Affective bias as a rational response to the statistics of rewards and punishments
Abstract
Affective bias, the tendency to differentially prioritise the processing of negative relative to positive events, is commonly observed in clinical and non-clinical populations. However, why such biases develop is not known. Using a computational framework, we investigated whether affective biases may reflect individuals' estimates of the information content of negative relative to positive events. During a reinforcement learning task, the information content of positive and negative outcomes was manipulated independently by varying the volatility of their occurrence. Human participants altered the learning rates used for the outcomes selectively, preferentially learning from the most informative. This behaviour was associated with activity of the central norepinephrine system, estimated using pupilometry, for loss outcomes. Humans maintain independent estimates of the information content of distinct positive and negative outcomes which may bias their processing of affective events. Normalising affective biases using computationally inspired interventions may represent a novel approach to treatment development.
Article and author information
Author details
Funding
Medical Research Council (MR/N008103/1)
- Michael Browning
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: All participants provided written informed consent. The study was reviewed and approved by the Medical Sciences Interdepartmental Research Ethics Committee of Oxford University (ref number MSD-IDREC-C1-2014-216).
Copyright
© 2017, Pulcu & Browning
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.
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Further reading
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- Neuroscience
- Stem Cells and Regenerative Medicine
Sensory dorsal root ganglion (DRG) neurons have a unique pseudo-unipolar morphology in which a stem axon bifurcates into a peripheral and a central axon, with different regenerative abilities. Whereas peripheral DRG axons regenerate, central axons are unable to regrow. Central axon regeneration can however be elicited by a prior conditioning lesion to the peripheral axon. How DRG axon asymmetry is established remains unknown. Here we developed a rodent in vitro system replicating DRG pseudo-unipolarization and asymmetric axon regeneration. Using this model, we observed that from early development, central DRG axons have a higher density of growing microtubules. This asymmetry was also present in vivo and was abolished by a conditioning lesion that decreased microtubule polymerization of central DRG axons. An axon-specific microtubule-associated protein (MAP) signature, including the severases spastin and katanin and the microtubule regulators CRMP5 and tau, was found and shown to adapt upon conditioning lesion. Supporting its significance, interfering with the DRG MAP signature either in vitro or in vivo readily abolished central-peripheral asymmetries in microtubule dynamics and regenerative ability. In summary, our data unveil that axon-specific microtubule regulation drives asymmetric regeneration of sensory neuron axons.