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Hair Cells

  1. Walter Marcotti1,
  2. Sergio Masetto2

Published Online: 15 JAN 2010

DOI: 10.1002/9780470015902.a0000181.pub2

eLS

eLS

How to Cite

Marcotti, W. and Masetto, S. 2010. Hair Cells. eLS. .

Author Information

  1. 1

    University of Sheffield, Department of Biomedical Science, Sheffield, United Kingdom

  2. 2

    University of Pavia, Department of Physiology, Pavia, Italy

Publication History

  1. Published Online: 15 JAN 2010
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Figure 1. Morphological organization of the inner ear. (a) Different sensory structures of the inner ear. P.C., perilymphatic compartment and E.C., endolymphatic compartment. (b)–(d) Sensory neuroepithelia and accessory structures present in the semicircular canals (b), otolith organs (c) and the cochlea (d). Type I and II hair cells are found in the cristae and maculae; inner (IHCs) and outer (OHCs) hair cells are found in the organ of Corti. In the semicircular canals, the stereocilia are embedded in a gelatinous material called the cupula (b). Movement of the cupula, as a consequence of head rotation (white arrow), results in stereociliar deflection. In the saccule and utricle, the tips of the stereocilia are embedded in the otolith membrane (c), note the presence of several small pebbles called otoliths made of calcium carbonate and proteins. Otolith movement produced by vertical or horizontal head accelerations (white arrows) displaces the otolith membrane, which deflects the stereocilia. In the cochlea (d), sound-induced vibration of the basilar membrane causes a shear force between the tectorial membrane and the inner and outer hair cells, resulting in hair bundle displacement. For clarity, only one afferent or efferent fibre is shown to contact an IHC and OHC. This composite figure has been partially redrawn and reprinted with permission from Hennig Arzneimittel GmbH & Co. KG, Wiesbaden, Germany (www.hennig-arzneimittel.de).

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Figure 2. Schematic diagram of the adult mammalian vestibular neuroepithelium. Two Type II hair cells (II), one Type I hair cell (I), three supporting cells (S.C.), afferent (Aff., red) and efferent (Eff., light blue) nerve fibres are shown. Type II hair cells are contacted by bouton terminals whereas the Type I cell's basolateral membrane is enveloped by the calyx terminal. Synaptic vesicles containing the neurotransmitter (glutamate) and the efferent neurotransmitter (acetylcholine) are also shown. Presynaptic vesicles in hair cells are shown tethered to the synaptic body (ribbon). For simplicity, only few afferent terminals are shown that face the presynaptic ribbons. The efferent synapse onto Type II hair cell is marked by a subsynaptic cistern (c.). An outer face (o.f.) synapse between the Type II hair cell and the calyx is also shown. The apical surface of hair cells is characterized by the hair bundle, whereas supporting cells have short microvilli. Only supporting cells contact the basement membrane. Below the basement membrane afferent nerve fibres become coated by the myelin sheath.

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Figure 3. Myosin-mediated mechano-transducer adaptation. In the absence of stimuli the stereocilia are in their resting position, where approximately 15% of the mechano-sensitive (MET) channels are open. For simplicity, only two stereocilia per bundle are shown. During an excitatory stimulus (gray arrow), stereocilia deflection produces an increase in tension of the rigid tip links, which pull down the MET channels. Sliding of the MET channel stretches a still unidentified elastic component (gating spring) connecting the MET channel and the myosin-1c protein. The interaction of the myosin-1c with the actin filaments inside the stereocilia is Ca2+/calmodulin-dependent. Stretching of the gating spring results in the opening of MET channels. The influx of Ca2+ ions into the stereocilia causes myosin-1c to slip down the actin cytoskeleton. This reduces tension at the gating spring and permits the MET channel closure (adaptation). As Ca2+ is removed by the stereocilia, mainly by Ca2+ pumps located in the stereocilia membrane (not shown), myosin-1c rebinds to the actin filament, although at a lower point. This interaction is able to exert sufficient tension on the gating spring to restore the normal (resting) sensitivity. At the end of the stimulus, while the hair bundle returns to its resting position, myosin-1c climbs along the actin filament to restore the normal sensitivity. This is a generally accepted model of adaptation, which is based on the assumption that the MET channels are located at the top of the tip link (e.g. on the taller stereocilia; for a review see: LeMasurier and Gillespie 2005. However, recent findings using fast Ca2+ imaging have shown that the MET channel is likely to be located at the bottom of the tip link (on the shorter stereocilia), questioning the above mechanism (Beurg et al., 2009).