electromotility

e·lec·tro·mo·til·ity

(ē-lek'trō-mō-til'i-tē),
The motility of the cochlear outer hair cells in response to electrical stimulation.
Farlex Partner Medical Dictionary © Farlex 2012

e·lec·tro·mo·til·i·ty

(ĕ-lek'trō-mō-til'i-tē)
The motility of the auditory outer hair cells in response to electrical stimulation.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
References in periodicals archive ?
The mechanoelectrical transduction (MET), electromotility, and synapse transmission are fundamental functions of HCs and are critical for normal hearing [10].
In OHCs, NLC and electromotility are typically coupled [20, 23].
In healthy subjects, acetylcholine (ACh), the primary neurotransmitter of the efferent auditory system, has been found to enhance the electromotility of outer hair cells (OHC) binding to acetylcholine receptors (AChRs), which are localized on the postsynaptic membrane of OHC [113].
In patients with MG, autoantibodies against AChRs were reported to bind with AChRs on OHCs, inducing a progressive loss of AChRs that decreases OHC electromotility [114].
This electromotility, thought to be the basis of cochlear amplification, is mediated by a voltage sensitive motor molecule recently identified as the membrane protein prestin.
Although electromotility is not directly dependent on ATP or other chemical intermediates [3, 4], these rapid changes in body length must consume a great deal of energy.
How glucose is transported across the three membrane structures, whether they participate in energy transport, and whether glucose transporters are related to electromotility are unknown.
By hyperpolarizing the OHCs, the MOC efferents inhibit the electromotility of the OHCs, thereby reducing the gain of the cochlear amplifier, which manifests as a reduction in the DPOAEs.
These shape changes, termed electromotility, are assumed to be part of the mechanical feedback process that amplifies low-level sound [7, 9].
The electromotility of OHCs contributes significantly to the cochlear response.
LePage, "Transitory endolymph leakage induced hearing loss and tinnitus: depolarization, biphasic shortening and loss of electromotility of outer hair cells," European Archives of Oto-Rhino-Laryngology, vol.
In the cochlea, salicylate competitively binds to prestin in outer hair cells (OHC); this attenuates OHC electromotility, distortion product otoacoustic emissions (DPOAE), and the cochlear compound action potential (CAP) and contributes to SS-induced hearing loss [2, 8,9].