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J Neurophysiol 97: 2930-2936, 2007. First published January 31, 2007; doi:10.1152/jn.01183.2006
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Overexpression of SK2 Channels Enhances Efferent Suppression of Cochlear Responses Without Enhancing Noise Resistance

Stéphane F. Maison1,*, Lisan L. Parker2,*, Lucy Young2, John P. Adelman3, Jian Zuo2 and M. Charles Liberman1

1Department of Otology and Laryngology, Harvard Medical School and Eaton-Peabody Laboratory, Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, 2Department of Developmental Neurobiology, St Jude Children's Research Hospital, Memphis, Tennessee, and 3The Vollum Institute, Oregon Health Sciences University, Portland, Oregon

Submitted 7 November 2006; accepted in final form 25 January 2007

Cochlear hair cells express SK2, a small-conductance Ca2+-activated K+ channel thought to act in concert with Ca2+-permeable nicotinic acetylcholine receptors (nAChRs) {alpha}9 and {alpha}10 in mediating suppressive effects of the olivocochlear efferent innervation. To probe the in vivo role of SK2 channels in hearing, we examined gene expression, cochlear function, efferent suppression, and noise vulnerability in mice overexpressing SK2 channels. Cochlear thresholds, as measured by auditory brain stem responses and otoacoustic emissions, were normal in overexpressers as was overall cochlear morphology and the size, number, and distribution of efferent terminals on outer hair cells. Cochlear expression levels of SK2 channels were elevated eightfold without striking changes in other SK channels or in the {alpha}9/{alpha}10 nAChRs. Shock-evoked efferent suppression of cochlear responses was significantly enhanced in overexpresser mice as seen previously in {alpha}9 overexpresser mice; however, in contrast to {alpha}9 overexpressers, SK2 overexpressers were not protected from acoustic injury. Results suggest that efferent-mediated cochlear protection is mediated by other downstream effects of ACh-mediated Ca2+ entry different from those involving SK2-mediated hyperpolarization and the associated reduction in outer hair cell electromotility.

Address for reprint requests and other correspondence: S. F. Maison, Massachusetts Eye and Ear Infirmary, 243 Charles St., Boston, MA 02114-3096 (E-mail: sfm{at}epl.meei.harvard.edu)




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Contextual memory deficits observed in mice overexpressing small conductance Ca2+-activated K+ type 2 (KCa2.2, SK2) channels are caused by an encoding deficit
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