ADDITIONAL FINDINGS ON HERITABILITY AND PRENATAL MASCULINIZATION OF COCHLEAR MECHANISMS - CLICK-EVOKED OTOACOUSTIC EMISSIONS

A previous demonstration of a substantial genetic contribution to the expression of spontaneous otoacoustic emissions (SOAEs) is here extend ed to an aspect of click-evoked otoacoustic emissions (CEOAEs). CEOAEs were measured in the same twins and non-twins used for the SOAE herit ability study. The stimuli were 100-mu s clicks presented at a nominal rate of 2/s; the emitted waveforms from 50 clicks were summed, and a 20-ms sample of that averaged waveform (beginning 6 ms after click pre sentation) was subjected to spectral analysis, The total power in the spectrum from 1 to 5 kHz in this temporal segment of the CEOAE wavefor m was used as the primary dependent variable. This overall power was s ignificantly greater in female and right ears than in male and left ea rs, but the difference between dark- and light-eyed subjects was not s ignificant. The overall power in the two left, and two right, ears of monozygotic co-twins was more highly correlated than in dizygotic co-t wins, and structural modeling indicated that about 65-85% of the indiv idual variation in the expression of CEOAE power could be attributed t o genes-essentially the same heritability estimate as obtained previou sly from the SOAE data. Within-subject correlations between CEOAE powe r and number of SOAEs ranged from about 0.3 to 0.7, suggesting that th ese two forms of otoacoustic emission may depend upon somewhat differe nt aspects of the same underlying mechanism and, thus, that heritabili ty estimates based on one measure are not completely redundant to thos e from the other. While the average spectral power of the CEOAEs in op posite-sex dizygotic (OSDZ) females was smaller than that in same-sex dizygotic (SSDZ) females-and thus approached the value for males-the d ifference did not achieve statistical significance. Thus, the evidence for a prenatal masculinizing effect was less definitive in these CEOA E data than in the SOAE data obtained from the same subjects. An inter pretation that accounts for both the CEOAE and SOAE results is that th e strength of the so-called cochlear amplifiers is under genetic contr ol that is to some extent mediated and/or modified through prenatal ex posure to androgens. The indicated direction of effect is that weak co chlear amplifiers result when prenatal androgen levels are high. Under this view, then, androgen levels contribute both to the sex differenc es observed in otoacoustic emissions and the prenatal masculinizing ef fects observed in opposite-sex twins, and they may be a factor in indi vidual differences in OAE expression as well. Additionally it is shown that, although the powers of the CEOAE waveforms were reasonably high ly correlated for the two ears of subjects in all groups, and across M Z co-twins, cross-correlations on the fine structures of those same pa irs of CEOAE waveforms were essentially zero-presumably owing largely to the synchronizing of (different) SOAE frequencies in the ears being compared.