical density of the efferent terminals 1 day after AT and a rebound at 14 days, suggesting depletion of the terminals followed by a long-term compensatory response. Such a synthesis recovery was significantly higher upon cortical stimulation. No significant correlation was found between ChAT optical density and size of the buttons in sham controls (SC) and ES/AT + 1day animals; however, significant negative correlations were shown in all other experimental conditions. Therefore, our comparative analysis suggests that cochleotopic cholinergic neurotransmission is also better preserved after multisession epidural stimulation.
Highlights
The medial olivocochlear (MOC) efferent system enhances hearing sound detection throughout cochlear amplifier regulation (Guinan, 2006, 2010; Lopez-Poveda, 2018), in addition to inducing hearing suppression, as shown in the seminal study by Robert Galambos (Galambos reflex) (Galambos, 1956)
We have shown that multisession electrical stimulation (ES) prevents threshold shifts and minimizes inflammatory reaction after acoustic overstimulation in our animal model of TTS
choline acetyltransferase (ChAT) quantitative immunocytochemistry results indicate that TTS induces short-term neurotransmitter depletion of cholinergic terminals apposed on outer hair cell (OHC), which recovers in the long term
Summary
The medial olivocochlear (MOC) efferent system enhances hearing sound detection throughout cochlear amplifier regulation (Guinan, 2006, 2010; Lopez-Poveda, 2018), in addition to inducing hearing suppression, as shown in the seminal study by Robert Galambos (Galambos reflex) (Galambos, 1956). In line with its role in regulating hearing sensitivity, efferent system activation induces a protective effect against noise overstimulation (Handrock and Zeisberg, 1982; Patuzzi and Thompson, 1991; Zheng et al, 1997; Tong et al, 2013; Dinh et al, 2015; Boero et al, 2018). Electrophysiological evidence shows that, despite the mechanism of self-regulation of the Galambos’ reflex in the low auditory pathway, the brain cortex controls efferent olivocochlear (OC) responses (Xiao and Suga, 2002; Terreros and Delano, 2015). The same effect is detected in humans after cortical epidural electrical stimulation (Fenoy et al, 2006; Perrot et al, 2006)
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