Locally produced androgens act via granulosa cell androgen receptors t
o modulate follicular responsiveness to gonadotrophins and thereby con
tribute to the paracrine regulation of ovarian function. We used quant
itative androgen receptor immunocytochemistry to assess androgen recep
tor distribution in relation to pre-ovulatory follicular development i
n the common marmoset (Callithrix jacchus), a New World primate that o
vulates two to four follicles in each similar to 28 day ovarian cycle.
Ovaries from four adult females in the late follicular phase and from
four in the luteal phase were fixed in 4% paraformaldehyde and subjec
ted to an immunocytochemical analysis using a polyclonal androgen rece
ptor antibody with detection by a standard avidin-biotin-peroxidase te
chnique for alkaline phosphatase. Specific androgen receptor immunosta
ining occurred mainly in granulosa cell nuclei, with little or no spec
ific staining in theca, stroma or oocytes. Granulosa cell androgen rec
eptor immunostaining was most abundant in healthy preantral/early antr
al follicles, being low or absent from pre-ovulatory follicles and cor
pora lutea. Differences in granulosa cell androgen receptor immunostai
ning between immature (0.1-1.0 mm diameter) and preovulatory (greater
than or equal to 2.0 mm diameter) follicles were quantified using a vi
deodensitometric analysis of grey-scale values. Readings were taken fr
om the granulosa cell layers of 53 immature follicles and 10 pre-ovula
tory follicles in late follicular phase ovaries. The average androgen
receptor level in granulosa cells of immature follicles proved to be 4
.2-fold higher (P < 0.01) than that in granulosa cells of pre-ovulator
y follicles. Because other evidence suggests that paracrine androgen a
ction in granulosa cells converts from stimulation to inhibition as fo
llicles mature, we speculate that a development-related reduction in a
ndrogen receptor numbers serves to 'protect' granulosa cells against t
he inhibitory action of androgen, thereby promoting pre-ovulatory foll
icular dominance in primate ovarian cycles.