Androgen receptor immunoreactivity in the male and female Syrian hamster brain
โ Scribed by Wood, R. I. ;Newman, S. W.
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 682 KB
- Volume
- 39
- Category
- Article
- ISSN
- 0022-3034
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โฆ Synopsis
To investigate potential mechanisms for sex differences in the physiologic response to androgens, the present study compared the hormonal regulation of intracellular androgen receptor partitioning and the distribution of androgen receptor immunoreactivity in select brain regions from male and female hamsters. Androgen receptors were visualized on coronal brain sections. Two weeks after castration, androgen receptor immunoreactivity filled the neuronal nuclei and cytoplasm in males and females. In gonad-intact males and females, androgen receptor immunoreactivity was limited to the cell nucleus. Whereas exogenous dihydrotestosterone prevented cytoplasmic immunoreactivity, estrogen at physiologic levels did not. These results suggest that nuclear androgen receptor immunoreactivity in gonad-intact females is maintained by endogenous androgens, and that androgens have the potential to influence neuronal activity in either sex. However, sex differences in the number and staining intensity of androgen-responsive neurons were apparent in select brain regions. In the ventral premammillary nucleus, ventromedial nucleus of the hypothalamus, and medial amygdaloid nucleus, androgen receptor staining was similar in gonadectomized males and females. In the lateral septum, posteromedial bed nucleus of the stria terminalis (BNSTpm), and medial preoptic nucleus, the number of androgen receptor-immunoreactive neurons was significantly lower in females (p < .05). Moreover, the integrated optical density/cell in BNSTpm was significantly less in females (1.28+/-0.3 units) than in males (2.21+/-0.2 units; p < .05). These sex differences in the number and staining intensity of androgen-responsive neurons may contribute to sex differences in the behavioral and neuroendocrine responses to androgens.
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