First-pass extracted concept

GRP/GRPR signaling

Candidate: concept label1 source documents5 linked claims

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Aliases

gastrin-releasing peptide/gastrin-releasing peptide receptor system

Extracted Explainers

What the tool is doing

The paper identifies GRP/GRPR signaling in the MO-to-NAc pathway as critical for regulating chronic pain and affective phenotypes. Reduced GRP release and reduced NAc Grpr neuron excitability are reported in chronic pain.

Source 1DOI PubMed

Resources required

The abstract indicates that studying this signaling system required fiber photometry, chemogenetics, optogenetics, Raman spectroscopy, and GRPR knockdown or GRP supplementation in mice.

Source 1DOI PubMed

What problem it solves

It provides a molecularly specified mechanism for a pain-affect circuit. The paper also frames it as a dual therapeutic target.

Source 1DOI PubMed

What it does not solve

The abstract does not establish a clinically deployable therapy or define all upstream causes of GRP down-regulation. It also does not compare GRP/GRPR directly against other molecular targets.

Source 1DOI PubMed

Alternatives

Within the abstract, pathway activation, receptor knockdown, chemogenetic inhibition, and GRP supplementation are contrasted as different manipulations of the same signaling axis.

Source 1DOI PubMed

Evidence Snippets

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.

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1primary paper2025MEDDOI PubMed

1 evidence snippet 5 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1causal perturbationsupports2025Source 1DOI PubMed

Chemogenetic inhibition or GRPR knockdown in NAc Grpr neurons induces pain phenotypes in naive mice.

Quoted textsource-backed

Chemogenetic inhibition or GRPR knockdown in NAcGrpr neurons induces pain phenotypes in naive mice

Claim 2disease associated changesupports2025Source 1DOI PubMed

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.

Claim 3mechanistic rolesupports2025Source 1DOI PubMed

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.

Claim 4quantified changesupports2025Source 1DOI PubMed

Raman mapping shows that NAc GRP is fivefold lower after nerve injury and this reduction correlates with reduced neuronal activity.

Quoted textsource-backed

Raman mapping shows fivefold lower NAc GRP after nerve injury, correlating with reduced neuronal activity.

Claim 5therapeutic effectsupports2025Source 1DOI PubMed

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.