ASA 128th Meeting - Austin, Texas - 1994 Nov 28 .. Dec 02

2pPP4. Evidence for heritability and prenatal masculinization of cochlear mechanisms from measures of otoacoustic emissions.

Dennis McFadden

John C. Loehlin

Dept. of Psychol. and Inst. for Neurosci., Mezes Hall 330, Univ. of Texas, Austin, TX 78712

Spontaneous and click-evoked otoacoustic emissions (SOAEs and CEOAEs) were measured in twin pairs of various sorts---monozygotic (MZ), same-sex dizygotic (SSDZ), and opposite-sex dizygotic (OSDZ)---as well as in nontwins. Comparison of the number of SOAEs exhibited by MZ and SSDZ twin pairs previously led to the conclusion that about 75% of the individual variation in SOAE expression can be attributed to genes. Parallel calculations will be shown for the CEOAE data. In accord with past surveys, females generally exhibited more SOAEs than males; however, OSDZ females exhibited, on average, less than half as many SOAEs as other females, and thus were comparable to males on this measure. Similarly, the strength of the CEOAEs was generally greater in females than in males, but not in OSDZ females. The interpretation is that the cochleas of OSDZ females have been masculinized by exposure to the high levels of androgens produced prenatally by their male co-twins. (Prenatal masculinizing effects are well known in other mammals.) If correct, the genes apparently lay a groundwork for the expression of emissions---and, correspondingly, good hearing sensitivity---and prenatal exposure to androgens operates to reduce both emission strength and sensitivity. [Work supported by NIDCD.]