https://pubmed.ncbi.nlm.nih.gov/24021919/ Inner ear insult suppresses the respiratory response to carbon dioxide Compensated respiratory acidosis has been observed in a significant number of patients with active vestibular disease. We therefore hypothesized that the inner ear may play an unrecognized integral role in respiratory control. To test this premise, we investigated whether mice with induced inner ear injury demonstrated any alteration in their respiratory response to inhaled carbon dioxide (CO(2)). Experimental mice and control mice were included in two separate experiments. Intra-tympanic gentamycin injections were administered to induce inner ear damage in experimental animals. Hearing loss and vestibular dysfunction were tested 1-week after injections to confirm presence of inner ear insult, following which the animal's respiratory response to inhalation of 8% CO(2) was examined. Mice with inner ear injury (n=60) displayed a significantly diminished hypercapnic ventilatory response (HCVR). This contrasted with the normal HCVR seen in control mice that had not undergone tympanic injections (n=30), controls that received tympanic injections with saline (n=5), and controls that had gentamicin administered systemically (n=5). In response to inspired CO(2), the mean respiratory frequency of control mice increased by an average of 50% over their baseline values for both parts of the experiment. In contrast, the ear-damaged experimental group mean values increased by only three breaths per minute (bpm) (2%) in the first experiment and by 28 bpm (11%) in the second experiment. Inner ear damage significantly reduces the respiratory response to CO(2) inhalation. In addition to the established role of the inner ear organ in hearing and balance, this alludes to an unidentified function of the inner ear and its interconnecting neuronal pathways in respiratory regulation. This finding may offer valuable new clues for disease states with abnormal respiratory control where inner ear dysfunction may be present. 5.2. The vestibular nucleus and its potential link to SIDS Allen et al. developed an experimental mouse model that uses gentamicin-induced loss of hair cells in the inner ear to examine the potential relationship between auditory/vestibular and respiratory physiology (Allen et al., 2011). These gentamicin-exposed mice exhibited an attenuated ventilatory response to a hypercapnic stimulus. Post-mortem histological analysis revealed a decrease in hair cell number accompanied with a decrease in the number of large neurons within the lateral vestibular nucleus and no discernible changes in the cochlear nucleus (Allen et al., 2011). These findings not only support the potential interaction between hair cell loss and attenuated responses to respiratory stimuli, but also suggest that the mechanism leading to this deficit may involve the central nervous system at the level of the vestibular nucleus (VN).