Neurochronometry of choice-induced preference changes: when do preferences actually change?

According to cognitive dissonance theory, a discrepancy between preferences and actions may lead to the revaluation of preferences, increasing preference for the chosen options and decreasing for the rejected options. This phenomenon is known as the spreading of alternatives (SoA), which results in a choice-induced preference change (CIPC). Previous neuroimaging studies have identified several brain regions that play a role in cognitive dissonance. However, the neurochronometry of the cognitive mechanisms underlying CIPC is a topic of debate. In other words, does it occur during the difficult choice, immediately after the choice, or when people encounter the options again? Furthermore, it remains unclear what is the exact time point, relative to the onset of facing options, either within the choice or after it, when the attitudes start to be revised. We argue that applying online protocols of transcranial magnetic stimulation (TMS), during or immediately after the choice process, could be the most efficient way to better understand the temporal dynamics of the SoA effect. TMS allows for achieving high temporal and spatial resolution, modulating the activity of areas of interest, and examining the causal relationships. Besides, unlike the offline TMS, the online instrument allows tracking of the neurochronometry of attitude change, by varying stimulation onsets and durations with respect to the option stimuli. Based on scrupulous analysis of previous findings, employing online TMS studies of conflict monitoring, cognitive control, and CIPC neuroimaging results, we conclude that the use of online TMS is critical to examine the neurochronometry of CIPC.

Neural mechanisms of expert persuasion on willingness to pay for sugar.

Introduction: Sugar consumption is associated with many negative health consequences. It is, therefore, important to understand what can effectively influence individuals to consume less sugar. We recently showed that a healthy eating call by a health expert can significantly decrease the willingness to pay (WTP) for sugar-containing food. Here, we investigate which aspects of neural responses to the same healthy eating call can predict the efficacy of expert persuasion. Methods: Forty-five healthy participants performed two blocks of a bidding task, in which they had to bid on sugar-containing, sugar-free and non-edible products, while their electroencephalography (EEG) was recorded. In between the two blocks, they listened to a healthy eating call by a nutritionist emphasizing the risks of sugar consumption. Results: We found that after listening to the healthy eating call, participants significantly decreased their WTP for sugar-containing products. Moreover, a higher intersubject correlation of EEG (a measure of engagement) during listening to the healthy eating call resulted in a larger decrease in WTP for sugar-containing food. Whether or not a participant's valuation of a product was highly influenced by the healthy eating call could also be predicted by spatiotemporal patterns of EEG responses to the healthy eating call, using a machine learning classification model. Finally, the healthy eating call increased the amplitude of the P300 component of the visual event-related potential in response to sugar-containing food. Disussion: Overall, our results shed light on the neural basis of expert persuasion and demonstrate that EEG is a powerful tool to design and assess health-related advertisements before they are released to the public.

Pro- and Anti-Inflammatory Cytokines in the Context of NK Cell-Trophoblast Interactions.

During pregnancy, uterine NK cells interact with trophoblast cells. In addition to contact interactions, uterine NK cells are influenced by cytokines, which are secreted by the cells of the decidua microenvironment. Cytokines can affect the phenotypic characteristics of NK cells and change their functional activity. An imbalance of pro- and anti-inflammatory signals can lead to the development of reproductive pathology. The aim of this study was to assess the effects of cytokines on NK cells in the presence of trophoblast cells in an in vitro model. We used TNFα, IFNγ, TGFß and IL-10; the NK-92 cell line; and peripheral blood NK cells (pNKs) from healthy, non-pregnant women. For trophoblast cells, the JEG-3 cell line was used. In the monoculture of NK-92 cells, TNFα caused a decrease in CD56 expression. In the coculture of NK cells with JEG-3 cells, TNFα increased the expression of NKG2C and NKG2A by NK-92 cells. Under the influence of TGFß, the expression of CD56 increased and the expression of NKp30 decreased in the monoculture. After the preliminary cultivation of NK-92 cells in the presence of TGFß, their cytotoxicity increased. In the case of adding TGFß to the PBMC culture, as well as coculturing PBMCs and JEG-3 cells, the expression of CD56 and NKp44 by pNK cells was reduced. The differences in the effects of TGFß in the model using NK-92 cells and pNK cells may be associated with the possible influence of monocytes or other lymphoid cells from the mononuclear fraction.