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Distribution and hormonal regulation of androgen receptor immunoreactivity in the forebrain of the male European ferret
Author(s) -
Kashon Michael L.,
Arbogast Jonathan A.,
Sisk Cheryl L.
Publication year - 1996
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19961223)376:4<567::aid-cne6>3.0.co;2-#
Subject(s) - stria terminalis , endocrinology , medicine , androgen receptor , biology , forebrain , androgen , castration , testosterone (patch) , preoptic area , hypothalamus , estrogen , hormone , central nervous system , prostate cancer , cancer
The distribution and hormonal regulation of androgen‐receptor‐immunoreactive (AR‐ir) cells in the male European ferret forebrain were examined. AR‐ir cells were found in many limbic and hypothalamic structures, and their distribution was similar to that reported for cells that either bind androgen or contain AR protein or mRNA in other species. Regulation of brain AR immunoreactivity by gonadal steroids was brain‐region dependent. In most regions examined, including the preoptic area, amygdala, and several hypothalamic nuclei, castration reduced the density of AR‐ir profiles and the intensity of immunocytochemical staining, and long‐term (days) androgen, but not estrogen, replacement restored these parameters of AR immunoreactivity. Other areas, such as the bed nucleus of the stria terminalis, appeared to be relatively resistant to modulation of AR immunoreactivity by castration and long‐term androgen treatment. The ability of testosterone to increase AR‐ir profile density is not a simple consequence of translocation of AR from the cytoplasm to the nucleus, because short‐term (hours) treatment with testosterone did not result in an increase in AR‐ir profile density equivalent to that seen after 10 days of testosterone treatment. Thus, androgens appear to be able to increase AR levels within certain brain cell groups, thereby altering target tissue responsiveness to their own action. © 1996 Wiley‐Liss, Inc.