title: Enhanced cochlear acoustic sensitivity and susceptibility to endotoxin are induced by adrenalectomy and reversed by corticosterone supplementation in rat.
abstract: Glucocorticoid receptors are widely distributed in the cochlea but their role remains poorly known. Previous studies provided contradictory reports on a possible cochlear acoustic hypersensitivity induced by adrenal insufficiency, while several experiments agree on a significant action of glucocorticoid receptors in adverse conditions such as acoustic trauma and restraint stress. The present experiments confirmed a cochlear acoustic hypersensitivity induced by adrenalectomy and reversed by corticosterone supplementation. These observations point to a significant role of corticosteroids in basal cochlear functioning. The glucocorticoids are known to be essential for limiting and resolving inflammatory processes. The endotoxin Escherichia coli lipopolysaccharide is widely used to induce inflammatory reactions. However, in various organs several toxic processes of this endotoxin are not influenced by glucocorticoids. From previous experiments on the cochlea there is no evidence that glucocorticoids are an essential factor against endotoxin cochlear toxicity. In the present experiments it was found that adrenalectomy greatly increased the cochlear susceptibility to endotoxin; the effect was reversed by providing corticosterone supplementation. This shows the essential role of corticosterone in this cochlear inflammation model. In previous studies local administration (at the cochlear base) of endotoxin was used and losses of cochlear acoustic sensitivity were found predominantly at high frequencies; in contrast, the systemic injection used in this study produced a cochlear loss of acoustic sensitivity at all frequencies, indicating a uniform cochlear sensitivity to the toxic effects of endotoxin.
authors.affiliation: Inserm EPI9902, Faculté de Médecine Marseille Nord, Boulevard P Dramard 13916 Marseille Cedex 20, France.
authors.forename: Philippe
authors.initials: P
authors.lastname: Siaud
authors.forename: Daniel
authors.initials: D
authors.lastname: Maurel
authors.forename: Michel
authors.initials: M
authors.lastname: Lucciano
authors.forename: Erzebet
authors.initials: E
authors.lastname: Kosa
authors.forename: Yves
authors.initials: Y
authors.lastname: Cazals
mesh_terms: D000161:Acoustic Stimulation / Q000379:methods; D000315:Adrenalectomy; D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage* / Q000097:blood; D001309:Auditory Threshold / Q000187:drug effects; D001522:Behavior, Animal; D003051:Cochlea / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D015834:Cochlear Diseases / Q000139:chemically induced / Q000178:diet therapy*; D003345:Corticosterone / Q000008:administration & dosage* / Q000097:blood; D004307:Dose-Response Relationship, Radiation; D004731:Endotoxins / Q000633:toxicity*; D007249:Inflammation / Q000139:chemically induced / Q000178:diet therapy; D008070:Lipopolysaccharides; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000893:Anti-Inflammatory Agents; D004731:Endotoxins; D008070:Lipopolysaccharides; D003345:Corticosterone