Sex Differences in the Regulation of Oxytocin Receptors by Ovarian Steroids in the Ventromedial Hypothalamus of the Rat

Coirini, Héctor; Johnson, Allan E.; Schumacher, Michaël; McEwen, Bruce S.

doi:10.1159/000126125

Cited by 38 publications

(24 citation statements)

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“…Treatment of females with estradiol benzoate induced a 4-fold increase in oxy tocin binding in the VMH [ 15,17,20,21,27,37] as well as in surrounding neuropil [41], The time course of the increase in oxytocin receptor density in the VMH after estrogen treatment pleads in favor of synthesis of new receptors [24]. We observed an increase of 4-fold after estrogen treatment in the VMH, in concordance with recent reports from Bale and Dorsa [42], It has been sug gested that the sequential action of estrogen and proges terone acts to bring the neuropeptide oxytocin and its receptor into register thereby enabling it to exert sexual behavioral effects [22,41,43], Since the neurons in the VMH, MeAmyg and hippocampus contain a high density of estradiol receptors [40], the oxytocin receptor mRNA levels in the CNS may be locally regulated by estrogen.…”

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confidence: 91%

“…For example, ovarian hormones influence the concentration of binding sites for oxytocin and the responsiveness of the uterus to oxytocin [3,18,19]. In the rat, the regulation of uterine oxytocin receptors has been correlated with estro gen and progesterone ratios [2], In the CNS of both sexes, estrogen treatment leads to an increase in oxytocin bind ing sites in some regions of the brain including the ven tromedial nucleus of the hypothalamus (VMH) [15,17,[20][21][22], medial amygdala [17.21], bed nucleus of the stria terminalis [17] and the anterior olfactory nucleus [23]. The time course of the estrogen effect on oxytocin binding sites is consistent with that for the induction of lordosis [ 15,24], Thus, it has been postulated that estrogen causes an increase in oxytocin receptor leading to a potentiation of the neuronal responsiveness to oxytocin, that in turn results in the facilitation of lordosis by oxytocin [7], Fur thermore.…”

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Effects of Estrogen on Oxytocin Receptor Messenger Ribonucleic Acid Expression in the Uterus, Pituitary, and Forebrain of the Female Rat

et al. 1997

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Oxytocin receptors are regulated during parturition and lactation. Gonadal steroids are thought to be key players in this regulation. It is not well documented how oxytocin receptor gene expression is regulated in the CNS. In this study we analyzed potential estrogen effects on the oxytocin receptor mRNA levels in some areas integral to the limbic-hypothalamic system, namely the ventromedial nucleus of the hypothalamus (VMH), posterior medial nucleus of amygdala (MeAmyg), and arcuate nucleus (ARC), as well as the caudate putamen (CPu), CA1 region of the hippocampus, anterior pituitary, and uterine tissue of ovariectomized (OVX) female rats. By in situ hybridization we observed a 4.4-fold increase in oxytocin receptor mRNA levels in the VMH after 48 h of estrogen treatment when compared to OVX rats. Smaller increases were observed in the MeAmyg, hippocampus, and anterior pituitary (3.18, 1.76, and 2.55, respectively). No changes in oxytocin receptor mRNA levels were observed in the CPu or ARC after estrogen treatment. A similar finding resulted from slot-blot analysis of total mRNA extracts. In uterine tissue, 48 h of estrogen treatment increased oxytocin receptor mRNA level in the myometrium (3.13-fold). No changes in oxytocin receptor mRNA levels were observed after 12 and 24 h of estrogen treatment. These findings suggest that the estrogenic regulation of oxytocin receptor binding in both CNS and uterine tissues may in part be mediated by de novo synthesis of oxytocin receptor mRNA or by alterations in the stability of oxytocin receptor gene transcripts.

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confidence: 91%

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Effects of Estrogen on Oxytocin Receptor Messenger Ribonucleic Acid Expression in the Uterus, Pituitary, and Forebrain of the Female Rat

et al. 1997

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“…In the ventromedial nucleus of the hypothalamus, there are developmentally programmed sex differences in the pattern of synaptic connections on dendritic shafts and spines (10) and developmentally regulated sex differences in the inducibility of progesterone receptors (11). However, there are no major sex differences in estrogen induction of oxytocin receptors, but there is a sex difference in the effects of progesterone on these receptors (12). Thus, in the nucleus studied by Cooke et al (2), the lack of a sex difference in cell body diameter or size of the neuroanatomical nucleus does not rule out the existence of developmentally programmed sex differences in neurochemistry or in fine-grained neuroanatomy of synaptic connections.…”

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Permanence of brain sex differences and structural plasticity of the adult brain

McEwen

1999

Proc. Natl. Acad. Sci. U.S.A.

