We directly compare IH to CH activity, and IL to CL activity, bel

We directly compare IH to CH activity, and IL to CL activity, below in the Reward Anticipation section. For the FEF and PFC populations, CH versus CL differences failed to reach significance not only during the interstage epoch, as described previously, but also in every epoch (Table 2, top and middle rows). IH and IL activity differences were similarly insignificant across epochs (except for one epoch in the FEF; Supplemental Results, IH versus

IL section). Finally, no CH-CL or IH-IL differences were significant in any epoch for the subsets of FEF and PFC neurons that were significantly active in each epoch (data not shown). We varied the SOA in the task to elicit large numbers of correct and incorrect trials (and their associated bets) to analyze. This raises two questions. Pomalidomide Did varying SOAs contribute to differences in trial durations between trial outcomes (e.g., CH versus CL) that could have influenced our neuronal results? And, more to the point, did metacognition-related signals in SEF vary with SOA? Regarding the first question, we did not expect SOA distributions (and thus trial lengths) to vary appreciably between trial outcomes, given that metacognitive behavior was stable across SOAs (e.g., Figure 1C). Betting

depended on trial-by-trial decisions, not SOAs. The only exception might be if a monkey “guessed” during the more difficult, shorter SOA trials; it might choose a target randomly and then bet low to be safe. If its choice was correct, the outcome would be a CL trial. find more Hence, short SOAs might be slightly more prevalent in CL trials than in CH trials. Consistent with this expectation, we found that average SOAs were 48.3 ms (SD

17.9 ms) in CH trials and 45.1 ms (SD 18.2 ms) in CL trials, a slight but significant difference (Mann-Whitney U test, p < 0.001). This 3.2 ms difference mafosfamide in mean trial duration was negligible compared to the overall trial duration of ∼2 s, so it is unlikely to have influenced our neuronal data. Regarding the second question, we analyzed whether our main indicators of metacognitive signals, CH firing rates, CL firing rates, and differential CH-CL activity, varied across SOAs. We analyzed each of these three data sets for all six epochs of Table 2 (baseline through interstage), for contralateral directions and all directions. Firing rates did not vary significantly as a function of SOA for any of the 36 tests (ANOVAs, p > 0.05 for all). In sum, variations in SOA were critical for the task design but had no significant influence on the neuronal effects that we found, just as they had no influence on metacognitive behavior (e.g., Figure 1C). We also analyzed CH versus CL differences for time periods after the interstage epoch, through the bet stage of the task. Briefly, at the population levels, none of the three cortical areas had activity correlated with metacognition after the interstage epoch and before the bet.

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