Motility-associated hair-bundle motion in mammalian outer hair cells
Citation: Shuping Jia, David Z Z He (2005/06/24) Motility-associated hair-bundle motion in mammalian outer hair cells. Nature Neuroscience (RSS)
DOI (original publisher): doi:10.1038/nn1509
Semantic Scholar (metadata): doi:10.1038/nn1509
Sci-Hub (fulltext): doi:10.1038/nn1509
Internet Archive Scholar (search for fulltext): Motility-associated hair-bundle motion in mammalian outer hair cells
Tagged: Neuroscience (RSS) hearing (RSS), cochlea (RSS), somatic motility (RSS)
Mammalian hearing depends on mechanical feedback in he cochlea. The outer hair cells (OHCs) function as the key elements in this feedback loop. Both somatic motility and "active movement" of hair bundles are considered possible sources of motion-driven cochlear ampliﬁcation. Active movement is known to be the source of such amplification in non-mammals, where somatic motility does not occur. This experiment distinguishes which drives movement in part of the mammalian cochlea.
Goals and Methods
The goal is to distinguish between somatic motility and other active movement of hair bundles in the mammalian cochlea, focusing in part on past studies of gerbils and rats which linked hair bundle movement to active movement for gerbil inner hair cells (IHCs), and rat OHCs.
To gain precision in measurement, cochlea from four groups of subjects were studied: Adult and neonatal gerbils, he latter of which have mechanotransduction but no OHC motility yet; and both wild and prestin-knockout mice, the latter of which have normal hair bundles and mechanotransducer function, but no OHC somatic motility at all.
Somatic motility was measured by applying a voltage across a bundle and looking for voltage-evoked motion. Mechanotransducer currents were also measured. To fully separate the functions of the two different source of motion, streptomycin was used as an inhibitor - it entirely blocks mechanotransducer channels and elimiates spontaneous bundle motion.
Hair motion was measured by looking at the magnified image of bundles at 1260x magnification, in which regime they looked like bright V-shaped lines and movement could be measured at up to 1200 Hz and down to 5nm.
Results and Analysis
The OHCs showed bundle movement with peak responses of up to 830 nm. The movement was insensitive to manipulations that block mechanotransduction. Adjacent OHCs were found to move in tandem with a target OHC when somatic motility was applied; a linkage which disappeared when the target OHC lost its turgor pressure. This suggests the motion resulted from something like rotation of its reticular lamina, a feature of somatic motility.
Finally, movement was entirely absent in neonatal OHCs and prestin-knockout OHCs. This strongly suggests that bundle movement originated in somatic motility for these specieis, and that it plays a central role in cochlear amplification in mammals.
Sharp extracellular potential changes would be needed to drive OHCs at high frequency. There is evidence that the organ of Corti could provide that drive, and theoretical models of OHC piezoelectric properties suggest ways their frequency response might be increased, addressing one outstanding concern with this theory.
Finally, OHC motility can also stimulate freestanding IHC cilia, leading to their motion as well - formerly attributed to mechanotransduction. Further study is needed to determine the source of IHC motion.
Theoretical and Practical Relevance
This study distinguishes between two potential sources of hair-bundle motion: the reclosing of mechanotransduction channels and somatic electromotility. Previous analyses had mainly demonstrated the possibility of either (including the possible presence of mechanotransduction-driven motion in IHCs of gerbils).
It demonstrate conclusively that such motion is due predominantly to electromotility in the OHCs of some gerbils and mice. It also suggests ways in which this motion in OHCs might excite IHCs and stimulate observed motion there as well, including possibly the observed motion of gerbil IHCs, which would make electromotility the primary mechanism for cochlear amplification in mammals. This indicates avenues for future research.