Search bioRxiv⌕ Search

bioRxiv · 10.1101/2021.07.21.453253

Transfer of learned cognitive flexibility to novel stimuli and task sets

Abstract

Adaptive behavior requires learning about the structure of ones environment to derive optimal action policies, and previous studies have documented transfer of such structural knowledge to bias choices in new environments. Here, we asked whether people could also acquire and transfer more abstract knowledge across different task environments, specifically expectations about cognitive control demands. Over three experiments, participants performed a probabilistic card-sorting task in environments of either a low or high volatility of task rule changes (requiring low or high cognitive flexibility respectively) before transitioning to a medium-volatility environment. Using reinforcement learning modeling, we consistently found that previous exposure to high task rule volatilities led to faster adaptation to rule changes in the subsequent transfer phase. These transfers of expectations about cognitive flexibility demands were both task- (Experiment 2) and stimulus- (Experiment 3) independent, thus demonstrating the formation and generalization of environmental structure knowledge to guide cognitive control. Statement of RelevanceWe investigated whether structural knowledge of one task environment can be transferred to guide cognitive control strategies in new environments. Past research has found that while learning generally improves subsequent performance, it does so only for the learned task ("near transfer") and has little or no generalizability to novel task rules and stimuli ("far transfer"). However, recent studies suggest that learning more abstract, structural task features (e.g., cognitive maps) allows for that knowledge to be applied to new environments. Here, we took a critical additional step and showed that people can acquire and transfer expectations about cognitive control demands (specifically cognitive flexibility) across different task environments. To our knowledge, this is the first demonstration of peoples ability to extract and re-use cognitive control learning parameters that transcend specific stimuli and tasks. This transfer of learned cognitive flexibility is particularly noteworthy because such flexibility is impaired in several common psychiatric conditions.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Wen, T., Geddert, R. M., Madlon-Kay, S., Egner, T.. 2021-07-23. Transfer of learned cognitive flexibility to novel stimuli and task sets. https://doi.org/10.1101/2021.07.21.453253

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The Unreasonable Effectiveness of Cell Types in Describing Neuronal Physiological Features

Single-cell RNA sequencing (scRNA-seq) captures detailed gene expression profiles at scale, while patch-clamp recordings measure intrinsic neuronal electrophysiological properties. Modeling the relations between these two modalities remains a challenge. Here, we compare how well electrophysiological features can be predicted by traditional transcriptomic cell type classification, representations derived from a foundational model (scGPT) pretrained on large-scale scRNA-seq datasets, ion channel-coding genes, and highly variable genes. Using paired transcriptomic and electrophysiological patch-sequencing data from 495 human neurons from neurosurgical tissue, we find that cluster-level cell type representations consistently outperform highly variable gene selection, ion channel gene selection, and context-enriched scGPT embeddings. Notably, performance varies across model architectures and initializations, and the best results are obtained by combining the outputs of separate cell type and scGPT-based models. Together, these findings suggest that traditional discrete cellular classification is highly effective in predicting physiological features. For maximum performance it can be complemented by pretrained transformer models.

neuroscience↗

A nonlinear inhibition pathway underlying cortical responses to tuned holographic optogenetic perturbations

Optogenetics enables causal manipulation of cortical activity. Perturbation responses can be counterintuitive due to network interactions, making theory essential for predicting them. Existing approaches often rely on linear approximations, which fail for many biologically relevant perturbations. Here we develop a nonlinear theory of responses to holographic perturbations in cell-type-specific recurrent networks with structured connectivity. We fit a nonlinear model to mouse V1 data, which shows cotuned-ensemble suppression: perturbing spatially clustered neurons with similar preferred orientations yields markedly stronger short-range suppression than perturbing untuned ensembles. We show that cotuned-ensemble suppression arises from a feature-tuned, nonlinear inhibition pathway implicating somatostatin-positive (SST) interneurons. The theory predicts that cotuned ensembles suppress parvalbumin-positive (PV) neurons but facilitate SST neurons, and links the degree of cotuned-ensemble suppression or facilitation to the variance of the SST response. This framework identifies mechanisms by which nonlinear inhibition sculpts cortical dynamics and establishes a predictive basis for targeted optogenetic interventions.

neuroscience↗

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimers disease

The apolipoprotein E {varepsilon}4 (APOE {varepsilon}4) allele is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, the underlying molecular mechanisms remain unclear. This study included 1691 participants from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP), 1226 participants from the Accelerating Medicines Partnership - Alzheimers Disease (AMP-AD) Diverse Cohorts Study, and 735 participants from the Alzheimers Disease Neuroimaging Initiative (ADNI). To characterise APOE {varepsilon}4 molecular effects, we analysed proteomic data from plasma, cerebrospinal fluid (CSF), and induced pluripotent stem cell (iPSC)-derived astrocytes and neurons, as well as transcriptomic and proteomic data from multiple brain regions. The association of APOE {varepsilon}4 with AD neuropathology was also examined. APOE {varepsilon}4 carriers shared a plasma proteomic signature enriched for immune processes, irrespective of AD diagnosis. A machine learning classifier trained on this signature discriminated APOE {varepsilon}4 carriers from non-carriers in an independent cohort using CSF proteomics. APOE {varepsilon}4 carriage was associated with higher Braak stages and Consortium to Establish a Registry for Alzheimers Disease (CERAD) score. However, only limited APOE {varepsilon}4-associated transcriptomic and proteomic changes were observed in bulk brain tissue, with poor cross-layer concordance. Proteomic analyses of iPSC-derived astrocytes and neurons further revealed cell-type-specific APOE {varepsilon}4-associated changes. APOE {varepsilon}4 is associated with a consistent proteomic signature across plasma and CSF. Its molecular effects in the brain differ across cell types, brain regions and molecular layers. These findings support the need for cell-type-resolved multi-omic studies to elucidate how APOE {varepsilon}4 confers AD risk.

neuroscience↗