Changes in brain content of nociceptin/orphanin FQ and endomorphin 2 in a rat model of neuropathic pain
Section snippets
Acknowledgements
This work was supported by the National Natural Science Foundation of China (39830160, 39800198), the National Basic Research Program (G1999054000) of China and a grant from NIDA, USA (DA03983).
References (20)
- et al.
Quantitative assessment of tactile allodynia in the rat paw
J. Neurosci. Methods
(1994) - et al.
The cold plate as a test of nociceptive behaviors: description and application to the study of chronic neuropathic and inflammatory pain models
Pain
(1998) - et al.
Functional antagonism of mu-, delta- and kappa-opioid antinociception by orphanin FQ
Neurosci. Lett.
(1996) - et al.
Opioid supraspinal analgesic synergy between the amygdala and periaqueductal gray in rats
Brain Res.
(1998) - et al.
Spinal analgesic action of endomorphins in acute, inflammatory and neuropathic pain in rats
Eur. J. Pharmacol.
(1999) - et al.
Central changes in nociceptin, dynorphin B and Met-enkephalin-Arg-Phe in different models of nociception
Brain Res.
(2000) - et al.
Accelerated release and production of orphanin FQ in brain of chronic morphine tolerant rats
Brain Res.
(1999) - et al.
Orphanin FQ potentiates formalin-induced pain behavior and antagonizes morphine analgesia in rats
Neurosci. Lett.
(1997) Efficient analysis of experimental observations
Ann. Rev. Pharmacol. Toxicol.
(1980)- et al.
Possible involvement of opioid peptides of caudate nucleus in acupuncture analgesia
Pain
(1985)
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Endogenous opioid peptides in the descending pain modulatory circuit
2020, NeuropharmacologyCitation Excerpt :β-endorphin release in the PAG is associated with stress-induced analgesia (Kulling et al., 1989), as well as peripheral injury (Nakamura et al., 2013). Similar increases in endomorphin 2 levels were reported following neuropathic pain (Sun et al., 2001). In addition, stimulation of the amygdala induces release of the KOR agonist dynorphin in the PAG (Nakamura et al., 2013) but dynorphin does not elicit analgesia when microinjected into the PAG (Fang et al., 1989).
Central N/OFQ-NOP Receptor System in Pain Modulation
2016, Advances in PharmacologyCitation Excerpt :For example, NOP receptor positive cells in the PAG and RVM were increased, while N/OFQ was increased in cingulate cortex, but not PAG and RVM, in rats under CCI (Ma, Xie, Dong, Wang, & Wu, 2005; Rosen et al., 2000). Furthermore, N/OFQ expression was upregulated in the PAG at a later period in SNL rats (Sun, Wang, Zhao, Chang, & Han, 2001). The direction of pain modulation via supraspinal N/OFQ-NOP receptor system might be changed along with temporal upregulation and functional plasticity of the NOP receptor henceforth (Schröder et al., 2014).
Nociceptin/orphanin FQ receptor and pain: Feasibility of the fourth opioid family member
2015, European Journal of PharmacologyCitation Excerpt :Similary, the number of NOP receptor mRNA positive cells increased also in the periaqueductal gray (PAG) and RVM after CCI (Ma et al., 2005). N/OFQ immunoreactivity increased in DRG, PAG and RVM of CCI rats (Chen and Sommer, 2006) or in other animal model of neuropathic pain (Sun et al., 2001). In these conditions spinally infused N/OFQ reduced mechanical and thermal hypersensitivity in trauma-induced models (Yamamoto and Nozaki-Taguchi, 1997).
Endomorphins
2013, Handbook of Biologically Active PeptidesChronic neuropathic pain in mice reduces μ-opioid receptor-mediated G-protein activity in the thalamus
2011, Brain ResearchCitation Excerpt :The observation that the reduction in G-protein activation in CCI mice was observed only at day 10 post-surgery and not earlier time points supports this hypothesis because tonic pain has been reported to increase levels of ß-endorphin in several brain areas including the thalamus (Porro et al., 1988, 1991). Elevated levels of endomorphin, another putative endogenous ligand for the μ-opioid receptor, were also observed in the rat brain following CCI surgery (Sun et al., 2001). Increased levels of endogenous opioid peptides could produce receptor desensitization by inducing G-protein-coupled receptor kinase-mediated phosphorylation and subsequent β-arrestin binding as previously described (Liu and Anand, 2001).