内リンパ水腫とNa⁺-K⁺-2Cl^-共輸送体

―モルモット蝸牛の免疫組織化学的検討―

抄録

Na⁺-K⁺-2Cl^- cotransporter 1 (NKCC1) and c-Jun N-terminal kinase (JNK) were immunohistochemically studied in guinea pig cochlea following the induction of endolymphatic hydrops by blocking the endolymphatic duct. Postoperative survivals were set to 1 day (n=3), 3 days (n=4), 1 week (n=3), 2 weeks (n=4), 1 month (n=4) and 3 months (n=4). The most striking finding was an increase in the immunoreactivity for NKCC1 at type 1 fibrocytes of the spiral ligament throughout the survival times. This suggests that the affected cells shrink as the result of surgical intervention and upregulate NKCC1 to restore the volume of the cells. The shrinkage of type 1 fibrocytes should reduce gap junctional connectivity among cells of the ligament, which could reduce K⁺ supply into the stria vascularis and disturb ionic homeostasis in the endolymph. On the other hand, JNK, which has been reported to activate NKCC1 by phosphorylation, showed a consistent decrease in immunoreactivity in the types 1 and 2 fibrocytes in hydropic ears, indicating that JNK does not play an important role in the activation of NKCC1 in the cochlea.
The findings in the present study suggested that endolymphatic homeostasis depends on cell integrity within the spiral ligament and that NKCC1 in type 1 fibrocytes is crucial in maintaining cochlear fluid homeostasis.