Endogenous mammalian RF-amide peptides, including PrRP, kisspeptin and 26RFa, modulate nociception and morphine analgesia via NPFF receptors

Elhabazi, Khadija; Humbert, Jean-Paul; Bertin, Isabelle; Schmitt, Martine; Bihel, Frédéric; Bourguignon, Jean‐Jacques; Bucher, Bernard; Becker, Jérôme A.J.; Sorg, Tania; Méziane, Hamid; Petit-Demoulière, Benoît; Ilien, Brigitte; Simonin, Frédéric

doi:10.1016/j.neuropharm.2013.07.012

Cited by 93 publications

(132 citation statements)

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“…We have previously shown that endogenous RF-amide peptides Kp-10, PrRP-20 and 26RFa bind and activate their cognate receptors as well as NPFF1R and NPFF2R subtypes [13]. This work shows that this is also true with the shorter N-terminus benzoylated forms of these peptides.…”

Section: Discussionmentioning

confidence: 54%

“…Competition experiments with membranes from CHO cells stably expressing hNPFF1R, hNPFF2R, GPR10, GPR54 and GPR103 were performed essentially as described [13]. Briefly, hNPFF1R or hNPFF2R membranes (5-10 g of proteins) were incubated (1 h at 25 • C; 0.25 mL total volume) with 10 nM or 3 nM …”

Section: Binding Experimentsmentioning

confidence: 99%

“…These RF-amide neuropeptides are implicated in a large diversity of biological activities, such as neuroendocrine and cardiovascular functions, energy homeostasis, feeding, as well as pain modulation [12]. Recently, we reported a systematic study of the five cloned human RF-amide receptors (NPFF1R, NPFF2R, GPR10, GPR54 and GPR103) in terms of affinity and functional activity towards each endogenous RF-amide neuropeptide [13]. Altogether our results showed that NPFF1R and NPFF2R displayed high affinity for all the RF-amide peptides, while GPR10, GPR54 and GPR103 only bind their cognate ligands.…”

Section: Introductionmentioning

confidence: 99%

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Effects of systematic N-terminus deletions and benzoylations of endogenous RF-amide peptides on NPFF1R, NPFF2R, GPR10, GPR54 and GPR103

et al. 2015

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Section: Discussionmentioning

confidence: 54%

Section: Binding Experimentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of systematic N-terminus deletions and benzoylations of endogenous RF-amide peptides on NPFF1R, NPFF2R, GPR10, GPR54 and GPR103

et al. 2015

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“…In that study, Lapatto et al [17] reported that, compared to Kiss1r -/- female mice, Kiss1 -/- female mice displayed a more variable phenotype and they suggested that it could be the result of modest constitutive Kiss1r activity in the complete absence of endogenous KP. It is unlikely that the variable reproductive phenotype is the result of other RF-amide peptides activating Kiss1r since binding experiments, performed on membranes from CHO cells expressing KISS1R, revealed a high affinity and remarkable selectivity for KP; this is in contrast to the NPFF1/GPR147 and NPFF2/GPR74 receptors which display a high affinity for all RF-amides, including KP [52]. …”

Section: Kiss1r Displays Basal Constitutive Signaling and Kp-independmentioning

confidence: 99%

KISS1R: Hallmarks of an Effective Regulator of the Neuroendocrine Axis

Millar

Babwah

2015

Neuroendocrinology

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Kisspeptin (KP) is now well recognized as a potent stimulator of gonadotropin-releasing hormone (GnRH) secretion and thereby a major regulator of the neuroendocrine-reproductive axis. KP signals via KISS1R, a G protein-coupled receptor (GPCR) that activates the G proteins Gα_q/11. Modulation of the interaction of KP with KISS1R is therefore a potential new therapeutic target for stimulating (in infertility) or inhibiting (in hormone-dependent diseases) the reproductive hormone cascade. Major efforts are underway to target KISS1R in the treatment of sex steroid hormone-dependent disorders and to stimulate endogenous hormonal responses along the neuroendocrine axis as part of in vitro fertilization protocols. The development of analogs modulating KISS1R signaling will be aided by an understanding of the intracellular pathways and dynamics of KISS1R signaling under normal and pathological conditions. This review focuses on KISS1R recruitment of intracellular signaling (Gα_q/11- and β-arrestin-dependent) pathways that mediate GnRH secretion and the respective roles of rapid desensitization, internalization, and recycling of resensitized receptors in maintaining an active population of KISS1R at the cell surface to facilitate prolonged KP signaling. Additionally, this review summarizes and discusses the major findings of an array of studies examining the desensitization of KP signaling in man, domestic and laboratory animals. This discussion highlights the major effects of ligand efficacy and concentration and the physiological, developmental, and metabolic status of the organism on KP signaling. Finally, the potential for the utilization of KP and analogs in stimulating and inhibiting the reproductive hormone cascade as an alternative to targeting the downstream GnRH receptor is discussed.

