Increased accumulation of oxytocin messenger ribonucleic acid in the hypothalamus of the female rat: induction by long term estradiol and progesterone administration and subsequent progesterone withdrawal.

Crowley, Rebecca S.; Insel, Thomas R.; O'Keefe, J A; Kim, N B; Amico, Janet A.

doi:10.1210/endo.136.1.7828535

Cited by 68 publications

(51 citation statements)

References 42 publications

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“…The oxytocin receptor gene is expressed in various tissues of the reproductive tract that are considered as target sites for oxytocin actions (21)(22)(23)(24). Oxytocin receptors have been found in other peripheral tissues, such as the kidney (25), mammary and pituitary glands (22), and in several brain regions (26)(27)(28). The rat oxytocin receptor gene has been cloned and characterized, and the availability of specific rat oxytocin receptor cDNA probes (29) prompted us to study the heart as a site of oxytocin receptor gene expression.…”

Section: ؊6mentioning

confidence: 99%

Oxytocin releases atrial natriuretic peptide by combining with oxytocin receptors in the heart

Gutkowska

Jankowski

Lambert

et al. 1997

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

227

217

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Previous studies indicated that the central nervous system induces release of the cardiac hormone atrial natriuretic peptide (ANP) by release of oxytocin from the neurohypophysis. The presence of specific transcripts for the oxytocin receptor was demonstrated in all chambers of the heart by amplification of cDNA by the PCR using specific oligonucleotide primers. Oxytocin receptor mRNA content in the heart is 10 times lower than in the uterus of female rats. Oxytocin receptor transcripts were demonstrated by in situ hybridization in atrial and ventricular sections and confirmed by competitive binding assay using frozen heart sections. Perfusion of female rat hearts for 25 min with KrebsHenseleit buffer resulted in nearly constant release of ANP. Addition of oxytocin (10 ؊6 M) significantly stimulated ANP release, and an oxytocin receptor antagonist (10 ؊7 and 10 ؊6 M) caused dose-related inhibition of oxytocin-induced ANP release and in the last few minutes of perfusion decreased ANP release below that in control hearts, suggesting that intracardiac oxytocin stimulates ANP release. In contrast, brain natriuretic peptide release was unaltered by oxytocin. During perfusion, heart rate decreased gradually and it was further decreased significantly by oxytocin (10 ؊6 M). This decrease was totally reversed by the oxytocin antagonist (10 ؊6 M) indicating that oxytocin released ANP that directly slowed the heart, probably by release of cyclic GMP. The results indicate that oxytocin receptors mediate the action of oxytocin to release ANP, which slows the heart and reduces its force of contraction to produce a rapid reduction in circulating blood volume.There is considerable evidence that the central nervous system is critically involved in release of the cardiac hormone atrial natriuretic peptide (ANP) in response to volume expansion (1-4). For example, lesions in the median eminence or neural lobe of the pituitary gland which interrupt neuronal projections to the neurohypophysis, thereby blocking the release of neurohypophyseal hormones, block volume expansioninduced ANP release (5). The two major neurohypophyseal hormones are vasopressin and oxytocin, both of which are important to control hydromineral homeostasis (6, 7). Sonnenberg and Veress (8) showed that vasopressin enhances ANP release from isolated atria. These in vitro studies have not been confirmed, but later experiments showed that vasopressin-stimulated ANP release is related to hemodynamic changes, as only pressor doses of vasopressin produced an immediate increase in plasma ANP (9).Oxytocin is involved in reproductive functions such as induction of myometrial contractions during parturition and milk ejection during lactation. The presence of similar numbers of magnocellular oxytocin-secreting neurons (10), and the similar plasma oxytocin concentrations in rats of both sexes suggest that oxytocin also subserves other important physiologic functions. Indeed, there is substantiated evidence that oxytocin is important in ingestive (11), sexual (12), m...

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Section: ؊6mentioning

confidence: 99%

Oxytocin releases atrial natriuretic peptide by combining with oxytocin receptors in the heart

Gutkowska

Jankowski

Lambert

et al. 1997

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

227

217

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“…In fact, the steroid treatment regimen designed to artificially facilitate rat maternal behavior (13 days of estrogen and progesterone followed by 2 days of estrogen alone) has recently been shown to be the ideal schedule for inducing oxytocin gene expression in the hypothalamus (45). In addition, estrogen regulates the number of oxytocin receptors, not only in the uterus and mammary myoepithelium but also in a few discrete nuclei in the brain (reviewed in reference 12).…”

Section: Parental Behaviormentioning

confidence: 99%

A neurobiological basis of social attachment

Insel

1997

AJP

425

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S ince Bowlby's seminal contributions (1), attachment and separation have become familiar theoretical components of ego psychology, developmental psychology, and psychodynamic theory. In spite of the important roles these concepts have played in studies of psychological development, relatively little is known about their neurobiological basis. If one considers that abnormal social attachments characterize virtually every form of psychopathology, it seems especially remarkable that the chemistry, the anatomy, and the physiology of social bond formation remain largely unexplored. To be sure, there is a considerable literature on the neurobiology and psychobiology of separation (2), but this work may not prove instructive for understanding social bond formation. Attachment is not simply the absence of separation. Accordingly, there is no obvious reason why attachment and separation should be subserved by the same neural pathways.Attachment, of course, is not a thing but a process (3). More specifically, it is a social process and thus not likely to be defined by a single neurochemical pathway nucleus or represented in a single anatomic nucleus. As Harlow noted throughout his insightful writings on this subject (4), attachment includes several quite different processes depending on the social context: parent-infant, filial, and pair (male-female) bond formation are all forms of attachment. All of these forms involve seeking proximity and all involve a response to separation, but the strategy for and the consequences of achieving proximity vary depending on the relationship. None of these forms of attachment is uniquely human, suggesting that the neural basis can be investigated in animal models. It is also possible (and experimentally testable) that these various forms of attachment use similar neural pathways, suggesting that, biologically, attachment is a singular process that is manifested with different behaviors depending on the external (e.g., social) or internal (e.g., endocrine) context. This review will describe research on two neuropeptides, oxytocin and vasopressin, that have been implicated in the central mediation of attachment. I will de-

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“…Oxytocin mRNA and immunoreactivity increased in the hypothalamus of OVX rats treated with E2 for more than 2 weeks [46,47]. It has been also reported that intracerebroventricular administration of oxytocin and its agonist significantly decreased food intake in a dose-related manner in fasted rats [48].…”

Section: Discussionmentioning

confidence: 82%

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

Hua

Narita

Ichimaru

et al. 2011

Journal of Reproduction and Development

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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...

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Increased accumulation of oxytocin messenger ribonucleic acid in the hypothalamus of the female rat: induction by long term estradiol and progesterone administration and subsequent progesterone withdrawal.

Cited by 68 publications

References 42 publications

Oxytocin releases atrial natriuretic peptide by combining with oxytocin receptors in the heart

Oxytocin releases atrial natriuretic peptide by combining with oxytocin receptors in the heart

A neurobiological basis of social attachment

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

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