zonotikk

Here's a paper which includes a review of the above studies (see section 5.2) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812300/

The movement response is not my interest, but more so the fact that mice with damaged inner ears did not breathe faster in response to high CO2 levels during sleep, which implies reduced chemosensation.

There are these papers which strongly imply that the inner ear hair cells, and not the medulla, is primarily the driving factor in the CO2 drive reflex https://www.ncbi.nlm.nih.gov/pubmed/21130842 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988803/ But every fMRI study done on chemoreceptors has shown only areas of the brain and carotid bodies light up in response to CO2. I could not find any fMRI study papers showing that the inner ears light up in response to CO2 or any histological evidence that the hair cells of the inner ear are chemosensitive and play a larger role in chemosensation than the brain like these studies are trying to imply. It is said the central chemoreceptors in the brain contribute to 85% of the CO2 drive reflex and the peripheral chemoreceptors contribute 15%, which seems to leave little room for the inner ear hair cells to play such a vital and significant part (53% of the respiratory drive was lost when both ears were damaged). The papers in question were trying to link SIDs to inner ear damage.