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“…Similarly, both the hypothalamus and brainstem contain neurons that secrete prolactin-releasing peptide, an RF-amide peptide that can cause prolactin release along with a variety of other functions. 4 The RF-amide peptides are a broad class of neuropeptides that are believed to modulate stress responses, energy metabolism, and analgesia. Due to the low receptor affinity of these peptides there are probably significant cross-interactions, and it is possible that the headache pain experienced by patients with spontaneous intracranial hypotension is significant enough to affect the release of RF-amides that cross-react with prolactin-releasing peptide and cause prolactin release in the pituitary.…”

Section: Discussionmentioning

confidence: 99%

Hyperprolactinemia due to spontaneous intracranial hypotension

Schievink¹,

Nuño²,

Rozen

et al. 2015

JNS

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SpontaneouS intracranial hypotension is an important cause of new, daily, persistent headaches that usually afflicts young to middle-aged adults, with a female predominance and a peak incidence in the 5th decade of life. 16 The headache is typically orthostatic and is often accompanied by nausea, neck pain, and hearing abnormalities. Spontaneous intracranial hypotension is uncommon, with an estimated incidence of approximately 5 per 100,000 per year. The cause of spontaneous intracranial hypotension is almost always a spontaneous spinal CSF leak, and a systemic connective tissue disorder affecting the spinal dura mater is often suspected.14 In spontaneous intracranial hypotension, pituitary enlargement is one of the 5 main imaging features that can be found on brain MRI (Sagging of the brain, Enhancement of the pachymeninges, Engorgement of venous structures, Pituitary enlargement, and Subdural fluid collections [SEEPS]). 16Pituitary enlargement in spontaneous intracranial hypotension has now been well documented and can resemble a pituitary tumor. 2,9,11,13,18 Moreover, sagging of the brain often is associated with distortion of the pituitary stalk. However, a systematic evaluation of pituitary function has not been reported in patients with spontaneous intracranial hypotension. Therefore, we investigated pituitary hormones in patients with this disorder. OBJect Spontaneous intracranial hypotension is an increasingly recognized cause of headaches. Pituitary enlargement and brain sagging are common findings on MRI in patients with this disorder. The authors therefore investigated pituitary function in patients with spontaneous intracranial hypotension. MethODS Pituitary hormones were measured in a group of 42 consecutive patients with spontaneous intracranial hypotension. For patients with hyperprolactinemia, prolactin levels also were measured following treatment. Magnetic resonance imaging was performed prior to and following treatment. reSultS The study group consisted of 27 women and 15 men with a mean age at onset of symptoms of 52.2 ± 10.7 years (mean ± SD; range 17-72 years). Hyperprolactinemia was detected in 10 patients (24%), ranging from 16 ng/ml to 96.6 ng/ml in men (normal range 3-14.7 ng/ml) and from 31.3 ng/ml to 102.5 ng/ml in women (normal range 3.8-23.2 ng/ml). In a multivariate analysis, only brain sagging on MRI was associated with hyperprolactinemia. Brain sagging was present in 60% of patients with hyperprolactinemia and in 19% of patients with normal prolactin levels (p = 0.02). Following successful treatment of the spontaneous intracranial hypotension, hyperprolactinemia resolved, along with normalization of brain MRI findings in all 10 patients. cONcluSiONS Spontaneous intracranial hypotension is a previously undescribed cause of hyperprolactinemia. Brain sagging causing distortion of the pituitary stalk (stalk effect) may be responsible for the hyperprolactinemia. Methods

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Endogenous mammalian RF-amide peptides, including PrRP, kisspeptin and 26RFa, modulate nociception and morphine analgesia via NPFF receptors

Cited by 93 publications

References 46 publications

Effects of systematic N-terminus deletions and benzoylations of endogenous RF-amide peptides on NPFF1R, NPFF2R, GPR10, GPR54 and GPR103

Effects of systematic N-terminus deletions and benzoylations of endogenous RF-amide peptides on NPFF1R, NPFF2R, GPR10, GPR54 and GPR103

KISS1R: Hallmarks of an Effective Regulator of the Neuroendocrine Axis

Hyperprolactinemia due to spontaneous intracranial hypotension

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