Lack of feminization of the cremaster nucleus in cryptorchid androgen insensitive rats.

Androgens may control rat testicular descent via effects on the genitofemoral nerve or cranial gonadal ligaments. Androgen-mediated release of calcitonin gene-related peptide from the genito-femoral nerve (whose motoneuron cell bodies reside in the sexually dimorphic cremaster nucleus) may stimulate cremaster sac formation and testicular descent. Alternatively, androgens may cause regression of cranial gonadal ligaments and thereby allow the testes to descend. To evaluate these theories testicular position, and the cremaster sac and nucleus were studied in Tfm (androgen insensitive) rats. Testes were abdominal, inguinal and scrotal in 20%, 67% and 13% of Tfm male rats, respectively, and cranial ligaments were present in all cases. Mean cremaster nucleus motoneuron number was lower in female rats (70 +/- 14) but not significantly different between normal male (256 +/- 44) and Tfm male (231 +/- 42) rats, and it correlated poorly with testicular position. Calcitonin gene-related peptide immunoreactivity was rarely observed in cremaster motoneurons. These data suggest that the cremaster nucleus is not androgen-dependent, calcitonin gene-related peptide release from cremaster motoneurons is not the likely mechanism of testicular descent and persistent cranial ligaments may cause cryptorchidism in the Tfm rat.