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The present study presents the results of a collaborative registered replication of Griskevicius et al. (2010, Experiment 1). As part of the Collaborative Replication and Education Project, 24 student groups from six countries (N = 3,774) investigated whether pro-environmental behavior can be promoted by priming status motives (desires for social status and prestige). This large, multi-site replication showed no evidence to support the hypothesis that hypothetical pro-environmental behavior can be stimulated by having participants read a story designed to prime status motives. We performed several exploratory analyses to investigate whether extension variables (i.e., equating “green” choices with prosocial behavior, political beliefs, sampling methods, location, duration of data collection, and gender) moderated the hypothesized effect of status motives on pro-environmental choices, but these analyses produced null results. One limitation of the study is that most data collection sites did not include a manipulation check, and the one site that did found a much weaker effect (d = 0.32) than the extremely large effect originally reported (d = 3.69). As a result, it remains unclear whether the null result reflects a failure of this specific priming method or a challenge to the underlying theory.

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. MS15203, 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.