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

Kehoe, Lesley; Parman, Rebecca; Janik, James; Callahan, Phyllis

doi:10.1159/000126448

Cited by 32 publications

(30 citation statements)

References 20 publications

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“…Administration of either the µ or ĸ receptor antagonists inhibited prolactin release during suckling [19], but only the µ site seemed to mediate inhibition of hypothalamic dopaminergic neural activity [30]. Furthermore, β-endorphin stimulated prolactin secretion in both virgin and postpartum female rats and this response was antagonized by specific µ 1 [21], µ, δ and ĸ [22]sites, indicating the involvement of multiple receptor subtypes. Taken together, we conclude that the EOP are necessary for normal lactation and that dynorphin and the enkephalins exert their effects by modulating TIDA neuronal activity, but β-endorphin may affect the activity of releasing factors or the THDA neurons.…”

Section: Discussionmentioning

confidence: 99%

“…cannulations were performed on dams on day 2 postpartum under ketamine/xylazine (80 mg/kg, 14 mg/kg i.m. respectively) anesthesia following the coordinate system of Pelligrino et al [40]as previously described [22]. When dams were fully awake, approximately 4–5 h after surgery, they were returned to their pups.…”

Section: Methodsmentioning

confidence: 99%

“…Endogenous opioid peptides (EOP) are clearly involved in the regulation of prolactin secretion [19, 20, 21, 22, 23]and elicit their effects via multiple opiate receptors which have been biochemically and pharmacologically characterized [24, 25]and cloned [26, 27, 28, 29]. β-Endorphin stimulated prolactin secretion in postpartum and virgin female rats to levels that mimicked the suckling-induced prolactin increase.…”

Section: Introductionmentioning

confidence: 99%

“…β-Endorphin stimulated prolactin secretion in postpartum and virgin female rats to levels that mimicked the suckling-induced prolactin increase. This response was abolished by antagonizing the µ 1 [21], µ, δ or ĸ sites [22]indicating that β-endorphin activates a pathway involving multiple receptor subtypes. In lactating female rats, antagonism of either the µ or ĸ receptor site inhibited prolactin release during suckling [19], but only the µ site seemed to mediate inhibition of hypothalamic dopaminergic neural activity [30].…”

Section: Introductionmentioning

confidence: 99%

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Immunoneutralization of Endogenous Opioid Peptides Prevents the Suckling-Induced Prolactin Increase and the Inhibition of Tuberoinfundibular Dopaminergic Neurons

Callahan

Klosterman²,

Prunty³

et al. 2000

Neuroendocrinology

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Previous studies have shown that the endogenous opioid peptides, acting at specific opiate receptor subtypes, are involved in the suckling-induced prolactin secretory response. The prolactin increase elicited by suckling is due, at least in part, to an inhibition of tuberoinfundibular dopaminergic (TIDA) neurons in the hypothalamus. We investigated the effects of immunoneutralization of dynorphin, leu-enkephalin and met-enkephalin on the suckling-induced prolactin increase and on the activity of the TIDA neurons in lactating female rats between days 7 and 12 postpartum. Rats were injected into the right lateral ventricle with antiserum specific for one of these three peptides. Control rats were administered equal amounts of immunoglobulin proteins. Suckling produced a profound and significant increase in prolactin levels, as well as a decrease in DOPA accumulation in the median eminence of lactating rats. Administration of immunoglobulin concentrations of up to 3.6 µg did not inhibit the prolactin secretory response to the suckling stimulus and did not prevent the suckling-induced inhibition of TIDA neurons. Antisera to all three endogenous opioid peptides abolished the suckling-induced prolactin increase and prevented the inhibition in DOPA accumulation in the median eminence. Thus, the endogenous opioid peptides, dynorphin, leu-enkephalin and met-enkephalin, are essential for the prolactin secretory response to suckling and inhibition of TIDA neuronal activity is at least one of the mechanisms of action utilized by these peptides.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Immunoneutralization of Endogenous Opioid Peptides Prevents the Suckling-Induced Prolactin Increase and the Inhibition of Tuberoinfundibular Dopaminergic Neurons

Callahan

Klosterman²,

Prunty³

et al. 2000

Neuroendocrinology

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“…β-Endorphin and methionine enkephalin have been reported to play no apparent role in either initiating or modulating the release of turkey PRL [1]. Some studies indicate an interaction between multiple opiate receptor sites, of which the best characterized subtypes are the µ-, δ-, and ĸ-sites [42, 43], that might act upon a convergent neural pathway regulating mammalian PRL secretion [44]. Also, more than one receptor subtype may exist on the same nerve terminal [45].…”

