The temporal representation of experience in subjective mood
- National Institutes of Health / National Institute of Mental Health, United States
- University College London, United Kingdom
Abstract
Humans refer to their mood state regularly in day-to-day as well as clinical interactions. Theoretical accounts suggest that when reporting on our mood we integrate over the history of our experiences; yet, the temporal structure of this integration remains unexamined. Here we use a computational approach to quantitatively answer this question and show that early events exert a stronger influence on reported mood compared to recent events. We show that a Primacy model accounts better for mood reports compared to a range of alternative temporal representations across random, consistent or dynamic reward environments, different age groups and in both healthy and depressed participants. Moreover, we find evidence for neural encoding of the Primacy, but not the Recency, model in frontal brain regions related to mood regulation. These findings hold implications for the timing of events in experimental or clinical settings and suggest new directions for individualized mood interventions.
Data availability
To enable the reproducibility of this study we made scripts and datasets available online at: https://osf.io/vw7sz/?view_only=e8cb4ef6782e4735815867203971994a.This repository includes: Mood modeling code; Source-data of Figure 2 (tasks trial-wise values and mood ratings values of all participants); Neural analyses code; Files of the whole-brain neural images presented in Figure 4.The link to this repository is provided in the Methods (section 7. Availability of code and datasets), and figure captions as well as other sections of the Methods refer to it.
Article and author information
Author details
Funding
National Institute of Mental Health (Intramural Research Program,ZIAMH002957-01)
- Hanna Keren
Brain and Behavior Research Foundation
- Robb B Rutledge
National Institute of Mental Health (Intramural Research Program)
- Charles Zheng
National Institute of Mental Health (Intramural Research Program)
- David C Jangraw
National Institute of Mental Health (Intramural Research Program,ZIAMH002957-01)
- Katharine Chang
National Institute of Mental Health (Intramural Research Program,ZIAMH002957-01)
- Aria Vitale
National Institute of Mental Health (Intramural Research Program,ZIAMH002957-01)
- Dylan Nielson
National Institute of Mental Health (Intramural Research Program)
- Francisco Pereira
National Institute of Mental Health (Intramural Research Program,ZIAMH002957-01)
- Argyris Stringaris
Wellcome Trust
- Robb B Rutledge
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 signed informed consent to a protocol approved by the NIH Institutional Review Board. The protocol is registered under the clinical trial no. NCT03388606.
Copyright
This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
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The temporal representation of experience in subjective mood
eLife 10:e62051.
https://doi.org/10.7554/eLife.62051
Further reading
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- Cell Biology
- Neuroscience
Experience shapes the brain as neural circuits can be modified by neural stimulation or the lack of it. The molecular mechanisms underlying structural circuit plasticity and how plasticity modifies behaviour are poorly understood. Subjective experience requires dopamine, a neuromodulator that assigns a value to stimuli, and it also controls behaviour, including locomotion, learning, and memory. In Drosophila, Toll receptors are ideally placed to translate experience into structural brain change. Toll-6 is expressed in dopaminergic neurons (DANs), raising the intriguing possibility that Toll-6 could regulate structural plasticity in dopaminergic circuits. Drosophila neurotrophin-2 (DNT-2) is the ligand for Toll-6 and Kek-6, but whether it is required for circuit structural plasticity was unknown. Here, we show that DNT-2-expressing neurons connect with DANs, and they modulate each other. Loss of function for DNT-2 or its receptors Toll-6 and kinase-less Trk-like kek-6 caused DAN and synapse loss, impaired dendrite growth and connectivity, decreased synaptic sites, and caused locomotion deficits. In contrast, over-expressed DNT-2 increased DAN cell number, dendrite complexity, and promoted synaptogenesis. Neuronal activity modified DNT-2, increased synaptogenesis in DNT-2-positive neurons and DANs, and over-expression of DNT-2 did too. Altering the levels of DNT-2 or Toll-6 also modified dopamine-dependent behaviours, including locomotion and long-term memory. To conclude, a feedback loop involving dopamine and DNT-2 highlighted the circuits engaged, and DNT-2 with Toll-6 and Kek-6 induced structural plasticity in this circuit modifying brain function and behaviour.
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- Cell Biology
- Neuroscience
Sorting nexin 4 (SNX4) is an evolutionary conserved organizer of membrane recycling. In neurons, SNX4 accumulates in synapses, but how SNX4 affects synapse function remains unknown. We generated a conditional SNX4 knock-out mouse model and report that SNX4 cKO synapses show enhanced neurotransmission during train stimulation, while the first evoked EPSC was normal. SNX4 depletion did not affect vesicle recycling, basic autophagic flux, or the levels and localization of SNARE-protein VAMP2/synaptobrevin-2. However, SNX4 depletion affected synapse ultrastructure: an increase in docked synaptic vesicles at the active zone, while the overall vesicle number was normal, and a decreased active zone length. These effects together lead to a substantially increased density of docked vesicles per release site. In conclusion, SNX4 is a negative regulator of synaptic vesicle docking and release. These findings suggest a role for SNX4 in synaptic vesicle recruitment at the active zone.
