Statistical context dictates the relationship between feedback-related EEG signals and learning
Abstract
Learning should be adjusted according to the surprise associated with observed outcomes but calibrated according to statistical context. For example, when occasional changepoints are expected, surprising outcomes should be weighted heavily to speed learning. In contrast, when uninformative outliers are expected to occur occasionally, surprising outcomes should be less influential. Here we dissociate surprising outcomes from the degree to which they demand learning using a predictive inference task and computational modeling. We show that the P300, a stimulus-locked electrophysiological response previously associated with adjustments in learning behavior, does so conditionally on the source of surprise. Larger P300 signals predicted greater learning in a changing context, but less learning in a context where surprise was indicative of a one-off outlier (oddball). Our results suggest that the P300 provides a surprise signal that is interpreted by downstream learning processes differentially according to statistical context in order to appropriately calibrate learning across complex environments.
Data availability
All analysis code has been made available on GitHub (https://github.com/learning-memory-and-decision-lab/NassarBrucknerFrank_eLife_2019.git). All behavioral and EEG data has been made available on Dryad (doi:10.5061/dryad.570pf8n).
-
Data from: Statistical context dictates the relationship between feedback-related EEG signals and learningDryad Digital Repository, doi:10.5061/dryad.570pf8n.
Article and author information
Author details
Funding
National Institute of Mental Health (F32MH102009)
- Matthew R Nassar
National Institute on Aging (K99AG054732)
- Matthew R Nassar
National Institute of Mental Health (R01 MH080066-01)
- Michael J Frank
National Science Foundation (1460604)
- Michael J Frank
German Academic Exchange Service London (Promos travel grant)
- Rasmus Bruckner
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: Informed consent was obtained from each participant in the study and all procedures were performed in accordance with the Declaration of Helsinki. All procedures were approved by the Brown University Institutional Review Board (Brown University Federal Wide Assurance #00004460).
Copyright
© 2019, Nassar et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
Metrics
-
- 3,685
- views
-
- 517
- downloads
-
- 66
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
Further reading
-
- Computational and Systems Biology
- Genetics and Genomics
Root causal gene expression levels – or root causal genes for short – correspond to the initial changes to gene expression that generate patient symptoms as a downstream effect. Identifying root causal genes is critical towards developing treatments that modify disease near its onset, but no existing algorithms attempt to identify root causal genes from data. RNA-sequencing (RNA-seq) data introduces challenges such as measurement error, high dimensionality and non-linearity that compromise accurate estimation of root causal effects even with state-of-the-art approaches. We therefore instead leverage Perturb-seq, or high-throughput perturbations with single-cell RNA-seq readout, to learn the causal order between the genes. We then transfer the causal order to bulk RNA-seq and identify root causal genes specific to a given patient for the first time using a novel statistic. Experiments demonstrate large improvements in performance. Applications to macular degeneration and multiple sclerosis also reveal root causal genes that lie on known pathogenic pathways, delineate patient subgroups and implicate a newly defined omnigenic root causal model.