Sharpened cochlear tuning in a mouse with a genetically modified tectorial membrane
Ian J Russell, P Kevin Legan, Victoria A Lukashkina, Andrei N Lukashkin,
Richard J Goodyear &
Guy P Richardson
Nat Neurosci. 2007 Feb;10(2): 215-23
School of Life Sciences, University of Sussex, Falmer, Brighton, BN1
9QG, UK.
Abstract:
Frequency tuning in the cochlea is determined by the passive mechanical properties of the basilar membrane and active feedback from the outer hair cells, sensory-effector cells that detect and amplify sound-induced basilar membrane motions. The sensory hair bundles of the outer hair cells are imbedded in the tectorial membrane, a sheet of extracellular matrix that overlies the cochlea's sensory epithelium. The tectorial membrane contains radially organized collagen fibrils that are imbedded in an unusual striated-sheet matrix formed by two glycoproteins, alpha-tectorin (Tecta) and beta-tectorin (Tectb). In Tectb(-/-) mice the structure of the striated-sheet matrix is disrupted. Although these mice have a low-frequency hearing loss, basilar-membrane and neural tuning are both significantly enhanced in the high-frequency regions of the cochlea, with little loss in sensitivity. These findings can be attributed to a reduction in the acting mass of the tectorial membrane and reveal a new function for this structure in controlling interactions along the cochlea. (Bold text emphasis by Martin Braun)
Comment:
Experiments during the past two decades have confirmed two functions
of the tectorial membrane (TM) in the mammalian inner ear. 1) It provides
a tight hydromechanical coupling between outer and inner hair cells
(OHC & IHC) via the narrow subtectorial space. 2) It absorbs acoustical
energy due to mechanical resonances.
Russell et al. could now for the first time separate these two functions
by comprehensive anatomical and physiological investigations of gene deletion
animals. In Tectb(-/-) mice the first function is fully intact, but the
second function is disrupted due to a pathologic internal structure of
the TM.
Hearing sensitivity above 20 kHz remained unaffected, apparently
due to the unchanged OHC-IHC coupling. Frequency selectivity, however,
was improved. This outcome is surprising. It could hardly be expected
that a pathology would improve a key function in hearing. Why then - one
may wonder - did this mutation (or a similar one) not become established
in the gene pool a long time ago? It seems that during evolution a further
sharpening of frequency selectivity was of less value than dispersion
of acoustic energy via TM resonances. The latter reduces the risk
of damages at high sound levels.
Of most importance for future research may be the following findings from
Tectb(-/-) mice: a perfect symmetry of tuning curves (Figs. 4c
and 5abc) and a total absence of a tail in the neural tuning curves
(Figs. 5abc). Both facts impressively demonstrate a discrete, point-like,
local tuning within the organ of Corti. Thus they further strengthen
the well-known hypothesis that the OHCs are tuned amplifiers. (Comment
Martin Braun)