Abstract

AbstractAnterior pituitaries from 17 human fetuses, 9.5 to 16.5 weeks in gestational age, were obtained to study the morphological development of gonadotropes as a function of age and sex.Routine electron microscopy alone was inadequate in determining which granulated cells produced the gonadotropins, owing to the similarities among granulated cells in the youngest fetuses as well as to the continuing differentiation of these cells. Therefore, electron‐microscopic immunocytochemistry was employed for identification of gonadotropes. LHβ and FSHβ antisera were used, and dilution and absorption tests were performed to determine the degree of cross‐reactivity with LHβ, LH, FSHβ, FSH, CGβ, and CGα. Both antisera completely cross‐reacted in parallel fashion with their respective β subunits, as well as with their respective intact hormones. Cross‐reactivity with the other absorbents was minimal, partial or nonexistent. With the LHβ antiserum, LHβ and intact LH appeared to be equipotent in absorption studies; whereas with the FSHβ antiserum, 10 times as much intact FSH was required to effect displacement as with FSHβ. These specificity studies, coupled with the failure of previous investigators (Kaplan et al., 1976a) to find free β subunits in the human fetal pituitary, suggest that staining of the granules was due to the presence of intact LH or FSH.Cells containing LH and FSH were identified immunocytochemically in the pituitaries of all the fetuses examined. Sex and age differences were qualitatively assessed. The number of cells and granules per cell stained with either LHβ or FSHβ antiserum, as well as the staining intensity with both antisera, increased as a function of fetal age. A sex difference was also evident, in that pituitaries of older females revealed more granules per cell and more cells stained with either LHβ or FSHβ antisera than those of males of comparable ages.These findings agree with the concept that the human male fetal pituitary produces less gonadotropin prior to mid‐gestation than the female gland, perhaps because of feedback inhibition by testicular testosterone secretion at this time.

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