Abstract
The key auditory signature that may associate peripheral hearing with central auditory cognitive defects remains elusive. Suggesting the involvement of stress receptors, we here deleted the mineralocorticoid and glucocorticoid receptors (MR and GR) using a CaMKIIα-based tamoxifen-inducible CreERT2/loxP approach to generate mice with single or double deletion of central but not cochlear MR and GR. Hearing thresholds of MRGRCaMKIIαCreERT2 conditional knockouts (cKO) were unchanged, whereas auditory nerve fiber (ANF) responses were larger and faster and auditory steady state responses were improved. Subsequent analysis of single MR or GR cKO revealed discrete roles for both, central MR and GR on cochlear functions. Limbic MR deletion reduced inner hair cell (IHC) ribbon numbers and ANF responses. In contrast, GR deletion shortened the latency and improved the synchronization to amplitude-modulated tones without affecting IHC ribbon numbers. These findings imply that stress hormone-dependent functions of central MR/GR contribute to "precognitive" sound processing in the cochlea.