ArticleThe Journal of pharmacology and experimental therapeutics2011
The role of central gastrin-releasing peptide and neuromedin B receptors in the modulation of scratching behavior in rats.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Spinal Calcrl+ neurons amplify mechanical itch signaling via synaptic plasticity in chronic itch model.PloS one · 2025Article
- Neural pathways that compel us to scratch an itch.Journal of biosciences · 2024Review
- Functional roles of neuromedin B and gastrin-releasing peptide in regulating itch and pain in the spinal cord of non-human primates.Biochemical pharmacology · 2022Article
- Analgesic effect of gastrin-releasing peptide in the dorsal horn.Molecular pain · 2022Article
- Article
- Pain and itch processing by subpopulations of molecularly diverse spinal and trigeminal projection neurons.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Chemogenetic activation of central gastrin-releasing peptide-expressing neurons elicits itch-related scratching behavior in male and female mice.Pharmacology research & perspectives · 2021Article
- Neuromedin B Induces Acute Itch in Mice via the Activation of Peripheral Sensory Neurons.Acta dermato-venereologica · 2019Article
- Spinal Functions of B-Type Natriuretic Peptide, Gastrin-Releasing Peptide, and Their Cognate Receptors for Regulating Itch in Mice.The Journal of pharmacology and experimental therapeutics · 2016Article
- Neuromedin B and Its Receptor: Gene Cloning, Tissue Distribution and Expression Levels of the Reproductive Axis in Pigs.PloS one · 2016Article
- GRPR/PI3Kγ: Partners in Central Transmission of Itch.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Phoenixin: A candidate pruritogen in the mouse.Neuroscience · 2015Article
- Review
- Molecular and cellular mechanisms that initiate pain and itch.Cellular and molecular life sciences : CMLS · 2015Review
- Distinct functions of opioid-related peptides and gastrin-releasing peptide in regulating itch and pain in the spinal cord of primates.Scientific reports · 2015Article
- Role of spinal bombesin-responsive neurons in nonhistaminergic itch.Journal of neurophysiology · 2014Article
- Cross-inhibition of NMBR and GRPR signaling maintains normal histaminergic itch transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- The Gastrin-Releasing Peptide Receptor (GRPR) in the Spinal Cord as a Novel Pharmacological Target.Current neuropharmacology · 2014Article
- Itch elicited by intradermal injection of serotonin, intracisternal injection of morphine, and their synergistic interactions in rats.Neuroscience · 2014Article
- Itch-associated peptides: RNA-Seq and bioinformatic analysis of natriuretic precursor peptide B and gastrin releasing peptide in dorsal root and trigeminal ganglia, and the spinal cord.Molecular pain · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
Bombesin is a pruritogenic agent that causes intense itch-scratching activity in rodents. Bombesin has high affinity for the gastrin-releasing peptide (GRP) receptor (GRPr) and the neuromedin B (NMB) receptor (NMBr). The aim of this study was to investigate pharmacologically the ability of GRPr and NMBr to elicit scratching behavior in rats. The intracerebroventricular route was selected for drug delivery because the study focused on supraspinal sites of action. The magnitude and duration of scratching produced by the naturally occurring peptides GRP and NMB were characterized. Antagonists selective for GRPr [(d-Tpi6, Leu13Ψ(CH2-NH)-Leu14)Bombesin(6-14) (RC-3095)] and NMBr [(S)-α-methyl-α-[[[(4-nitrophenyl)amino]carbonyl]amino]-N-[[1-(2-pyridinyl)cyclohexyl]methyl]-1H-indole-3-propanamide (PD168368)] were used to define the role of GRPr and NMBr in the scratching response. After intracerebroventricular administration, GRP (0.03-0.3 nmol) and NMB (0.1-1 nmol) dose-dependently elicited marked scratching. There was a tolerance to scratching elicited by daily repeated administration of bombesin, GRP, or NMB. Presession administration of RC-3095 (0.1-1 nmol) and PD168368 (0.3-3 nmol) dose-dependently antagonized scratching elicited by GRP and NMB, respectively. More importantly, 1 nmol of RC-3095 failed to block NMB-elicited scratching, and 3 nmol of PD168368 failed to block GRP-elicited scratching. In addition, pretreatment with effective doses of RC-3095 or PD168368 alone or in combination did not block bombesin-elicited scratching. Through the use of the selective antagonists RC-3095 and PD168368, this study demonstrates that central GRPr and NMBr act independently to elicit scratching behavior and there is an additional, unidentified receptor mechanism underlying bombesin-elicited scratching.
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