One-shot learning and behavioral eligibility traces in sequential decision making
Abstract
In many daily tasks we make multiple decisions before reaching a goal. In order to learn such sequences of decisions, a mechanism to link earlier actions to later reward is necessary. Reinforcement learning theory suggests two classes of algorithms solving this credit assignment problem: In classic temporal-difference learning, earlier actions receive reward information only after multiple repetitions of the task, whereas models with eligibility traces reinforce entire sequences of actions from a single experience (one-shot). Here we show one-shot learning of sequences. We developed a novel paradigm to directly observe which actions and states along a multi-step sequence are reinforced after a single reward. By focusing our analysis on those states for which RL with and without eligibility trace make qualitatively distinct predictions, we find direct behavioral (choice probability) and physiological (pupil dilation) signatures of reinforcement learning with eligibility trace across multiple sensory modalities.
Data availability
The datasets generated during the current study are available on Dryad, at the following address https://dx.doi.org/10.5061/dryad.j7h6f69
-
Data from: One-shot learning and behavioral eligibility traces in sequential decision makingDryad Digital Repository, doi:10.5061/dryad.j7h6f69.
Article and author information
Author details
Funding
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (CRSII2 147636 (Sinergia))
- Marco P Lehmann
- He A Xu
- Vasiliki Liakoni
- Michael H Herzog
- Wulfram Gerstner
- Kerstin Preuschoff
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (CRSII2 200020 165538)
- Marco P Lehmann
- Vasiliki Liakoni
- Wulfram Gerstner
Horizon 2020 Framework Programme (Human Brain Project (SGA2) 785907)
- Michael H Herzog
- Wulfram Gerstner
H2020 European Research Council (268 689 MultiRules)
- Wulfram Gerstner
Horizon 2020 Framework Programme (Human Brain Project (SGA1) 720270)
- Michael H Herzog
- Wulfram Gerstner
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Thorsten Kahnt, Northwestern University, United States
Ethics
Human subjects: Experiments were conducted in accordance with the Helsinki declaration and approved by the ethics commission of the Canton de Vaud (164/14 Titre: Aspects fondamentaux de la reconnaissance des objets : protocole général). All participants were informed about the general purpose of the experiment and provided written, informed consent. They were told that they could quit the experiment at any time they wish.
Version history
- Received: April 5, 2019
- Accepted: November 1, 2019
- Accepted Manuscript published: November 11, 2019 (version 1)
- Version of Record published: December 6, 2019 (version 2)
Copyright
© 2019, Lehmann 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
-
- 2,700
- views
-
- 391
- downloads
-
- 15
- 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
-
- Neuroscience
Despite substantial progress in mapping the trajectory of network plasticity resulting from focal ischemic stroke, the extent and nature of changes in neuronal excitability and activity within the peri-infarct cortex of mice remains poorly defined. Most of the available data have been acquired from anesthetized animals, acute tissue slices, or infer changes in excitability from immunoassays on extracted tissue, and thus may not reflect cortical activity dynamics in the intact cortex of an awake animal. Here, in vivo two-photon calcium imaging in awake, behaving mice was used to longitudinally track cortical activity, network functional connectivity, and neural assembly architecture for 2 months following photothrombotic stroke targeting the forelimb somatosensory cortex. Sensorimotor recovery was tracked over the weeks following stroke, allowing us to relate network changes to behavior. Our data revealed spatially restricted but long-lasting alterations in somatosensory neural network function and connectivity. Specifically, we demonstrate significant and long-lasting disruptions in neural assembly architecture concurrent with a deficit in functional connectivity between individual neurons. Reductions in neuronal spiking in peri-infarct cortex were transient but predictive of impairment in skilled locomotion measured in the tapered beam task. Notably, altered neural networks were highly localized, with assembly architecture and neural connectivity relatively unaltered a short distance from the peri-infarct cortex, even in regions within ‘remapped’ forelimb functional representations identified using mesoscale imaging with anaesthetized preparations 8 weeks after stroke. Thus, using longitudinal two-photon microscopy in awake animals, these data show a complex spatiotemporal relationship between peri-infarct neuronal network function and behavioral recovery. Moreover, the data highlight an apparent disconnect between dramatic functional remapping identified using strong sensory stimulation in anaesthetized mice compared to more subtle and spatially restricted changes in individual neuron and local network function in awake mice during stroke recovery.
-
- Neuroscience
Dissection of neural circuitry underlying behaviors is a central theme in neurobiology. We have previously proposed the concept of chemoconnectome (CCT) to cover the entire chemical transmission between neurons and target cells in an organism and created tools for studying it (CCTomics) by targeting all genes related to the CCT in Drosophila. Here we have created lines targeting the CCT in a conditional manner after modifying GFP RNA interference, Flp-out, and CRISPR/Cas9 technologies. All three strategies have been validated to be highly effective, with the best using chromatin-peptide fused Cas9 variants and scaffold optimized sgRNAs. As a proof of principle, we conducted a comprehensive intersection analysis of CCT genes expression profiles in the clock neurons, uncovering 43 CCT genes present in clock neurons. Specific elimination of each from clock neurons revealed that loss of the neuropeptide CNMa in two posterior dorsal clock neurons (DN1ps) or its receptor (CNMaR) caused advanced morning activity, indicating a suppressive role of CNMa-CNMaR on morning anticipation, opposite to the promoting role of PDF-PDFR on morning anticipation. These results demonstrate the effectiveness of conditional CCTomics and its tools created here and establish an antagonistic relationship between CNMa-CNMaR and PDF-PDFR signaling in regulating morning anticipation.