Journal of Neuroscience, Vol 3, 933-941, Copyright © 1983 by Society for Neuroscience
A regional analysis of estrogen binding to hypothalamic cell nuclei in relation to masculinization and defeminization
EJ Nordeen and P Yahr
Gonadal steroids masculinize and defeminize neuroendocrine development,
including behavior. Defeminization makes males less sensitive than females
to estrogen for showing female sexual behavior and cyclic gonadotropin
secretion. Masculinization makes males more sensitive than females to
estrogen for showing male sexual behavior. Thus masculinization and
defeminization produce opposite effects on estrogen sensitivity. To study
the relationship between estrogen sensitivity and estrogen binding, we
studied sex differences in estrogen binding to hypothalamic cell nuclei on
a regional and temporal basis. We measured the amount of estradiol (E2)
bound to cell nuclei in the preoptic area (POA), mediobasal hypothalamus
(MBH), corticomedial amygdala, and cortex of gonadectomized male and female
rats 30 and 60 min after [3H]E2 was injected intravenously. In the MBH,
males consistently bound less E2 than females did. In the POA, males bound
less E2 than females after 60 min, but they bound more E2 than females
after 30 min. Decreased estrogen binding in the MBH may underlie
defeminized sexual behavior. Similarly, decreased estrogen binding in the
POA at 60 min may be a correlate of defeminized gonadotropin secretion,
whereas increased estrogen binding in the POA at 30 min may be a correlate
of masculinized sexual behavior. To test the hypothesis that decreased
estrogen binding in the MBH and POA are correlates of defeminization, we
measured E2 binding at 60 min in female rats in which masculinization and
defeminization were manipulated independently. Defeminization decreased E2
binding to cell nuclei in both the POA and MBH to the level seen in males
at this time point. Masculinization had no effect at this time point. The
data suggest that sex differences in E2 binding to hypothalamic cell nuclei
correlate reliably with sex differences in estrogen sensitivity even though
masculinization and defeminization produce opposing effects on these
parameters.