RFamide-related peptides signal through the neuropeptide FF receptor and regulate pain-related responses in the rat

Pertovaara, Antti; Östergård, Maria; Änkö, Minna‐Liisa; Lehti-Koivunen, Sirpa M.; Brandt, Annika; Hong, Wei; Korpi, Esa R.; Panula, Pertti

doi:10.1016/j.neuroscience.2005.04.050

Cited by 22 publications

(11 citation statements)

References 39 publications

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“…At the present time, such species differences are difficult to explain and require further investigation. The biological action of RFRPs may extend far beyond the modulation of reproductive activity, and RFRP-1 and RFRP-3 may fulfil different biological roles [122, 123,136,137,138]. The receptor for RFRPs is widely expressed in the forebrain [136], while RFRP-immunoreactive nerve fibres are broadly distributed in the brain [123, 124, 139, 140], suggesting that RFRPs may control a large palette of biological functions.…”

Section: Photoperiodic Genes Define New Seasonal Loci In the Brainmentioning

confidence: 99%

“…Importantly, the RFRPs share significant homology with another member of the RFamide peptide family, that of the neuropeptide FF. These neuropeptides have been reported to interact with each other’s receptor [136, 137, 141], and biological actions such as the central anti-opioid effect initially attributed to neuropeptide FF may occur via the RFRP receptor and may thus reflect endogenous RFRP activity [136, 142]. …”

Section: Photoperiodic Genes Define New Seasonal Loci In the Brainmentioning

confidence: 99%

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Melatonin Controls Seasonal Breeding by a Network of Hypothalamic Targets

et al. 2009

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In seasonal species, the photoperiod (i.e. day length) tightly regulates reproduction to ensure that birth occurs at the most favourable time of year. In mammals, a distinct photoneuroendocrine circuit controls this process via the pineal hormone melatonin. This hormone is responsible for the seasonal timing of reproduction, but the anatomical substrates and the cellular mechanisms through which melatonin modulates seasonal functions remain imprecise. Recently, several genes have been identified as being regulated by the photoperiod in the brain of seasonal mammals. These genes are thought to play active roles in the regulation of seasonal biology, notably for the adjustment of reproduction and body weight. Here, we briefly review findings associated with the control of seasonal breeding and describe recent data ascribing photoperiodic roles to type 2 and type 3 deiodinases, to the Kiss1/GPR54 system and to the RFamide-related peptides.Interestingly, these systems involve different hypothalamic nuclei, suggesting that several brain loci may be crucial for melatonin to regulate reproduction, and thus represent key starting points to identify the long-sought-after mode and site(s) of action of melatonin. Such findings raise great hopes for the future and could herald a new era of research in the field of seasonal biology.

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Section: Photoperiodic Genes Define New Seasonal Loci In the Brainmentioning

confidence: 99%

Section: Photoperiodic Genes Define New Seasonal Loci In the Brainmentioning

confidence: 99%

Melatonin Controls Seasonal Breeding by a Network of Hypothalamic Targets

et al. 2009

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“…Thomas et al (10) demonstrated that treatment of chick embryonic atrial myocytes with muscarinic agonists decreased levels of GIRK1 and GIRK4 proteins and mRNAs. RFamide-related peptides induced an outward current in Xenopus oocytes that depended on the expression of GIRK1 and GIRK4 and associated with pain in the rat (11). Most interestingly, chronic atrial fibrillation in humans has been associated with the downregulation of GIRK4, I KACh , and decreased muscarinic receptor–mediated shortening of the action potential duration (12).…”

Section: Introductionmentioning

confidence: 99%

Glycogen Synthase Kinase-3β Inhibition Ameliorates Cardiac Parasympathetic Dysfunction in Type 1 Diabetic Akita Mice

et al. 2014

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Decreased heart rate variability (HRV) is a major risk factor for sudden death and cardiovascular disease. We previously demonstrated that parasympathetic dysfunction in the heart of the Akita type 1 diabetic mouse was due to a decrease in the level of the sterol response element–binding protein (SREBP-1). Here we demonstrate that hyperactivity of glycogen synthase kinase-3β (GSK3β) in the atrium of the Akita mouse results in decreased SREBP-1, attenuation of parasympathetic modulation of heart rate, measured as a decrease in the high-frequency (HF) fraction of HRV in the presence of propranolol, and a decrease in expression of the G-protein coupled inward rectifying K+ (GIRK4) subunit of the acetylcholine (ACh)-activated inward-rectifying K+ channel (IKACh), the ion channel that mediates the heart rate response to parasympathetic stimulation. Treatment of atrial myocytes with the GSK3β inhibitor Kenpaullone increased levels of SREBP-1 and expression of GIRK4 and IKACh, whereas a dominant-active GSK3β mutant decreased SREBP-1 and GIRK4 expression. In Akita mice treated with GSK3β inhibitors Li+ and/or CHIR-99021, Li+ increased IKACh, and Li+ and CHIR-99021 both partially reversed the decrease in HF fraction while increasing GIRK4 and SREBP-1 expression. These data support the conclusion that increased GSK3β activity in the type 1 diabetic heart plays a critical role in parasympathetic dysfunction through an effect on SREBP-1, supporting GSK3β as a new therapeutic target for diabetic autonomic neuropathy.

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“…The signaling properties of the NPFF 2 receptor have been studied in several cellular models. The receptor was demonstrated to couple to G i/o heterotrimeric proteins to inhibit adenylyl cyclase (10) and N-type voltagegated calcium channels (11) and activate G protein-regulated inwardly rectifying potassium channels (12), as well as a putative delayed rectifier K ϩ channel (13). It was also shown to activate MAPK pathways (14).…”

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confidence: 99%

Identification and Functional Characterization of the Phosphorylation Sites of the Neuropeptide FF2 Receptor

Bray

Froment

Pardo

et al. 2014

Journal of Biological Chemistry

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Background: G protein-coupled receptor functions are regulated by phosphorylation. Results: Mass spectrometry was used to map the phosphorylation sites of the NPFF 2 neuropeptide FF receptor, and site-directed mutagenesis permitted the identification of their role in receptor regulation. Conclusion: Sites involved in desensitization and internalization do not fully overlap. Significance: This is the first mapping of NPFF 2 receptor phosphorylation.

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RFamide-related peptides signal through the neuropeptide FF receptor and regulate pain-related responses in the rat

Cited by 22 publications

References 39 publications

Melatonin Controls Seasonal Breeding by a Network of Hypothalamic Targets

Melatonin Controls Seasonal Breeding by a Network of Hypothalamic Targets

Glycogen Synthase Kinase-3β Inhibition Ameliorates Cardiac Parasympathetic Dysfunction in Type 1 Diabetic Akita Mice

Identification and Functional Characterization of the Phosphorylation Sites of the Neuropeptide FF2 Receptor

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