Changes in MAP2 and tyrosinated α-tubulin expression in cochlear inner hair cells after amikacin treatment in the rat

The expression of MAP2 (microtubule-associated protein 2) and of tyrosinated alpha-tubulin was investigated immunocytochemically in the cochleas of normal and amikacin-treated rats. For MAP2, two different antibodies were used: anti-MAP2ab, against the high molecular weight forms, and anti-MAP2abc, additionally against the embryonic form c. In the cochlea of the normal rat, the outer (OHCs) and inner (IHCs) hair cells were labeled for MAP2abc. The labeling was weaker in IHCs than in OHCs. The hair cells were rarely labeled for MAPab. Both OHCs and IHCs were labeled for tyrosinated alpha-tubulin. In the cochlea of the amikacin-treated rat, aggregates of anti-MAP2abc and anti-tyrosinated alpha-tubulin antibodies were seen in the apical region of the IHCs as early as the end of the antibiotic treatment. In rats investigated during the following week, the cell body of most of the surviving IHCs were not labeled for MAP2abc and tyrosinated alpha-tubulin. Then, labeling for these two antibodies reappeared in the surviving IHCs, including their giant stereocilia. Fewer surviving IHCs were labeled for tyrosinated alpha-tubulin than for MAP2abc. The amikacin-poisoned IHCs were rarely labeled for MAP2ab. These results suggest that cochlear hair cells essentially express form c of MAP2. In the amikacin-damaged cochlea, the apical aggregation of MAP2c and tyrosinated alpha-tubulin within the poisoned IHCs could be implicated in a cell degenerative process. By contrast, the extinction and recovery of MAP2c and tyrosinated alpha-tubulin labeling in the remaining IHCs suggest the occurrence of a limited repair process. A possible role of MAP2 and tubulin in hair cell survival is discussed.