bioRxivNeuroscience
A small molecule ligand for the novel pain target GPR171 produces minimal reward in mice
Maxwell McDermottiD, Akila RamiD, Matt T. Mattoon, Emmaline E. Haderlie, Megan C. RaddatziD, Madi K. Thomason, Erin N. BobeckiD
Abstract
ProSAAS is one of the most abundant proteins in the brain and is processed into several smaller peptides. One of which, BigLEN, is an endogenous ligand for the G protein-coupled receptor, GPR171. Recent work in rodent models has shown that a small-molecule ligand for GPR171, MS15203, increases morphine antinociception and is effective in lessening chronic pain. While these studies provide evidence for GPR171 as a possible pain target, its abuse liability has not yet been assessed which we evaluate in the current study. We first mapped the distribution of GPR171 and ProSAAS throughout the reward circuit of the brain using immunohistochemistry and showed that GPR171 and ProSAAS are localized in the hippocampus, basolateral amygdala, nucleus accumbens, prefrontal cortex. In the major dopaminergic structure, the ventral tegmental area (VTA), GPR171 appeared to be primarily localized in dopamine neurons while ProSAAS is outside of dopamine neurons. Next, MS15203 was administered to mice with or without morphine, and VTA slices were stained for the immediate early gene c-Fos as a marker of neuronal activation. Quantification of c-Fos-positive cells revealed no statistical difference between MS15203 and saline, suggesting that MS15203 does not increase VTA activation and dopamine release. Similarly, the results of a conditioned place preference experiment showed that treatment with MS15203 or MS15203 + Morphine produced no place preference compared to Saline indicating a lack of reward-related behavior. Taken together this data provides evidence that the novel pain therapeutic, MS15203, has minimal reward liability. Therefore, GPR171 deserves further exploration as a pain target. Significance StatementMS15203, a drug that activates the receptor GPR171, was previously shown to increase morphine analgesia. The authors use in vivo and histological techniques to show that it fails to activate the rodent reward circuitry, providing support for the continued exploration of MS15203 as a novel pain drug, and GPR171 a novel pain target.
- organism: mouse
- assay: proteomics
- research focus: drug response / drug discovery
- approach: statistical model
- Citations
- 2
- FWCI
- 0.11
- Field percentile
- 37th percentile
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- GPR171 Agonist Reduces Chronic Neuropathic and Inflammatory Pain in Male, but not in Female Mice
A. Ram, T. Edwards, … E. Bobeck·bioRxiv·Apr 16, 2021
- Discovery of a functionally selective serotonin 5-HT1A receptor agonist for the treatment of pain
A. Ullrich, J. Schneider, … P. Gmeiner·bioRxiv·Sep 11, 2023
- Comparison of morphine, oxycodone and the biased MOR agonist SR-17018 for tolerance and efficacy in mouse models of pain.
F. Pantouli, T. W. Grim, … L. M. Bohn·bioRxiv·Oct 16, 2020
- The Habenular Receptor GPR151 Regulates Addiction Vulnerability Across Drug Classes
Beatriz Antolin‐Fontes, Kun Li, … Inés Ibáñez-Tallon·bioRxiv·Jul 31, 2019
- Targeting Gi/o-coupled GPCRs to inhibit nociceptors: insights from the serotonin receptor Htr1b and triptans
Jing Peng, Brianna T Sanchez, … David D. Ginty·Cell Reports MedicinePeer-reviewed·Jul 30, 2026
- An endogenous GLP-1 circuit engages VTA GABA neurons to regulate mesolimbic dopamine neurons and attenuate cocaine seeking
Riley Merkel, Nicole S. Hernandez, … Heath D. Schmidt·Science AdvancesPeer-reviewed·Feb 26, 2025