Schweitzer L, Casseday J H, Sjoerdsma A, McCann P P, Bartolome J V
Brain Res Bull. 1986 Feb;16(2):215-8. doi: 10.1016/0361-9230(86)90035-3.
The occurrence of reversible hearing loss in patients treated with the polyamine biosynthesis inhibitor, alpha-difluoromethylornithine (DFMO), led to the hypothesis that this functional hearing deficit might be due to polyamine depletion in the cochlea. To test this hypothesis the polyamine content (putrescine, spermidine and spermine) of the cochleas of normal rats was measured and compared to that of DFMO-treated rats. For the first time, it was demonstrated that in the cochleas of normal rats there were substantial amounts of spermidine and spermine but no detectable putrescine. There was also no measurable ornithine decarboxylase. The DFMO treatments employed in this study were not effective, however, in depleting the cochlear polyamines to levels generally considered critical for disrupting polyamine-dependent processes in other systems. Thus, it is not surprising that auditory thresholds, which were evaluated using brainstem evoked potentials, remained unaltered in the DFMO-treated rats. Demonstration of a role for polyamines in hearing awaits further investigation with the use of more potent inhibitors or other model systems for hearing.
