Inhibition of suckling-induced prolactin release by μ- and κ-opioid antagonists

Baumann, Michael H.; Rabii, Jamshid

doi:10.1016/0006-8993(91)90799-2

Cited by 32 publications

(30 citation statements)

References 36 publications

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“…This possibility has been suggested by others [42], In this case, all three receptor subtypes on the nerve terminal would have to be activated in order for the neuron to re spond. Interestingly, Baumann and Rabii [27] also re ported an interaction between the p-and K-sites in the suckling induced prolactin increase. Their study did not investigate the involvement of the 8-site in prolactin re lease during suckling.…”

Section: Discussionmentioning

confidence: 99%

“…The nor-BNI dose was chosen based on our own preliminary studies indicating that this dose abolished the prolactin increase due to suckling during lactation [Calla han, unpubl.] In addition, 4 ug of norBNI attenuated the suckling-induced prolactin increase, while 16 ug abol ished this response [27], Even higher doses (25 ug) of norBNI were used by Manzanares et al [44] to reverse effects on DOPA accumulation by the K-specific agonist U-50,488. We are therefore confident that the doses of antagonists utilized in this study are acting specifically at their respective receptors.…”

Section: Discussionmentioning

confidence: 99%

“…However, in contrast to morphine, adminis tration of (3-endorphin or DADLE resulted in a signifi cant increase in prolactin release in both virgin and lactat ing female rats [26], Indeed, the prolactin response to [3-endorphin and DADLE was similar in magnitude to the suckling-induced prolactin response even in virgin fe males. Furthermore, Baumann and Rabii [27] reported that the suckling-induced prolactin increase involved the EOP acting through both p-and K-receptor subtypes since both [3-funaltrexamine ((3-FNA; a specific u-antagonist) and nor-binaltorphimine (norBNI; a specific K-antagonist) abolished the response. They did not determine the possible involvement of the 8-site in their study.…”

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confidence: 99%

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Opiate Receptor Subtype Involvement in the Stimulation of Prolactin Release by β-Endorphin in Female Rats

Kehoe

Parman²,

Janik³

et al. 1993

Neuroendocrinology

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The prolactin secretory response to β-endorphin and the involvement of opiate receptor subtypes in this response was determined in both diestrous and postpartum, lactating female rats. The involvement of the µ-, δ- and/or ĸ-site was determined by administering specific antagonists for each of these sites prior to β-endorphin. β-Funaltrexamine (β-FNA, 1 or 5 µg) was administered to block µ-sites, ICI 154,129 (5,10 or 25 µg) blocked δ-sites and nor-binaltor-phimine (norBNI, 8 µg) blocked ĸ-sites. The ability of β-FNA and ICI 154, 129 to block prolactin secretion following morphine administration was also determined. A dose response study for β-endorphin indicated that β-endorphin, at doses as low as 25 ng, was a potent stimulus for prolactin release producing an increase in prolactin that mimicked the suckling-induced prolactin increase. In addition, all three antagonists were capable of antagonizing the stimulatory effect of β-endorphin in both diestrous and postpartum female rats. These results indicate that β-endorphin is a potent stimulus for prolactin secretion and that these three opiate receptor subtypes interact to produce its stimulatory effect on prolactin release.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Opiate Receptor Subtype Involvement in the Stimulation of Prolactin Release by β-Endorphin in Female Rats

Kehoe

Parman²,

Janik³

et al. 1993

Neuroendocrinology

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“…Mu opioid agonists also stimulate PRL release under some conditions (Bowen et al, 2002;Hoehe et al, 1988;Saarialho-Kere et al, 1989), but inhibit ACTH and cortisol (Auernhammer et al, 1992(Auernhammer et al, , 1994. In contrast, selective mu-antagonists such as beta-FNA decrease PRL in rats (Baumann and Rabii, 1991;Koenig et al, 1984) and block morphine-induced ACTH release in rats (Pfeiffer et al, 1985). In rhesus monkeys, the mu antagonist quadazocine did not alter PRL levels significantly but antagonized the heroin-induced increase in PRL (Bowen et al, 2002).…”

Section: Introductionmentioning

confidence: 98%

“…Furthermore, Ur et al 1997 reported a dose-dependent stimulation of cortisol release by kappa-selective agonist spiradoline in healthy human volunteers. Kappa opioid antagonists, such as nor-BNI, tend to decrease PRL in rats (Baumann and Rabii, 1991;Manzanares et al, 1993) and increase ACTH and cortisol in rhesus monkeys (Williams et al, 2003). The mu antagonists naloxone and naltrexone, and the mixed mu/kappa antagonist nalmefene, increase ACTH and cortisol in human subjects (Hernandez-Avila et al, 2002;Mendelson et al, 1986Mendelson et al, 1991Schluger et al, 1998;Teoh et al, 1988;Wand et al, 1999a,b).…”

Section: Introductionmentioning

confidence: 99%

Effects of nalbuphine on anterior pituitary and adrenal hormones and subjective responses in male cocaine abusers

Goletiani

Mendelson

Sholar

et al. 2007

Pharmacology Biochemistry and Behavior

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Nalbuphine (Nubain®) is a mixed action mu-kappa agonist used clinically for the management of pain. Nalbuphine and other mu-kappa agonists decreased cocaine self-administration in preclinical models. Cocaine stimulates the hypothalamic-pituitary-adrenal (HPA) axis, but the effects of nalbuphine on the HPA axis are unknown. Analgesic doses (5 and 10 mg/70 kg) of IV nalbuphine were administered to healthy male cocaine abusers, and plasma levels of PRL, ACTH and cortisol were measured before and at 10, 17, 19, 23, 27, 31, 35, 40, 45, 60, 75, 105, 135 min after nalbuphine administration. Subjective effects were measured on a Visual Analog Scale (VAS). Prolactin (PRL) increased significantly within 17 min (P=.04) and reached peak levels of 22.1 ± 7.1 ng/ml and 54.1 ± 11.3 at 60 min after low and high dose nalbuphine administration, respectively. VAS reports of "Sick," "Bad" and "Dizzy" were significantly higher after 10 mg/70 kg than after 5 mg/70 kg nalbuphine (P=.05−.0001), and were significantly correlated with increases in PRL (P=.05−.0003). However, sedation and emesis were observed only after a 10 mg/70 kg dose of nalbuphine. Interestingly, ACTH and cortisol levels did not change significantly after administration of either dose of nalbuphine. Taken together, these data suggest that nalbuphine had both mu-and kappa-like effects on PRL (PRL increase) but did not increase ACTH and cortisol.

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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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Inhibition of suckling-induced prolactin release by μ- and κ-opioid antagonists

Cited by 32 publications

References 36 publications

Opiate Receptor Subtype Involvement in the Stimulation of Prolactin Release by β-Endorphin in Female Rats

Opiate Receptor Subtype Involvement in the Stimulation of Prolactin Release by β-Endorphin in Female Rats

Effects of nalbuphine on anterior pituitary and adrenal hormones and subjective responses in male cocaine abusers

Neuroendocrine Regulation of Lactation and Milk Production

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