1992
DOI: 10.1016/0960-0760(92)90024-d
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Estradiol increases the duration of nuclear androgen receptor occupation in the preoptic area of the male rat treated with dihydrotestosterone

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Cited by 35 publications
(11 citation statements)
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“…In peripheral tissues, estrogen has been shown to antagonize some of the cellular effects of androgens [15]. In brain, E 2 can increase AR concentration [10] and significantly augment the duration of AR occupation [11]. Our study demonstrated the presence of three types of hormone-sensitive neurons in male rat brain.…”
Section: Discussionmentioning
confidence: 72%
See 1 more Smart Citation
“…In peripheral tissues, estrogen has been shown to antagonize some of the cellular effects of androgens [15]. In brain, E 2 can increase AR concentration [10] and significantly augment the duration of AR occupation [11]. Our study demonstrated the presence of three types of hormone-sensitive neurons in male rat brain.…”
Section: Discussionmentioning
confidence: 72%
“…In addition, estrogen increases the number of androgen receptors (AR) and the duration of ligand occupancy [10, 11] within brain regions involved in the control of mating, and androgens downregulate the expression of ER [12, 13], suggesting an interaction between both steroids. Depending on the tissue, androgenic and estrogenic interactions may be either antagonistic or synergistic [14, 15].…”
Section: Introductionmentioning
confidence: 99%
“…Sodersten 1980). Estrogen might also increase the ef fectiveness of androgen receptors of vasopressin-producing cells by altering the duration of androgen receptor occupation, as has been observed in the preoptic area of male rats (Roselli and Fasasi 1992). Sex-related differences in androgen levels cannot fully explain sex-related dif ferences in vasopressin fiber staining and vasopressin mRNA levels observed in intact male and female rats (De Vries et al 1981;Miller et al 1989b).…”
Section: Cellular Basis Of Sex-related Differences In Vasopressin Expmentioning
confidence: 99%
“…Castration followed by hormone replacement disrupts normal homeostatic mechanisms regulating steroid hormone activity, and the potential exists for treatmentinduced activation of compensatory mechanisms not associated with normal development. For example, administration of estrogens alters androgen receptor concentration (Handa et al, 1987a,b), increases nuclear retention time of occupied androgen receptors (Roselli and Fasasi, 1992), and interferes with dihydrotestosterone catabolism (Soderstein and Gustafsson, 1980;Soderstein et al, 1986). Thus, it is possible that the observed trophic effects of estrogens on SNB dendritic development in castrated, estradiol/dihydrotestosterone-treated males may actually represent enhancement of androgenic activity induced by the presence of pharmacological doses of estradiol.…”
Section: Introductionmentioning
confidence: 97%