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Androgenic Regulation of Androgen Receptor Immunoreactivityin Motoneurons of the Spinal Nucleus of the Bulbocavernosusof Male Rats
Author(s) -
Matsumoto Akira,
Arai Yasumasa,
Prins Gail S.
Publication year - 1996
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1996.04899.x
Subject(s) - endocrinology , medicine , castration , testosterone propionate , androgen receptor , androgen , immunostaining , nucleus , bulbocavernosus reflex , testosterone (patch) , immunohistochemistry , biology , cytoplasm , chemistry , hormone , neuroscience , microbiology and biotechnology , prostate cancer , cancer , reflex
Androgenic regulation of androgen receptor (AR) immunoreactivity was examined in androgen‐sensitive motoneurons of the spinal nucleus of the bulbocavernosus (SNB) in adult male rats by immunohistochemistry using the polyclonal antibody, PG21. In intact controls, intense AR immunoreactivity was confined to the cell nucleus, but not in the nucleolus of SNB motoneurons, whereas cytoplasmic AR immunoreactivity was weak. Androgen withdrawal significantly reduced both the intensity of AR immunoreactivity in the nuclei and number of AR immunoreactive nuclei of the SNB motoneurons within 1 day of castration. AR immunostaining in the nucleus and cytoplasm was completely eliminated 5 or 10 days following castration. These changes were prevented by replacement of testosterone propionate (TP). The number of AR immunoreactive nuclei recovered to about half of the control levels within 20 min or 1 hr of TP administration to males 5 days after castration, although the intensity of AR immunoreactivity was almost the same as that of males 1 day following castration. Both the intensity of nuclear and cytoplasmic AR immunoreactivity and number of AR immunoreactive nuclei recovered to the control levels 2 or 6 hr after TP injection. These results suggest that androgen causes a significant up‐regulation in AR expression of SNB motoneurons.