|Budget Amount *help
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2009: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
To elucidate the pathogenesis of viral infection-induced hearing loss, cytomegalovirus (CMV) was inoculated into the neonatal BALB/c mice. Additional intracranial lipopolysaccharide administration brought effective CMV propagation into the inner ear organa, such as stria vascularis and stria ligament, which played an important role for electrolyte balance homeostasis and high-voltage state of the endolymphatic duct. The number of CMV antigen-positive cells transiently peaked at 7 to 10 days after infection, followed by gradual decrease and loss within 28 days after infection. The broad expressions of KvLQT1, a potassium channel in the stria vascularis, and carbonic anhydrase II in the stria ligament were constitutively observed from the early developmental stage. Whereas, Na^+, K^+-ATPase, Kir4.1, connexin 26 and connexin 30 were focally and weakly expressed at first, then were up-regulated and spread, according to the hearing development, in the control group analysis. However, in the CMV-infected group, the maturation of some ion transporter molecules was inhibited even after the disappearing of the CMV antigens. Hypoplasia of the stria vascularis and stria ligament was also noted in the 28 days after CMV-infected mice. These findings suggested that CMV infection in the developing inner ear indirectly caused functional disability of the organ of Corti, mediated by the continuous electrolyte imbalance of the endolymphatic duct, and resulted in the hypoplasia of the auditory neural circuit formation, leading progressive hearing disabilities.