Abstract
Sound and head movements are perceived through sensory hair cells in the inner ear. Mounting evidence indicates that this process is initiated by the opening of mechanically sensitive calcium-permeable channels, also referred to as the mechanoelectrical transducer (MET) channels, reported to be around the tips of all but the tallest stereocilia. However, the identity of MET channel remains elusive. Literature suggests that the MET channel is a non-selective cation channel with a high Ca2+ permeability and ∼100 picosiemens conductance. These characteristics make members of the transient receptor potential (TRP) superfamily likely candidates for this role. One of these candidates is the transient receptor potential melastatin 1 protein (TRPM1), which is expressed in various cells types within the cochlea of the mouse including the hair cells. Recent studies demonstrate that mutations in the TRPM1 gene underlie the inherited retinal disease complete congenital stationary night blindness in humans and depolarizing bipolar cell dysfunction in the mouse retina, but auditory function was not assessed. Here we investigate the role of Trpm1 in hearing and as a possible hair cell MET channel using mice homozygous for the null allele of Trpm1 (Trpm1−/−) or a missense mutation in the pore domain of TRPM1 (Trpm1tvrm27/tvrm27). Hearing thresholds were evaluated in adult (4–5 months old) mice with auditory-evoked brain stem responses. Our data shows no statistically significant difference in hearing thresholds in Trpm1−/− or Trpm1tvrm27/tvrm27 mutants compared to littermate controls. Further, none of the mutant mice showed any sign of balance disorder, such as head bobbing or circling. These data suggest that TRPM1 is not essential for development of hearing or balance and it is unlikely that TRPM1 is a component of the hair cell MET channel.
Highlights
Hearing functions depend on specialized mechanoreceptors of the inner ear called hair cells that convert sound vibrations into electrical stimuli
The hair bundle is deflected towards the tallest stereocilia and the tip links are tensioned and are thought to directly pull open mechanoelectrical transducer (MET) channels located at their lower ends [3]
To test this hypothesis we evaluated auditory function in mice carrying a null mutation or a point mutation in Trpm1
Summary
Hearing functions depend on specialized mechanoreceptors of the inner ear called hair cells that convert sound vibrations into electrical stimuli. These reports encouraged us to investigate the role of TRPM1 in hearing and possibly hair cell MET function by using these Trpm1 mouse mutants. The genotype of mice used to obtain ABR thresholds was confirmed by PCR for the Trpm12/2 allele (Fig. 2A) or DNA sequence analysis for the Trpm1tvrm27point mutation (Fig. 2B).
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