Androgen and Estrogen Receptors in Fetal Rhesus Monkey Brain and Anterior Pituitary*

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Abstract
Cytosolic androgen and estrogen receptors in the brain and anterior pituitary gland (AP) of fetal rhesus monkeys [Macaca mulatta] were identified and characterized using the technique of DNA-cellulsoe chromatography. Cytosolic extracts were prepared from fetal monkey (days 135-162 of gestation) tissues including hypothalamus-preoptic area/amygdala (HPOA/AMG), cerebral cortex, and AP. Extracts were incubated with [3H]testosterone, [3H]5.alpha.-dihydrotestosterone, or [3H] 17.beta.-estradiol and applied to DNA-cellulose columns. [3H]Androgen- and [3H]estrogen-binding activities from cytosolic extracts adhered to DNA-cellulose. After elution with a linear salt gradient (10-500 mM NaCl) [3H]androgen-binding activity exhibited elution maxima between 130-150 mM NaCl, while [3H] estrogen-binding activity exhibited elution maxima between 200-220 mM NaCl. These elution patterns were similar in every region examined and were characteristic of putative androgen and estrogen receptors found in other vertebrate species. Additional experiments established the high affinity-low capacity nature of both androgen- and estrogen-binding activities, as well as their inhibition by known competitors of receptor binding. Estimates of binding activity of ligand concentrations that approximated saturation suggested that the concentration (mol specific bound/mg cytosolic protein) of both androgen and estrogen receptor were highest in the AP, intermediate in the HPOA/AMG, and lowest in the cerebral cortex. Comparisons of androgen- and estrogen-binding activities revealed that in the AP, apparent concentrations of the estrogen receptor exceeded those of androgen. Androgen and estrogen receptor concentrations were roughly equivalent in the HPOA/AMG, whereas, in the cerebral cortex, androgen receptor concentration was greater than estrogen. Evidently in the fetal primate brain and AP, distinct androgen and estrogen receptors are present which might mediate the action of gonadal steroids on sexual differentiation.