This paper presents the MO-to-NAc GRP/GRPR pathway as a circuit that regulates chronic pain and its affective dimensions. The abstract describes reduced GRP release and reduced excitability in this pathway during chronic pain.
First-pass extracted concept
MO Grp-to-NAc Grpr circuit
Candidate: concept label1 source documents4 linked claims
Live refresh every 5sNext refresh in 5s
Aliases
medial orbitofrontal cortex to nucleus accumbens GRP/GRPR pathway, MO-Grp-NAc-Grpr circuit
Extracted Explainers
What the tool is doing
Resources required
What problem it solves
What it does not solve
Evidence Snippets
Supporting Sources
Linked Claims
Chronic pain reduces excitability of NAc Grpr neurons and reduces MO-to-NAc GRP release.
Quoted textsource-backed
Using multimodal approaches (fiber photometry, chemogenetics, optogenetics, and Raman spectroscopy), we show that chronic pain reduces NAcGrpr neuron excitability and MO-to-NAc GRP release.
The GRP/GRPR system in the medial orbitofrontal cortex to nucleus accumbens pathway is critical for regulating chronic pain and its affective dimensions.
Quoted textsource-backed
Here, we identify the gastrin-releasing peptide (GRP)/GRP receptor (GRPR) system in the medial orbitofrontal cortex (MO)-nucleus accumbens (NAc) pathway as critical for regulating chronic pain and its affective dimensions.
Activation of MO Grp-to-NAc projections mirrors the therapeutic effects seen with NAc Grpr neuron activation or NAc GRP supplementation.
Quoted textsource-backed
MOGrp-to-NAc activation mirrors therapeutic effects.
Optogenetic activation of NAc Grpr neurons or NAc GRP supplementation alleviates pain phenotypes in chronic pain mice.
Quoted textsource-backed
optogenetic activation of NAcGrpr neurons or NAc GRP supplementation alleviates these in chronic pain mice.