作者: Alexander Hess , Wilhelm Bloch , Jochen Huverstuhl , Jiping Su , Eberhard Stennert
DOI: 10.1016/S0006-8993(99)01433-X
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摘要: Abstract Since NO is believed to be involved in cochlear physiology, presence of the constitutive isoforms nitric oxide synthase (NOS), and target enzyme NO, soluble guanylyl cyclase (sGC) structures mammalian cochlea have been demonstrated. To date, no reports published regarding detection inducible isoform (NOS II) cochlea. In order show capability iNOS expression tissue, a mixture proinflammatory bacterial lipopolysaccharides (LPS) tumor necrosis factor α (TNF-α) was injected into tympanic cavity guinea pigs, vs. saline-solution as control. Paraffin sections LPS/TNF-α treated saline-treated cochleae (6 h) were examined immunohistochemically with specific antibodies neuronal, endothelial NOS sGC. Initiated observed wall blood vessels spiral ligament (SL) modiolus, supporting cells organ Corti, limbus, nerve fibers part perikarya ganglion after LPS/TNFα-treatment. not detected control tissue. Expression both NOS-isoforms (endothelial neuronal NOS) sGC showed significant differences experimental groups. Endothelial eNOS bNOS co-localized cells, fibers, SL but sensory cells. Strong labeling for became evident endosteum cochlea, while endothelium epithelium limbus only could labeled. SL, limbus-epithelium. While small amounts generated by eNOS, seem support flow auditory function well neurotransmission, high iNOS-generated dysregulative neurotoxic effects on inner ear during viral infections middle ear.