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Suppressing a motivationally-triggered action tendency engages a response control mechanism that prevents future provocation.

ABSTRACT: Reward-predicting stimuli can induce maladaptive behavior by provoking action tendencies that conflict with long-term goals. Earlier, we showed that when human participants were permitted to respond for a reward in the presence of a task-irrelevant, reward-predicting stimulus (i.e. goCS+ trials), the CS+ provoked an action tendency to respond compared to when a non-rewarding CS- stimulus was present (i.e. goCS- trials). However, when participants were not permitted to respond, response suppression was recruited to mitigate the action tendency that was triggered by the motivating CS+ stimulus (i.e. on nogoCS+ trials) (Freeman et al., 2014). Here we tested the hypothesis that repeated response suppression over a motivationally-triggered action tendency would reduce subsequent CS+ provocation. We compared groups of participants who had different proportions of nogoCS+ trials, and we measured CS+ provocation on go trials via reaction time. Our results showed that CS+ provocation on go trials was reduced monotonically as the proportion of nogoCS+ trials increased. Further analysis showed that these group differences were best explained by reduced provocation on goCS+ trials that followed nogoCS+ (compared to nogoCS-) trials. Follow-up experiments using a neurophysiological index of motor activity replicated these effects and also suggested that, following nogoCS+ trials, a response suppression mechanism was in place to help prevent subsequent CS+ provocation. Thus, our results show that performing response suppression in the face of a motivating stimulus not only controls responding at that time, but also prevents provocation in the near future.

SUBMITTER: Freeman SM

PROVIDER: S-EPMC4420638 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature

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Suppressing a motivationally-triggered action tendency engages a response control mechanism that prevents future provocation.

Freeman Scott M SM Alvernaz Dominic D Tonnesen Alexandra A Linderman David D Aron Adam R AR

Neuropsychologia 20150113

Reward-predicting stimuli can induce maladaptive behavior by provoking action tendencies that conflict with long-term goals. Earlier, we showed that when human participants were permitted to respond for a reward in the presence of a task-irrelevant, reward-predicting stimulus (i.e. goCS+ trials), the CS+ provoked an action tendency to respond compared to when a non-rewarding CS- stimulus was present (i.e. goCS- trials). However, when participants were not permitted to respond, response suppressi ...[more]

PMID: 25592370

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Project description:Background: Paeoniflorin (PF) is the main active component of Chinese herbaceous peony that has been shown to have an anti-tumor effect. However, there are few studies on the prevention and treatment of pancreatic cancer with PF. Methods: We gathered Microarray data pertaining to paeoniflorin intervention in pancreatic cancer by utilizing the GEO database (GSE97124). Then, the DEGs were filtered by the 33R program. RNA-seq data of pancreatic cancer and normal tissue samples were taken from the TCGA and GTEx databases, respectively, and the WGCNA technique was utilized to examine the pancreatic cancer-specific genes. Paeoniflorin target genes for the treatment of pancreatic cancer were determined based on the overlap between DEGs and WGCNA. GO and KEGG enrichment analyses were then performed on paeoniflorin target genes to discover which biological processes were impacted. Using the 3 hierarchical methods included in the Cytohubba plugin, we re-screened the hub genes in the target genes to find the genes most relevant to paeoniflorin treatment. The overall survival effects of hub genes were confirmed using the TCGA database. Finally, the paeoniflorin targets identified by the network pharmacology analysis were validated using PANC-1 and Capan-2 cells. Results: We identified 148 main potential PF targets, and gene enrichment analysis suggested that the aforementioned targets play a crucial role in the regulation of MAPK, PI3K-AKT, and other pathways. The further screening of the prospective targets resulted in the identification of 39 hub genes. Using the TCGA database, it was determined that around 33.33% of the hub gene's high expression was linked with a bad prognosis. Finally, we demonstrated that PF inhibits IL-6 and IL-10 expression and p38 phosphorylation in pancreatic cancer cells, thereby reducing inflammation. Conclusion: PF may regulate inflammatory factors mainly through the p38 MAPK signal pathway. These findings provide theoretical and experimental evidence suggesting the PF as a promising natural source of anti-tumor compounds for pancreatic cancer.

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Suppressing a motivationally-triggered action tendency engages a response control mechanism that prevents future provocation.

Publications

Suppressing a motivationally-triggered action tendency engages a response control mechanism that prevents future provocation.

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