ABSTRACT
Gap junction channels which are responsible for direct intercellular communication are composed of connexin proteins. Different connexins are distributed in a tissue-specific manner. Up to now only connexin26 has been identified to be widely expressed in the inner ear. In order to investigate the role of additional gap junction proteins, the expression of connexin30 and 43 was investigated in the rat cochlea. Connexin26 and connexin30 were both expressed in the spiral limbus, the spiral ligament, the stria vascularis and between supporting cells of the organ of Corti. Double-labeling experiments suggest that both connexins are partly colocalized between cells. Weak staining of connexin43 could only be detected in the stria vascularis, the spiral ligament and between organ of Corti supporting cells. The corresponding transcripts for connexin26, 30 and 43 could be detected by Northern blot analysis. The expression of different gap junction channels in the cochlea suggests functional diversity. Gap junctions in the inner ear may control ion concentrations of cochlear fluids or act as conduits through which glucose and other metabolites diffuse.
Subject(s)
Cochlea/metabolism , Connexins/biosynthesis , Animals , Cochlea/chemistry , Connexin 26 , Connexin 30 , Gap Junctions/chemistry , Gap Junctions/metabolism , Immunohistochemistry , Ligaments/chemistry , Ligaments/metabolism , Nerve Tissue Proteins/biosynthesis , Rats , Rats, Wistar , Stria Vascularis/chemistry , Stria Vascularis/metabolismABSTRACT
11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyzes the transformation of active glucocorticoid (GC) steroids to inactive 11-oxosteroids, as well as the reverse reaction. 11 beta-HSD was previously demonstrated specifically in the spiral ligament of the lateral cochlear wall where it was co-localized with adrenal steroid receptors. These findings imply that 11 beta-HSD regulates binding of corticoids to their inner ear receptors. The GC receptor expression initially occurs around the critical maturation period of the cochlear duct. 11 beta-HSD, which is an integral part of the cochlear steroid receptor system, could indirectly affect glucocorticoid-mediated induction processes. In this study the expression of 11 beta-HSD was studied in the postnatal rat cochlea from the 3rd to 30th postnatal day. Bouin's fixed, paraffin-embedded cochlear sections were processed for immunocytochemical detection of 11 beta-HSD using polyclonal antibodies against 11 beta-HSD. 11 beta-HSD expression appeared at the 12th postnatal day at low levels in spiral ligament tissues. From the 15th postnatal day, 11 beta-HSD expression was stronger and similar to that of the adult cochlea. No additional inner ear tissue region expressed 11 beta-HSD enzyme during the observed period. 11 beta-HSD expression coincides with the onset of functional maturity of the rat cochlear duct. The expression of 11 beta-HSD is preceded by the expression of GC receptors which appeared at the 7th postnatal day in the rat cochlea. These results further suggest an integrative role of the cochlear steroid receptor system in the homeostasis and functional maturation of the cochlea.
