L-type CaV1.2 deletion in the cochlea but not in the brainstem reduces noise vulnerability: implication for CaV1.2-mediated control of cochlear BDNF expression.

Zuccotti, Annalisa; Lee, Sze C; Campanelli, Dario; Singer, Wibke; Satheesh, Somisetty V; Patriarchi, Tommaso; Geisler, Hyun-Soon; Köpschall, Iris; Rohbock, Karin; Nothwang, Hans G; Hu, Jing; Hell, Johannes W; Schimmang, Thomas; Rüttiger, Lukas; Knipper, Marlies

Zuccotti, Annalisa; Lee, Sze C; Campanelli, Dario; Singer, Wibke; Satheesh, Somisetty V; Patriarchi, Tommaso; Geisler, Hyun-Soon; Köpschall, Iris; Rohbock, Karin; Nothwang, Hans G; Hu, Jing; Hell, Johannes W; Schimmang, Thomas; Rüttiger, Lukas; Knipper, Marlies.

Afiliação

Zuccotti A; Molecular Physiology of Hearing, Hearing Research Center Tübingen, Department of Otolaryngology, University of Tübingen Tübingen, Germany.

Front Mol Neurosci ; 6: 20, 2013.

Article em En | MEDLINE | ID: mdl-23950737

Palavras-chave

ABR; BDNF; CaV1.2; L-VGCCs; SOC; inner ear

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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Front Mol Neurosci Ano de publicação: 2013 Tipo de documento: Article País de afiliação: Alemanha

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