Section: Discussionmentioning

confidence: 99%

An Opioid Pathway in the Hypothalamus of the Turkey That Stimulates Prolactin Secretion

et al. 1999

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Circulating prolactin (PRL) levels increase when dynorphin is infused into the turkey brain. This study tested the hypothesis that centrally infused dynorphin requires an intact vasoactive intestinal peptide (VIP) system in order to stimulate turkey PRL secretion. It also investigated the roles of the dopaminergic and serotonergic systems in dynorphin-induced PRL release. Drugs were infused into the third ventricle of anesthetized laying turkeys via stereotaxically guided cannulae and circulating blood was assayed for changes in PRL levels. When a highly selective ĸ opioid receptor antagonist was given prior to dynorphin injection, the PRL response to dynorphin was almost totally blocked. The coinfusion of either a serotonin (5-HT) or a D₁ dopamine (DA) receptor antagonist with dynorphin prevented the increase in PRL observed in birds when dynorphin was infused alone. On the other hand, the ĸ opioid receptor antagonist failed to prevent the 5-HT-induced release of PRL. In hens actively immunized against VIP, infused dynorphin was unable to increase plasma PRL levels and infused VIP gave a muted PRL rise, while large increases in PRL were seen in nonimmunized birds receiving the same infusions. These data show that: (1) dynorphin stimulates PRL secretion by activating ĸ opioid receptors in the avian hypothalamus, and (2) dynorphin, 5-HT, DA, and VIP stimulate avian PRL secretion via a common pathway expressing ĸ opioid, serotonergic, dopaminergic, and VIPergic receptors at synapses arranged serially in that functional order, with the VIPergic system as the final mediator (releasing factor).

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μ‐opioid receptor mRNA expression in identified hypothalamic neurons

Zheng

Bosch

Rønnekleiv

2005

J of Comparative Neurology

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It has been known for a number of years that mu-opioid receptor agonists (e.g., morphine, beta-endorphin, and enkephalin) inhibit luteinizing hormone (LH), vasopressin (VP), and oxytocin (OT) release and stimulate prolactin secretion in rodents and primates by an action at the level of the brain. Also, electrophysiological studies have established that hypothalamic neurons, including gonadotropin-releasing hormone (GnRH), VP, OT, beta-endorphin, and dopamine neurons, are responsive to mu-receptor activation. Although mu-receptor expression has been demonstrated in the hypothalamus, there have been few studies localizing these receptors in neurosecretory neurons. Therefore, we sought to document mu-opioid receptor mRNA expression in immunocytochemically identified hypothalamic neurons. The brains from both female and male guinea pigs were examined by using in situ hybridization and immunocytochemistry. The studies revealed that mu-receptor mRNA was expressed in different diencephalic regions including the preoptic area, the bed nuclei stria terminalis, the paraventricular nucleus thalamus, and the anterior hypothalamus, as well as the supraoptic (SON), paraventricular (PVH), ventromedial, dorsomedial, and arcuate nuclei of the hypothalamus. Importantly, mu-opioid receptors were expressed in subpopulations of GnRH neurons (33.25 +/- 4.6% and 33.6 +/- 3.7% in females and males, respectively), dopamine neurons (51.7 +/- 5.8% to 75.0 +/- 2.6%, depending on neuronal location), beta-endorphin neurons (68.3.0 +/- 4.4%), and VP neurons (41-70%, depending on neuronal location). Because mu-opioid receptors couple via G-proteins to activate inwardly rectifying potassium channels and to inhibit calcium channels, the presence of these receptors is likely to play a major role in directly controlling the excitability of hypothalamic neurons.

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

Cited by 32 publications

References 20 publications

Immunoneutralization of Endogenous Opioid Peptides Prevents the Suckling-Induced Prolactin Increase and the Inhibition of Tuberoinfundibular Dopaminergic Neurons

Immunoneutralization of Endogenous Opioid Peptides Prevents the Suckling-Induced Prolactin Increase and the Inhibition of Tuberoinfundibular Dopaminergic Neurons

An Opioid Pathway in the Hypothalamus of the Turkey That Stimulates Prolactin Secretion

μ‐opioid receptor mRNA expression in identified hypothalamic neurons

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