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. Author manuscript; available in PMC: 2023 Sep 15.
Published in final edited form as: Hear Res. 2021 Nov 11;423:108376. doi: 10.1016/j.heares.2021.108376

Fig. 5. A hypothetical electromotility mechanism driven by turgor pressure and voltage-dependent OHC axial stiffness.

Fig. 5.

(A) Voltage-dependent OHC axial stiffness, kv, deduced from the NLC parameters of WT (black) and C1/499 compound heterozygotes (magenta). In this model, OHC electromotility is driven by turgor pressure, P (indicated by red arrow heads) and a prestin-associated voltage-dependent change in the axial stiffness (Δkv). OHC contraction or elongation (Δd) is expressed as Δd = P/ΔkV. Circumferential inflation of an OHC due to positive turgor pressure with reduced axial stiffness is exaggerated for clarity. Note that this model is mathematically similar to the widely accepted prestin area motor-based electromotility mechanism (F = kV × Δd). (B) Schematic representations of the OHC lateral membrane with prestin-associated unitary voltage-dependent stiffness, k. n1 and n2 indicate the numbers of unitary stiffness components connected in series and in parallel, respectively. On the right, the total number of the unitary stiffness components is only 25% of those on the left, yet the overall stiffness, kall, remains unchanged.