Morphine does not stimulate prolactin release during lactation

Callahan, Phyllis; Janik, James; Grandison, Lindsey; Rabii, Jamshid

doi:10.1016/0006-8993(88)91506-5

Cited by 27 publications

(34 citation statements)

References 20 publications

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“…With respect to the preceding discussion, it is quite surprising to find that morphine treatment does not elicit a PRL secretory response during lactation (24,25). In an extensive series of experiments, Callahan et al (24) demonstrated that in lactating rats, morphine sulfate delivered by any route of administration failed to increase plasma PRL.…”

Section: Discussionmentioning

confidence: 97%

“…In an extensive series of experiments, Callahan et al (24) demonstrated that in lactating rats, morphine sulfate delivered by any route of administration failed to increase plasma PRL. The observed opiate insensitivity is dependent upon the suckling stimulus (25).…”

Section: Discussionmentioning

confidence: 99%

“…The observed insensitivity of the PRLreleasing mechanism to opiates is dependent upon the suckling stimulus (25) and apparently not related to changes in drug metabolism (24, 25). The lack of response to morphine seems specific for PRL since morphine-induced G H responses are virtually identical in lactating and non-lactating rats (24). One possible explanation for the altered opiate sensitivity during lactation could be related to reduced number and/or affinity of mu opioid receptors (24,25).…”

mentioning

confidence: 98%

“…The lack of response to morphine seems specific for PRL since morphine-induced G H responses are virtually identical in lactating and non-lactating rats (24). One possible explanation for the altered opiate sensitivity during lactation could be related to reduced number and/or affinity of mu opioid receptors (24,25).…”

mentioning

confidence: 98%

“…Interestingly, we have discovered that in the lactating female, the opiate agonist morphine does not elicit a P R L secretory response (24,25). The observed insensitivity of the PRLreleasing mechanism to opiates is dependent upon the suckling stimulus (25) and apparently not related to changes in drug metabolism (24, 25).…”

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confidence: 99%

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Mu‐Selective Opioid Peptides Stimulate Prolactin Release in Lactating Rats

Baumann

Rabii

1990

J Neuroendocrinology

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The fact that opiates elicit prolactin secretion is well known. However, we have recently discovered that morphine does not stimulate prolactin release in lactating rats. The physiological basis for this alteration in opiate sensitivity during lactation is not known. Since morphine-induced prolactin secretion in male rats is mediated via the mu opioid receptor subtype, one possible explanation is that mi1 receptors are down-regulated during lactation. To address this possibility, the effects of mu opioid peptides on prolactin secretion were examined in lactating rats. The presumed mu-selective peptides DAGO ([D-Ala', Me-Phe4, Gly-01'1-enkephalin) and PLO-17 ("Me-Phe3, D-Pro4]-morphiceptin) were administered to primiparous lactating rats and the resulting hormone responses measured. Both DAGO and PLO-17 caused a rapid and significant rise in plasma prolactin during lactation. The prolactin-releasing effects of both peptides were naloxone reversible, suggesting involvement of opioid receptors. Moreover, the DAGO-induced secretion of prolactin could be completely abolished by pretreatment with the irreversible mu antagonist b-funaltrexamine. In lactating rats, DAGO and PLO-17 were poor growth hormone-releasing agents, providing further evidence for the mu specificity of these peptides. These results imply that during lactation, as in other reproductive states, mu opioid receptor sites are positively coupled to the prolactin secretory mechanism. Thus, the previously observed inability of morphine to elicit prolactin release in lactating rats cannot be explained on the basis of down-regulation of mu opioid receptors.The \timulatory effect of opioids on prolactin (PRL) release is well estaidished for several mammalian species, including man (1, 2). In tile rat, opioid antagonists such as naloxone, suppress basal and stimulus-induced PRL release suggesting that endogenous opiclid peptides (EOPs) may have an important role in the phqyiological regulation of PRL secretion (1, 2). Although most evidLmce points to central sites of EOP action (3-9, direct opioid effects at the level of the anterior pituitary cannot be completely m1eC out (6). Recently, the concept of multiple opioid receptors has gained wide acceptance, and many investigators have attempted to correlate specific neuroendocrine functions with particular opioid receptor subtypes (7-1 6).There is general agreement that at least three major opioid receptor populations are present: mu, kappa, and delta sites (17 19). The characterization of receptor subtypes is based largely on !he affinities of opioid ligands for particular binding sites in Vitvri Thus, morphine is the prototypical mu receptor agonist while enkephalin peptides interact preferentially with delta sites. Kelaocine-like drugs are potent, though non-selective, kappa agonists, and dynorphins appear to be the endogenous ligands for the kappa site (17,19). Unfortunately, determining the functional importance of specific opioid receptor subtypes has been difficult due to the fact that few opioid...

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

mentioning

confidence: 98%

mentioning

confidence: 99%

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