Estrogen Increases c-Fos Expression in the Paraventricular Nucleus along with its Anorexic Effect in Developing Rats

Abstract

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 EBinduced 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). Key words: c-Fos, Development, Estrogen, Food intake, Hypothalamus (J. Reprod. Dev. 57: [365][366][367][368][369][370][371][372] 2011) nderstanding of the mechanism regulating eating is very important for human health because of obesity and eating disorders, such as anorexia and bulimia nervosa. Anorexia nervosa mainly occurs in young women around puberty, and the increasing estrogen level in the circulation during the puberty has been suggested to be involved in anorexia [1]. Estrogen exerts a potent physiological and inhibitory effect on feeding in a variety of species. During the menstrual cycle for example, meal size decreases during the periovulatory phase, just after the period of increased plasma estradiol (E2) concentration [2,3]. In nonhuman primates like monkeys, food intake is reduced at the time of ovulation when estrogen is at its peak and increases after ovulation when progesterone is elevated [4]. In rats, food intake is decreased at proestrus when plasma E2 increases during the estrous cycle [5,6], and ovariectomy increases food intake and body weight and E2 treatment normalizes these increases in ovariectomized (OVX) rats [7][8][9].In rats, the anorexic effect of estrogen has been only reported to appear in 45-day-old rats ovariectomized either on the day of birth or at weaning [10,11], and daily treatment of estradiol benzoate (EB) did not decrease food intake or body weight from postnatal day 30 (P30) until approximate P40 in OVX rats [12]. In contrast, the periodic alterations in food intake and meal size have been reported to occur prior to the vaginal opening in intact female rats [13], suggesting that the anorexic effect of est...

Differential Effects of E2 on MAPK Activity in the Brain and Heart of Aged Female Rats

“…This treatment paradigm approximately resembles the period of the estrous cycle with higher levels of circulating estrogens. Similar acute treatment paradigms (1x/day for 1 to 4 days) resulted in physiological and behavioral improvements in ovariectomized rats [ 38 , 39 ] [ 40 ] [ 41 – 43 ] [ 44 , 45 ]. Animals were euthanized 24 hours after the last injection, trunk blood was collected, brain and heart rapidly removed and flash frozen.…”

Abnormal feeding behaviour in spinalised rats is mediated by hypothalamus: Restorative effect of exposure to extremely low frequency magnetic field

“…Cells were considered c-Fos immunoreactive, if they contained dark, punctuate, nuclear immunostaining. 49…”