Cytoplasmic oxytocin and vasopressin gene transcripts decline postpartum in the hypothalamus of the lactating rat.

Crowley, Rebecca S.; Tr, Insel; O'Keefe, J.P.; Ja, Amico

doi:10.1210/endo.133.6.7612074

Cited by 46 publications

(36 citation statements)

References 15 publications

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“…It is likely that other factors are also involved in the retention of this behavior. Nevertheless, based on the documented changes in the AVP system around parturition [11,[13][14][15], and the present V1a receptor antagonist treatments, we propose that peripartum change in V1a receptor activity is one important mechanism responsible for the establishment of maternal memory.…”

Section: Discussionmentioning

confidence: 88%

“…Zingg and Lefebvre found that hypothalamic AVP mRNA levels are increased 2-3 times during late pregnancy and lactation compared to controls [11], whereas vasopressin mRNA levels increase in the supraoptic nucleus during lactation [12]. Although AVP mRNA appears to be elevated during lactation compared to control animals, immunoreactive vasopressin typically peaks the day prior to parturition in several hypothalamic nuclei [13] and then declines following parturition [14,15]. Exogenous AVP is capable of inducing maternal behavior in rats [16], and the infusion of a V1 antagonist into the medial preoptic area suppresses the behavior [17].…”

Section: Introductionmentioning

confidence: 99%

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Arginine vasopressin V1a receptor antagonist impairs maternal memory in rats

Nephew

Bridges

2008

Physiology & Behavior

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Primiparous female rats rapidly respond to foster pups following an extended separation from pups after an initial maternal experience. This consolidation of maternal behavior has been referred to as maternal memory. The neurochemical regulation of maternal memory is not clearly understood. One neuropeptide that may mediate maternal memory is arginine vasopressin (AVP), a neuropeptide which is modulated around the time of parturition and has an established role in learning and memory processes. Thus, the present studies examine the possible involvement of AVP in the establishment of maternal memory in female rats. Pregnant rats were implanted with chronic cannulae connected to subcutaneous osmotic minipumps filled with a V1a receptor antagonist [d(CH2)5Tyr(Me)AVP, 0.1-12.5 ng/hr] or saline vehicle which were chronically infused either into the lateral ventricles or bilaterally into the medial amygdala beginning on day 18 of gestation. Both the osmotic pumps and the newborn pups were removed 24 hours following parturition. The effects of the V1a antagonist treatments on social recognition and maternal behavior were measured following parturition and maternal memory was assessed following a ten day separation from pups. Whereas none of the AVP treatments affected the initial establishment of maternal behavior postpartum, maternal memory was impaired in rats infused into the amygdala with the AVP antagonist (1.25 and 12.5 ng/hr). Social recognition was not impaired by intracerebroventricular infusion of either the 0.1 or 1.0 ng/hr dose of the V1a antagonist. The present results suggest a role for medial amygdaloid V1a receptors in the establishment of maternal memory.

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Arginine vasopressin V1a receptor antagonist impairs maternal memory in rats

Nephew

Bridges

2008

Physiology & Behavior

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“…Whether this pervading influence of gonadal ste roids is specific to a hyperosmotic stimulus is not yet known. Our previous studies in the lactating rat [12] sug gest a broader role for gonadal steroid modulation of AVP mRNA accumulation in other states in which the AVP neuron may be activated.…”

Section: Discussionmentioning

confidence: 86%

“…Gonadal steroid-filled silastic capsules were prepared using the methods of Smith [13], and as described by this laboratory [9,12]. LISA).…”

Section: Silastic Capsulesmentioning

confidence: 99%

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Effect of Testosterone and Its Metabolites upon the Level of Vasopressin Messenger Ribonucleic Acid in the Hypothalamus of the Hyperosmotically Stimulated Male Rat

O'Keefe¹,

Crowley²,

Hrivnak³

et al. 1995

Neuroendocrinology

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We previously reported that gonadal steroids modify the expression of arginine vasopressin (AVP) in the hypothalamus of rats administered 2% sodium chloride solution for 5 days. Gonadectomy prevented, and testosterone (T) replacement restored, enhanced AVP mRNA levels in the supraoptic nucleus (SON) of male rats receiving this hyperosmotic challenge. The present study investigated the effects of the androgenic and estrogenic metabolites of T on hypothalamic AVP mRNA levels in response to chronic hyperosmolality. Gonadectomized male rats receiving 2% NaCl for 5 days and treated with T, dihydrotestosterone (DHT), or DHT + estradiol (E₂), but not E₂ alone or empty implants, had increased AVP mRNA levels compared to gonadectomized animals receiving tap water. Our results support a role for T and DHT-mediated effects upon the enhanced accumulation of AVP mRNA in the SON of male rats receiving a chronic hyperosmotic challenge.

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Neuroendocrine Regulation of Lactation and Milk Production

Crowley

2014

Comprehensive Physiology

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Prolactin (PRL) released from lactotrophs of the anterior pituitary gland in response to the suckling by the offspring is the major hormonal signal responsible for stimulation of milk synthesis in the mammary glands. PRL secretion is under chronic inhibition exerted by dopamine (DA), which is released from neurons of the arcuate nucleus of the hypothalamus into the hypophyseal portal vasculature. Suckling by the young activates ascending systems that decrease the release of DA from this system, resulting in enhanced responsiveness to one or more PRL-releasing hormones, such as thyrotropin-releasing hormone. The neuropeptide oxytocin (OT), synthesized in magnocellular neurons of the hypothalamic supraoptic, paraventricular, and several accessory nuclei, is responsible for contracting the myoepithelial cells of the mammary gland to produce milk ejection. Electrophysiological recordings demonstrate that shortly before each milk ejection, the entire neurosecretory OT population fires a synchronized burst of action potentials (the milk ejection burst), resulting in release of OT from nerve terminals in the neurohypophysis. Both of these neuroendocrine systems undergo alterations in late gestation that prepare them for the secretory demands of lactation, and that reduce their responsiveness to stimuli other than suckling, especially physical stressors. The demands of milk synthesis and release produce a condition of negative energy balance in the suckled mother, and, in laboratory rodents, are accompanied by a dramatic hyperphagia. The reduction in secretion of the adipocyte hormone, leptin, a hallmark of negative energy balance, may be an important endocrine signal to hypothalamic systems that integrate lactation-associated food intake with neuroendocrine systems.

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Cytoplasmic oxytocin and vasopressin gene transcripts decline postpartum in the hypothalamus of the lactating rat.

Cited by 46 publications

References 15 publications

Arginine vasopressin V1a receptor antagonist impairs maternal memory in rats

Arginine vasopressin V1a receptor antagonist impairs maternal memory in rats

Effect of Testosterone and Its Metabolites upon the Level of Vasopressin Messenger Ribonucleic Acid in the Hypothalamus of the Hyperosmotically Stimulated Male Rat

Neuroendocrine Regulation of Lactation and Milk Production

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