{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T11:15:48Z","timestamp":1791112548950,"version":"4.1.0"},"reference-count":68,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2007,9,19]],"date-time":"2007-09-19T00:00:00Z","timestamp":1190160000000},"content-version":"vor","delay-in-days":18,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,9]]},"abstract":"<jats:p>Voltage\u2010gated calcium channels support both spontaneous and sound\u2010evoked neurotransmitter release from ribbon synapses of cochlear hair cells. A variety of regulatory mechanisms must cooperate to ensure the appropriate level of activity in the restricted pool of synaptic calcium channels (\u223c100) available to each synaptic ribbon. One potential feedback mechanism, calcium\u2010dependent inactivation (CDI) of voltage\u2010gated, L\u2010type calcium channels, can be modulated by calmodulin\u2010like calcium\u2010binding proteins. CDI of voltage\u2010gated calcium current was studied in hair cells of the chicken's basilar papilla (analogous to the mammalian cochlea) after blocking the predominant potassium conductances. For inactivating currents produced by 2.5 s steps to the peak of the current\u2013voltage relation (1 m<jats:sc>m<\/jats:sc> EGTA internal calcium buffer), single exponential fits yielded an average decay time constant of 1.92 \u00b1 0.18 s (mean \u00b1<jats:sc>s.e.m.<\/jats:sc>, <jats:italic>n<\/jats:italic>= 12) at 20\u201322\u00b0C, while recovery occurred with a half\u2010time of \u223c10 s. Inactivation produced no change in reversal potential, arguing that the observed relaxation did not result from alternative processes such as calcium accumulation or activation of residual potassium currents. Substitution of external calcium with barium greatly reduced inactivation, while inhibition of endoplasmic calcium pumps with t\u2010benzohydroquinone (BHQ) or thapsigargin made inactivation occur faster and to a greater extent. Raising external calcium 10\u2010fold (from 2 to 20 m<jats:sc>m<\/jats:sc>) increased peak current 3\u2010fold, but did not alter the extent or time course of CDI. However, increasing levels of internal calcium buffer consistently reduced the rate and extent of inactivation. With 1 m<jats:sc>m<\/jats:sc> EGTA buffering and in 2 m<jats:sc>m<\/jats:sc> external calcium, the available pool of calcium channels was half\u2010inactivated near the resting membrane potential (\u221250 mV). CDI may be further regulated by calmodulin\u2010like calcium\u2010binding proteins (CaBPs). mRNAs for several CaBPs are expressed in chicken cochlear tissue, and antibodies to CaBP4 label hair cells, but not supporting cells, equivalent to the pattern seen in mammalian cochlea. Thus, molecular mechanisms that underlie CDI appeared to be conserved across vertebrate species, may provide a means to adjust calcium channel open probability, and could serve to maintain the set\u2010point for spontaneous release from the ribbon synapse.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.135582","type":"journal-article","created":{"date-parts":[[2007,7,27]],"date-time":"2007-07-27T00:30:00Z","timestamp":1185496200000},"page":"909-922","source":"Crossref","is-referenced-by-count":23,"title":["Calcium\u2010dependent inactivation of calcium channels in cochlear hair cells of the 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