PT  - JOURNAL ARTICLE
AU  - A. J. Ricci
AU  - Y-C. Wu
AU  - R. Fettiplace
TI  - The Endogenous Calcium Buffer and the Time Course of Transducer Adaptation in Auditory Hair Cells
AID  - 10.1523/JNEUROSCI.18-20-08261.1998
DP  - 1998 Oct 15
TA  - The Journal of Neuroscience
PG  - 8261--8277
VI  - 18
IP  - 20
4099  - http://www.jneurosci.org/content/18/20/8261.short
4100  - http://www.jneurosci.org/content/18/20/8261.full
SO  - J. Neurosci.1998 Oct 15; 18
AB  - Mechanoelectrical transducer currents in turtle auditory hair cells adapt to maintained stimuli via a Ca2+-dependent mechanism that is sensitive to the level of internal calcium buffer. We have used the properties of transducer adaptation to compare the effects of exogenous calcium buffers in the patch electrode solution with those of the endogenous buffer assayed with perforated-patch recording. The endogenous buffer of the hair bundle was equivalent to 0.1–0.4 mm BAPTA and, in a majority of cells, supported adaptation in an external Ca2+concentration of 70 μm similar to that in turtle endolymph. The endogenous buffer had a higher effective concentration, and the adaptation time constant was faster in cells at the high-frequency end than at the low-frequency end of the cochlea. Experiments using buffers with different Ca2+-binding rates or dissociation constants indicated that the speed of adaptation and the resting open probability of the transducer channels could be differentially regulated and imply that the endogenous buffer must be a fast, high-affinity buffer. In some hair cells, the transducer current did not decay exponentially during a sustained stimulus but displayed damped oscillations at a frequency (58–230 Hz) that depended on external Ca2+ concentration. The gradient in adaptation time constant and the tuned transducer current at physiological levels of calcium buffer and external Ca2+ suggest that transducer adaptation may contribute to hair cell frequency selectivity. The results are discussed in terms of feedback regulation of transducer channels mediated by Ca2+ binding at two intracellular sites.