title: Sound conditioning protects hearing by activating the hypothalamic-pituitary-adrenal axis.
abstract: Sound conditioning primes the auditory system to low levels of acoustic stimuli and reduces damage caused by a subsequent acoustic trauma. This priming activates the HPA axis resulting in the elevation of plasma corticosterone with a consequent upregulation of glucocorticoid receptors (GR) in the cochlea and the paraventricular nucleus (PVN) of the hypothalamus in the mouse. This protective effect is blocked by adrenalectomy or pharmacological treatment with RU486 + metyrapone. Sound conditioning prevents GR down-regulation induced by acoustic trauma and subsequently enhances GR activity in spiral ganglion neurons. Increased SRC-1 expression, triggered by sound conditioning, positively correlates with the upregulation of GR in the cochlea. These findings will help to define the cellular mechanisms responsible for protecting the auditory system from hearing loss by sound conditioning.
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institute, 171 77 Stockholm, Sweden.
authors.forename: Yeasmin
authors.initials: Y
authors.lastname: Tahera
authors.forename: Inna
authors.initials: I
authors.lastname: Meltser
authors.forename: Peter
authors.initials: P
authors.lastname: Johansson
authors.forename: Hazim
authors.initials: H
authors.lastname: Salman
authors.forename: Barbara
authors.initials: B
authors.lastname: Canlon
mesh_terms: D000161:Acoustic Stimulation; D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D015153:Blotting, Western; D003051:Cochlea / Q000503:physiopathology; D003213:Conditioning, Psychological / Q000502:physiology*; D003345:Corticosterone / Q000097:blood; D004791:Enzyme Inhibitors / Q000494:pharmacology; D016057:Evoked Potentials, Auditory, Brain Stem / Q000502:physiology; D005938:Glucocorticoids / Q000037:antagonists & inhibitors / Q000502:physiology; D006309:Hearing / Q000502:physiology*; D006317:Hearing Loss, Noise-Induced / Q000503:physiopathology*; D051548:Histone Acetyltransferases / Q000096:biosynthesis / Q000235:genetics; D006727:Hormone Antagonists / Q000494:pharmacology; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D007150:Immunohistochemistry; D008297:Male; D008797:Metyrapone / Q000494:pharmacology; D051379:Mice; D008808:Mice, Inbred CBA; D009474:Neurons / Q000378:metabolism; D056920:Nuclear Receptor Coactivator 1; D010286:Paraventricular Hypothalamic Nucleus / Q000166:cytology / Q000378:metabolism; D010913:Pituitary-Adrenal System / Q000502:physiology*; D011965:Receptors, Glucocorticoid / Q000096:biosynthesis; D015398:Signal Transduction / Q000502:physiology; D013136:Spiral Ganglion / Q000187:drug effects / Q000473:pathology; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics
chemical_list: D004791:Enzyme Inhibitors; D005938:Glucocorticoids; D006727:Hormone Antagonists; D011965:Receptors, Glucocorticoid; D014157:Transcription Factors; D000324:Adrenocorticotropic Hormone; D051548:Histone Acetyltransferases; C538861:Ncoa1 protein, mouse; D056920:Nuclear Receptor Coactivator 1; D003345:Corticosterone; D008797:Metyrapone