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Sex differences in brain structure have been widely recognized since the pioneering studies of Raisman and Field (1). For the most part, brain sex differences are thought to arise in perinatal development through the actions of testosterone secreted by the developing testes, and these sex differences are believed to persist in the absence of gonadal hormones in adult life, very much like the basic plan of the male and female reproductive tracts, which are also developmentally determined. As shown in Fig. 1, the basic plan of brain and body sex differences is the result of a cascade of events beginning with the role of the sex-determining genes in sexual differentiation and continuing with the actions of hormones in embryonic, neonatal, peripubertal, and adult life. The emphasis on early developmental programming of brain structural sex differences was reinforced over several decades by the long-standing view that the brain is not capable of significant structural changes in adulthood. However, this view is changing, and in this issue of the Proceedings, Cooke et al. (2) describe a brain sex difference controlled entirely by circulating androgens. The postereodorsal nucleus of the medial amygdala is larger in male rats and females, but castration of adult males causes the volume of the nucleus to decrease to female levels within 4 weeks, whereas testosterone treatment of adult females for 4 weeks enlarges volume of this nucleus to male levels. Not only is the volume of the anatomical nucleus affected, but the individual cell soma areas are also increased in size by androgen, irrespective of genetic sex of the animal. These interesting findings are not as heretical as they might have seemed a few years ago, and they should be interpreted in light of new evidence for the structural plasticity of the adult brain at different levels of neuroanatomical and functional analysis in relation to the actions of circulating androgens, estrogens, and glucocorticoids. Moreover, as the authors point out, the findings of this new study also raise interesting issues pertaining to the interpretation of sex differences found in the human brain.Adult Neuronal Plasticity in Sexually Dimorphic Systems. Hormone actions in the adult brain affect not only neurochemistry but also structure of nerve cells in meaningful ways, and this realization constitutes a paradigm shift in our thinking about the plasticity of the adult brain. The first recognition of this came from studies on some of the recognized sexually dimorphic systems of the brain, in which adults treated with hormones showed sex-specific morphological changes. For example, androgen actions in the adult spinal nucleus of the bulbocavernosus (SNB), which innervates the penis, regulate both size and functional connectivity of these motor neurons, even though a significant part of the size of this nucleus is determined by developmental events (3, 4). Moreover, estrogen actions in the ventromedial nucleus of the adult female hypothalamus induce new synapses (5-7), and these effects ...

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“…Furthermore, estra diol benzoate influences oxytocin-immunoreactive brain systems [12,13], and induces the expression of oxytocin receptors in several brain nuclei, especially in the ven tromedial nucleus of the hypothalamus [14-16], an effect that resembles the induction of oxytocin receptors in the pregnant uterus [17], Progesterone further enhances estra diol benzoate-induced oxytocin receptors [18,19], and is required after estrogen priming for the expression of sev eral effects of oxytocin [20][21][22], Oxytocin receptors are also increased in the ventromedial nucleus of castrated male rats by testosterone, which probably induces this effect after its conversion to estradiol benzoate by brain aromatase [23]. However, progesterone was much less effective in male rats than in female rats [24], The above results prompted us to study the effect of sexual steroids on apomorphine-and oxytocin-induced penile erection and yawning in intact and castrated male rats.…”

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Apomorphine- and Oxytocin-Induced Penile Erection and Yawning in Intact and Castrated Male Rats: Effect of Sexual Steroids

Melis

Mauri²,

Argiolas³

1994

Neuroendocrinology

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The effect of apomorphine (80 µg/kg s.c.) and oxytocin (30 ng i.c.v.) on penile erection and yawning was studied in intact and castrated male rats. In castrated rats both apomorphine and oxytocin responses were abolished. In these animals, testosterone (100 µg/kg s.c. once a day for 3 days), restored penile erection while estradiol benzoate (10 µg/kg s.c. once a day for 3 days) restored yawning induced by both compounds. 5-Dihydrotestosterone (DHT) or progesterone (each at a dose of 100 µg/kg s.c. once a day for 3 days) were ineffective. Given together, estradiol benzoate and DHT partially restored apomorphine- and oxytocin-induced yawning and penile erection, whereas estradiol benzoate and progesterone restored only yawning. Estradiol benzoate-induced recovery of yawning was prevented by the antiestrogen tamoxifen (1 mg/kg s.c. once a day for 3 days). In intact rats, progesterone increased and estradiol benzoate decreased apomorphine- and oxytocin-induced yawning without modifying penile erection, although oxytocin-induced yawning was prevented much less by estradiol benzoate than that induced by apomorphine. Testosterone or DHT were ineffective on both responses. Estradiol benzoate inhibition of apomorphine- and oxytocin-induced yawning was prevented by tamoxifen, which per se failed to modify apomorphine and oxytocin responses, as well as by testosterone or progesterone. The present results suggest that apomorphine-and oxytocin-induced penile erection and yawning are endocrine-dependent and differentially modulated by sexual steroids, suggesting that the mechanisms controlling the two behaviors are different even though they are often associated.

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Sex Differences in the Regulation of Oxytocin Receptors by Ovarian Steroids in the Ventromedial Hypothalamus of the Rat

Cited by 38 publications

References 30 publications

Effects of Estrogen on Oxytocin Receptor Messenger Ribonucleic Acid Expression in the Uterus, Pituitary, and Forebrain of the Female Rat

Effects of Estrogen on Oxytocin Receptor Messenger Ribonucleic Acid Expression in the Uterus, Pituitary, and Forebrain of the Female Rat

Permanence of brain sex differences and structural plasticity of the adult brain

Apomorphine- and Oxytocin-Induced Penile Erection and Yawning in Intact and Castrated Male Rats: Effect of Sexual Steroids

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