title: N/OFQ system in brain areas of nerve-injured mice: its role in different aspects of neuropathic pain.
abstract: Several studies showed that chronic pain causes reorganization and functional alterations of supraspinal brain regions. The nociceptin-NOP receptor system is one of the major systems involved in pain control and much evidence also suggested its implication in stress, anxiety and depression. Therefore, we investigated the nociceptin-NOP system alterations in selected brain regions in a neuropathic pain murine model. Fourteen days after the common sciatic nerve ligature, polymerase chain reaction (PCR) analysis indicated a significant decrease of pronociceptin and NOP receptor mRNA levels in the thalamus; these alterations could contribute to the decrease of the thalamic inhibitory function reported in neuropathic pain condition. Nociceptin peptide and NOP mRNA increased in the anterior cingulate cortex (ACC) and not in the somatosensory cortex, suggesting a peculiar involvement of this system in pain regulating circuitry. Similarly to the ACC, an increase of nociceptin peptide levels was observed in the amygdala. Finally, the pronociceptin and NOP mRNAs decrease observed in the hypothalamus reflects the lack of hypothalamus-pituitary-adrenal axis activation, already reported in neuropathic pain models. Our data indicate that neuropathic pain conditions affect the supraspinal nociceptin-NOP system which is also altered in regions known to play a role in emotional aspects of pain.
authors.affiliation: Department of Pharmacy and Biotechnology, Alma Mater Studiorum - University of Bologna, Bologna, Italy.
authors.forename: M
authors.initials: M
authors.lastname: Palmisano
authors.affiliation: Department of Pharmacy and Biotechnology, Alma Mater Studiorum - University of Bologna, Bologna, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Mercatelli
authors.affiliation: Department of Pharmacy and Biotechnology, Alma Mater Studiorum - University of Bologna, Bologna, Italy.
authors.forename: F F
authors.initials: FF
authors.lastname: Caputi
authors.affiliation: Department of Pharmacy and Biotechnology, Alma Mater Studiorum - University of Bologna, Bologna, Italy.
authors.forename: D
authors.initials: D
authors.lastname: Carretta
authors.affiliation: Department of Pharmacy and Biotechnology, Alma Mater Studiorum - University of Bologna, Bologna, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Romualdi
authors.affiliation: Department of Pharmacy and Biotechnology, Alma Mater Studiorum - University of Bologna, Bologna, Italy.
authors.forename: S
authors.identifier: 0000-0001-8905-7393
authors.initials: S
authors.lastname: Candeletti
mesh_terms: D000679:Amygdala / Q000378:metabolism / Q000502:physiology; D000818:Animals; D006179:Gyrus Cinguli / Q000378:metabolism* / Q000502:physiology; D008297:Male; D051379:Mice; D009437:Neuralgia / Q000378:metabolism* / Q000503:physiopathology; D018847:Opioid Peptides / Q000235:genetics / Q000378:metabolism*; D011957:Receptors, Opioid / Q000235:genetics / Q000378:metabolism*; D012584:Sciatic Nerve / Q000293:injuries*; D013003:Somatosensory Cortex / Q000378:metabolism / Q000502:physiology; D013788:Thalamus / Q000378:metabolism / Q000502:physiology; D000094942:Nociceptin Receptor; D000097629:Nociceptin
chemical_list: D018847:Opioid Peptides; D011957:Receptors, Opioid; D000094942:Nociceptin Receptor; D000097629:Nociceptin; C000722287:Oprl1 protein, mouse
keywords: Amygdala; NOP receptor; cingulate cortex; gene expression; neuropathic pain; nociceptin; supraspinal areas; thalamus