Estrogen Increases c-Fos expression in the paraventricular nucleus along with its anorexic effect in developing rats
Jing Hua Chi1, Kazumi Narita, Toru Ichimaru
1Department of Integrative Physiology, Faculty of Medical Sciences, University of Fukui, Fukui, Japan.
Insights
Estrogen
Area of Science:
- Neuroscience
- Endocrinology
- Developmental Biology
Background:
- Estrogen is known to suppress appetite in female mammals.
- Understanding the developmental regulation of this estrogenic anorexic system is crucial.
Purpose of the Study:
- To investigate the developmental timeline of estrogen's anorexic effects in rats.
- To identify the brain regions involved in estrogen-induced appetite suppression during development.
Main Methods:
- Rats at different developmental stages (postnatal days 11-31) and adult ovariectomized rats were treated with estradiol benzoate (EB) or vehicle.
- Food intake, body weight gain, and brain c-Fos expression were measured.
Main Results:
- Estradiol benzoate (EB) reduced food intake and weight gain starting from postnatal day 27.
- EB increased c-Fos expression in the parvocellular paraventricular nucleus of the hypothalamus (pPVN) in developing rats, correlating with appetite suppression.
- In adult rats, EB affected c-Fos expression in the nucleus tractus solitarius (NTS), central amygdala (CeA), and ventromedial hypothalamus (VMH).
Conclusions:
- The parvocellular paraventricular nucleus of the hypothalamus (pPVN) is critical for estrogen's anorexic effects.
- The rat feeding system starts responding to estrogen before puberty, around postnatal days 25-28.
Abstract:
Estrogen inhibits food intake in cycling females in a variety of species. To determine how the development of the anorexic system by estrogen is regulated, rat pups at four developmental stages, postnatal day 11 (P11)-13, P20-22, P25-27 and P29-31, and adult ovariectomized (OVX) rats received a daily subcutaneous injection of 20 µg/kg of estradiol benzoate (EB) or vehicle for three days. Food intake, body weight gain and immunohistochemical c-Fos expression in the brain were measured after each injection. EB treatment decreased both food intake and body weight gain from P27 onwards and significantly increased c-Fos expression in the parvocellular division of the paraventricular nucleus of the hypothalamus (pPVN), which is coincident with its anorexic effect in developing rats. The pattern of EB-induced c-Fos activation in other feeding-related nuclei did not coincide with its anorexic effect in developing pups. However, in adult OVX rats, EB treatment increased c-Fos expression in the nucleus tractus solitarius (NTS), the central nucleus of the amygdala (CeA), and, to a lesser degree, the ventromedial nucleus of the hypothalamus (VMH). These results suggested that the pPVN is an essential site in the brain for controlling the anorexic effect of estrogen and that the feeding system of rat begins to respond to estrogen before the onset of puberty (P25-28).
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