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The Journal of Neuroscience, December 8, 2004, 24(49):11160-11164; doi:10.1523/JNEUROSCI.3674-04.2004
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A "Synaptoplasmic Cistern" Mediates Rapid Inhibition of Cochlear Hair Cells
Maria Lioudyno,1
Hakim Hiel,1
Jee-Hyun Kong,2
Eleonora Katz,3
Erik Waldman,1
Suchitra Parameshwaran-Iyer,1
Elisabeth Glowatzki,1 and
Paul A. Fuchs1
1The Cochlear Neurotransmission Laboratory, Center for Hearing and Balance, Department of Otolaryngology-Head and Neck Surgery, and 2Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2195, and 3Instituto de Investigaciones en Ingenieria Genetica y Biologia Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas, Universidad de Buenos Aires, Buenos Aires 1428, Argentina
Cochlear hair cells are inhibited by cholinergic efferent neurons. The acetylcholine (ACh) receptor of the hair cell is a ligand-gated cation channel through which calcium enters to activate potassium channels and hyperpolarize the cell. It has been proposed that calcium-induced calcium release (CICR) from a near-membrane postsynaptic store supplements this process. Here, we demonstrate expression of type I ryanodine receptors in outer hair cells in the apical turn of the rat cochlea. Consistent with this finding, ryanodine and other store-active compounds alter the amplitude of transient currents produced by synaptic release of ACh, as well as the response of the hair cell to exogenous ACh. Like the sarcoplasmic reticulum of muscle, the "synaptoplasmic" cistern of the hair cell efficiently couples synaptic input to CICR.
Key words: acetylcholine; calcium; cochlea; hair cell; inhibition; nicotinic
Received Sep 6, 2004;
revised November 5, 2004;
accepted November 5, 2004.
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