| Literature DB >> 31510846 |
Ulf R Heinrich1, Irene Schmidtmann2, Regina Meuser2, Benjamin P Ernst1, Desiree Wünsch1, Svenja Siemer1, Alena Gribko1, Roland H Stauber1, Sebastian Strieth1.
Abstract
Constitutively expressed endothelial nitric oxide synthase (eNOS) is supposed to play a role in noise-induced nitric oxide (NO)-production. It is commonly known that intense noise exposure results in inducible NOS (iNOS) expression and increased NO-production, but knowledge about a contribution of the eNOS isoform is still lacking. Effects of noise exposure on eNOS immunolabeling were determined in male guinea pigs (n=24). For light microscopic analysis, 11 animals were exposed to 90 dB for 1 hr and 6 animals were used as controls. After exposure, eNOS immunostaining was performed on paraffin sections, and the staining intensities were quantified for 4 cochlear regions. For electron microscopic analysis, 2 animals were exposed for 2 hr to 90 dB and 5 animals were used as controls. The intensity of eNOS immunolabeling was found to be already comprehensively increased 1 hr after noise exposure to 90 dB. At the ultrastructural level, a clear increase in eNOS immunolabeling was found in microtubules-rich areas of cochlear cuticular structures. Hence, our findings indicate that the reticular lamina forming the endolymph-perilymph barrier at the apical side of the organ of Corti is involved in a fast intrinsic otoprotective mechanism of the cochlea.Entities:
Keywords: NO; eNOS; noise-induced hearing loss (NIHL); otoprotection; reticular lamina
Year: 2019 PMID: 31510846 PMCID: PMC6824004 DOI: 10.1369/0022155419876644
Source DB: PubMed Journal: J Histochem Cytochem ISSN: 0022-1554 Impact factor: 2.479