Sex and regional differences in decrease of estrogen receptor α-immunoreactive cells by estrogen in rat hypothalamus and midbrain

Yamada, Shunji; Noguchi, Daisuke; Ito, Hiroyuki; Yamanouchi, Korehito

doi:10.1016/j.neulet.2009.07.074

Cited by 38 publications

(37 citation statements)

References 33 publications

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“…Because changing levels of E 2 may modify the detection of ER␣ immunoreactivity in the rodent brain (41,42,54), we evaluated the colocalization rate of ER␣ and GHSR in OVX and OVX ϩ E 2 females ( Table 1). As a control for E 2 levels, uterine weight was assessed at the time of euthanization.…”

Section: Resultsmentioning

confidence: 99%

Estradiol modulates Kiss1 neuronal response to ghrelin

Frazão

Lemko

Silva

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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Ghrelin is a metabolic signal regulating energy homeostasis. Circulating ghrelin levels rise during starvation and fall after a meal, and therefore, ghrelin may function as a signal of negative energy balance. Ghrelin may also act as a modulator of reproductive physiology, as acute ghrelin administration suppresses gonadotropin secretion and inhibits the neuroendocrine reproductive axis. Interestingly, ghrelin's effect in female metabolism varies according to the estrogen milieu predicting an interaction between ghrelin and estrogens, likely at the hypothalamic level. Here, we show that ghrelin receptor (GHSR) and estrogen receptor-␣ (ER␣) are coexpressed in several hypothalamic sites. Higher levels of circulating estradiol increased the expression of GHSR mRNA and the co-xpression of GHSR mRNA and ER␣ selectively in the arcuate nucleus (ARC). Subsets of preoptic and ARC Kiss1 neurons coexpressed GHSR. Increased colocalization was observed in ARC Kiss1 neurons of ovariectomized estradiol-treated (OVX ϩ E2; 80%) compared with ovariectomized oil-treated (OVX; 25%) mice. Acute actions of ghrelin on ARC Kiss1 neurons were also modulated by estradiol; 75 and 22% of Kiss1 neurons of OVX ϩ E2 and OVX mice, respectively, depolarized in response to ghrelin. Our findings indicate that ghrelin and estradiol may interact in several hypothalamic sites. In the ARC, high levels of E2 increase GHSR mRNA expression, modifying the colocalization rate with ER␣ and Kiss1 and the proportion of Kiss1 neurons acutely responding to ghrelin. Our findings indicate that E2 alters the responsiveness of kisspeptin neurons to metabolic signals, potentially acting as a critical player in the metabolic control of the reproductive physiology. kisspeptin; hypothalamus; metabolism; growth hormone secretagogue receptor; reproduction IN MAMMALS, THE ABILITY TO REPRODUCE is gated by the availability of energy stores (25,49). Reproduction is metabolically expensive, and during starvation fertility is stopped to conserve energy for basic survival. Accumulating evidence has implicated circulating hormones as a means of transmitting information regarding peripheral energy availability to the central circuitry that controls the reproductive system. Among these metabolic signals is the stomach-derived hormone ghrelin (23,46). Ghrelin was recognized originally for its growth hormonestimulating action, but extensive research has since demonstrated that ghrelin is also a direct regulator of metabolism and energy balance (22,28,55). Ghrelin promotes the storage of lipids as fat, induces glucagon release, and suppresses insulin secretion and sensitivity (4, 5, 47). Interestingly, the effects of ghrelin to increase body weight vary according to the estrogen milieu, as a more pronounced orexigenic effect is observed in females upon ovariectomy (3, 6). In cycling rats, ghrelin stimulation of food intake is observed only in females in diestrus (when estrogen levels are low). Moreover, males treated with estradiol are resistant to the stimulatory effects of ghrelin...

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Section: Resultsmentioning

confidence: 99%

Estradiol modulates Kiss1 neuronal response to ghrelin

Frazão

Lemko

Silva

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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“…In addition, low sex steroid levels were associated with a high expression of classical steroid receptors (i.e., AR and ER) in the brain of tropical male passerine birds [53]. In the brain of rodents, modifications in 17β-E levels are known to affect the expression and localization of ERs with regional specificity [54,55,56]. Moreover, it is interesting to note that finasteride treatment induces intersex animals in Western clawed frogs showing high expressions of AR and ER in the brain [57].…”

Section: Discussionmentioning

confidence: 99%

Effects of Subchronic Finasteride Treatment and Withdrawal on Neuroactive Steroid Levels and Their Receptors in the Male Rat Brain

et al. 2015

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The enzymatic conversion of progesterone and testosterone by the enzyme 5alpha-reductase exerts a crucial role in the control of nervous function. The effects of finasteride in the brain, an inhibitor of this enzyme used for the treatment of human benign prostatic hyperplasia and androgenic alopecia, have been poorly explored. Therefore, the effects of a subchronic treatment with finasteride at low doses (3 mg/kg/day) and the consequences of its withdrawal on neuroactive steroid levels in plasma, cerebrospinal fluid and some brain regions as well as on the expression of classical and non-classical steroid receptors have been evaluated in male rats. After subchronic treatment (i.e., for 20 days) the following effects were detected: (i) depending on the compartment considered, alteration in the levels of neuroactive steroids, not only in 5alpha-reduced metabolites but also in its precursors and in neuroactive steroids from other steroidogenic pathways and (ii) an upregulation of the androgen receptor in the cerebral cortex and beta3 subunit of the GABA-A receptor in the cerebellum. One month after the last treatment (i.e., withdrawal period), some of these effects persisted (i.e., the upregulation of the androgen receptor in the cerebral cortex, an increase of dihydroprogesterone in the cerebellum, a decrease of dihydrotestosterone in plasma). Moreover, other changes in neuroactive steroid levels, steroid receptors (i.e., an upregulation of the estrogen receptor alpha and a downregulation of the estrogen receptor beta in the cerebral cortex) and GABA-A receptor subunits (i.e., a decrease of alpha 4 and beta 3 mRNA levels in the cerebral cortex) were detected. These findings suggest that finasteride treatment may have broad consequences for brain function.

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“…For example, in the rat, estrogen acts to reduce ERb and ERb-mRNA expression in the PVN (Patisaul et al, 2001;Suzuki and Handa, 2004). Some studies have shown that estrogen can exert inhibitory control over the expression of both ERa (Simerly and Young, 1991;Yamada et al, 2009;Lauber et al, 2011) and ERb (Suzuki and Handa, 2004) and that castration increases levels of ERa-mRNA (DeVries et al, 1985;Handa et al, 1996).…”

Section: Discussionmentioning

confidence: 99%