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Journal of Neuroscience, Vol 12, 800-809, Copyright © 1992 by Society for Neuroscience
Cholinergic inhibition of short (outer) hair cells of the chick's cochlea
PA Fuchs and BW Murrow
Department of Physiology, University of Colorado School of Medicine, Denver 80262.
Cochlear hair cells are thought to be inhibited by the release of ACh from
efferent neurons. Several studies have implicated Ca2+ as a postsynaptic
intermediary in hair cell inhibition, but its role remains unproven. We
have made whole-cell, tight-seal recordings from single short hair cells
(the avian analog of outer hair cells in the mammalian cochlea), isolated
from the chick's cochlea, to determine the mechanism of cholinergic
inhibition. These cells hyperpolarized upon exposure to ACh, although a
brief depolarization preceded the much larger, longer- lasting
hyperpolarization. In voltage clamp ACh evoked an outward current that
reversed in sign near the K+ equilibrium potential. A small, transient
inward current preceded the predominant outward current. The ACh-evoked K+
current depended on Ca2+ in the external saline, or could be prevented when
the cell was dialyzed with the rapid Ca2+ buffer BAPTA. In BAPTA-loaded
cells a residual inward current was seen. This activated with very little
delay upon exposure of the cell to ACh and reversed near 0 mV membrane
potential. Thus, the hair cell ACh receptor appears to be a nonspecific
cation channel through which Ca2+ enters and triggers the opening of nearby
Ca(2+)-activated K+ channels. However, the ACh-evoked K+ channels are not
the same as the "maxi" K+ channels activated by Ca2+ influx through
voltage-gated Ca2+ channels in these same cells.
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