The cochlea outer hair cell (OHC) is a sensory hair cell that is also electromotile, that is, it converts electrical stimuli to a dynamic length change. OHC electromotility is thought to contribute to the sensitivity and sharp tuning of the mammalian cochlea and to be especially vulnerable to metabolic insult. The mature OHC is a cylindrical cell with a cortical cytoskeleton consisting of actin and spectrin but an otherwise relatively sparse internal structure. The OHC cortical cytoskeleton is thought to confer stiffness to the OHC membrane. The mechanical properties of the lateral membrane are important in determining how effectively OHC motility is communicated to the organ of Corti, the sensory organ of mammalian hearing. We show that only actin is present in the gerbil OHC cortical cytoskeleton at birth. However, spectrin is progressively incorporated in the OHC cortical cytoskeleton between post-natal day 3 (P3) and P9. We tested the contribution of spectrin to mechanical properties of OHCs by measuring the ratio of shear modulus μ to area modulus K, a key measure of membrane mechanics, in isolated developing gerbil OHCs. Length and diameter strains of OHCs in response to exposure to a hypo-osmotic solution were measured using video microscopy and the value of μ/K was calculated. In adult gerbil OHCs, μ/K was –0.050 (± 0.001, N = 37), the same as the value reported by Ratnanather et al. (J.A.S.A., 99:1025, 1996) for guinea pig OHCs. The values of μ/K obtained during development were significantly different from those of the adult, changing from 0.12 (± 0.02, N = 12) at P0, to 0.08 (± 0.01, N = 34) at P3, 0.16 (± 0.005, N = 60) at P6, and 0.04 (± 0.01, N = 36) at P12, close to the adult value. Thus, the μ/K ratio of the OHC lateral wall membrane is altered over the period in which the actin-spectrin cortical cytoskeleton is elaborated. We conclude that the addition of spectrin to the cortical cytoskeleton is a significant factor in determining the mechanical properties of the OHC lateral wall membrane. Supported by NIH (DC02053) and the Clare Booth Luce Foundation.
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