NDLI: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

Content Provider	Springer Nature : BioMed Central
Author	Mousa, Shaaban A. Khalefa, Baled I. Shaqura, Mohammed Al-Madol, Mohammed Treskatsch, Sascha Schäfer, Michael
Abstract	Background Under inflammatory conditions, the activation of corticotropin-releasing factor (CRF) receptor has been shown to inhibit pain through opioid peptide release from immune cells or neurons. CRF’s effects on human and animal pain modulation depend, however, on the distribution of its receptor subtypes 1 and 2 (CRF-R1 and CRF-R2) along the neuraxis of pain transmission. The objective of this study is to investigate the respective role of each CRF receptor subtype on centrally administered CRF-induced antinociception during inflammatory pain. Methods The present study investigated the role of intracerebroventricular (i.c.v.) CRF receptor agonists on nociception and the contribution of cerebral CRF-R1 and/or CRF-R2 subtypes in an animal model of Freund’s complete adjuvant (FCA)-induced hind paw inflammation. Methods used included behavioral experiments, immunofluorescence confocal analysis, and reverse transcriptase-polymerase chain reaction. Results Intracerebroventricular, but systemically inactive, doses of CRF elicited potent, dose-dependent antinociceptive effects in inflammatory pain which were significantly antagonized by i.c.v. CRF-R1-selective antagonist NBI 27914 (by approximately 60%) but less by CRF-R2-selective antagonist K41498 (by only 20%). In line with these findings, i.c.v. administration of CRF-R1 agonist stressin I produced superior control of inflammatory pain over CRF-R2 agonist urocortin-2. Intriguingly, i.c.v. opioid antagonist naloxone significantly reversed the CRF as well as CRF-R1 agonist-elicited pain inhibition. Consistent with existing evidence of high CRF concentrations in brain areas such as the thalamus, hypothalamus, locus coeruleus, and periaqueductal gray following its i.c.v. administration, double-immunofluorescence confocal microscopy demonstrated primarily CRF-R1-positive neurons that expressed opioid peptides in these pain-relevant brain areas. Finally, PCR analysis confirmed the predominant expression of the CRF-R1 over CRF-R2 in representative brain areas such as the hypothalamus. Conclusion Taken together, these findings suggest that CRF-R1 in opioid-peptide-containing brain areas plays an important role in the modulation of inflammatory pain and may be a useful therapeutic target for inflammatory pain control.
Related Links	https://jneuroinflammation.biomedcentral.com/counter/pdf/10.1186/s12974-022-02498-8.pdf
Ending Page	15
Page Count	15
Starting Page	1
File Format	HTM / HTML
ISSN	17422094
DOI	10.1186/s12974-022-02498-8
Journal	Journal of Neuroinflammation
Issue Number	1
Volume Number	19
Language	English
Publisher	BioMed Central
Publisher Date	2022-06-15
Access Restriction	Open
Subject Keyword	Neurosciences Neurology Neurobiology Immunology Inflammatory pain Corticotropin-releasing factor Brain Opioid peptide Immunofluorescence
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology Cellular and Molecular Neuroscience Neurology
Journal Impact Factor	9.3/2023
5-Year Journal Impact Factor	9.8/2023

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Adoptive transfer of M2 macrophages reduces neuropathic pain via opioid peptides

Mechanisms of the Analgesic Action of Corticotrophin-Releasing Factor on Somatic Pain Sensitivity in Rats

Inhibition of Schwann cell pannexin 1 attenuates neuropathic pain through the suppression of inflammatory responses

Anti-inflammatory properties of a novel peptide interleukin 1 receptor antagonist

Gastrin-Releasing Peptide Receptor Knockdown Induces Senescence in Glioblastoma Cells

Mu-opioid receptor and delta-opioid receptor differentially regulate microglial inflammatory response to control proopiomelanocortin neuronal apoptosis in the hypothalamus: effects of neonatal alcohol

Ginsenoside Re protects methamphetamine-induced dopaminergic neurotoxicity in mice via upregulation of dynorphin-mediated κ-opioid receptor and downregulation of substance P-mediated neurokinin 1 receptor

Colony-stimulating factor 1 receptor blockade prevents fractionated whole-brain irradiation-induced memory deficits

Mechanisms of the Analgesic Effect of Corticotropin-Releasing Factor in Conscious Rats

Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

Similar Documents

Adoptive transfer of M2 macrophages reduces neuropathic pain via opioid peptides

Mechanisms of the Analgesic Action of Corticotrophin-Releasing Factor on Somatic Pain Sensitivity in Rats

Inhibition of Schwann cell pannexin 1 attenuates neuropathic pain through the suppression of inflammatory responses

Anti-inflammatory properties of a novel peptide interleukin 1 receptor antagonist

Gastrin-Releasing Peptide Receptor Knockdown Induces Senescence in Glioblastoma Cells

Mu-opioid receptor and delta-opioid receptor differentially regulate microglial inflammatory response to control proopiomelanocortin neuronal apoptosis in the hypothalamus: effects of neonatal alcohol

Ginsenoside Re protects methamphetamine-induced dopaminergic neurotoxicity in mice via upregulation of dynorphin-mediated κ-opioid receptor and downregulation of substance P-mediated neurokinin 1 receptor

Colony-stimulating factor 1 receptor blockade prevents fractionated whole-brain irradiation-induced memory deficits

Mechanisms of the Analgesic Effect of Corticotropin-Releasing Factor in Conscious Rats

Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas