Pre-saccadic remapping relies on dynamics of spatial attention
Abstract
Each saccade shifts the projections of the visual scene on the retina. It has been proposed that the receptive fields of neurons in oculomotor areas are predictively remapped to account for these shifts. While remapping of the whole visual scene seems prohibitively complex, selection by attention may limit these processes to a subset of attended locations. Because attentional selection consumes time, remapping of attended locations should evolve in time, too. In our study, we cued a spatial location by presenting an attention-capturing cue at different times before a saccade and constructed maps of attentional allocation across the visual field. We observed no remapping of attention when the cue appeared shortly before saccade. In contrast, when the cue appeared sufficiently early before saccade, attentional resources were reallocated precisely to the remapped location. Our results show that pre-saccadic remapping takes time to develop suggesting that it relies on the spatial and temporal dynamics of spatial attention.
Data availability
All files are available from the OSF database: URL: https://osf.io/3tru6.
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Dataset of the Peripheral Remapping and Foveal Remapping of attention tasksOpen Science Framework, osf.io/3tru6.
Article and author information
Author details
Funding
Deutsche Forschungsgemeinschaft (SZ343/1)
- Martin Szinte
Deutsche Forschungsgemeinschaft (RA2191/1-1)
- Dragan Rangelov
Marie Skłodowska-Curie Individual Fellowship (704537)
- Martin Szinte
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Andrew J King, University of Oxford, United Kingdom
Ethics
Human subjects: Experiments were designed according to the ethical requirements specified by the Faculty for Psychology and Pedagogics of the Ludwig-Maximilians-Universität München (approval number 13_b_2015) for experiments involving eye tracking. All participants provided written informed consent, including a consent to publish anonymized data.
Version history
- Received: April 16, 2018
- Accepted: December 30, 2018
- Accepted Manuscript published: December 31, 2018 (version 1)
- Version of Record published: January 10, 2019 (version 2)
Copyright
© 2018, Szinte 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.
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Further reading
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- Medicine
- Neuroscience
Background:
Ketamine has emerged as one of the most promising therapies for treatment-resistant depression. However, inter-individual variability in response to ketamine is still not well understood and it is unclear how ketamine’s molecular mechanisms connect to its neural and behavioral effects.
Methods:
We conducted a single-blind placebo-controlled study, with participants blinded to their treatment condition. 40 healthy participants received acute ketamine (initial bolus 0.23 mg/kg, continuous infusion 0.58 mg/kg/hr). We quantified resting-state functional connectivity via data-driven global brain connectivity and related it to individual ketamine-induced symptom variation and cortical gene expression targets.
Results:
We found that: (i) both the neural and behavioral effects of acute ketamine are multi-dimensional, reflecting robust inter-individual variability; (ii) ketamine’s data-driven principal neural gradient effect matched somatostatin (SST) and parvalbumin (PVALB) cortical gene expression patterns in humans, while the mean effect did not; and (iii) behavioral data-driven individual symptom variation mapped onto distinct neural gradients of ketamine, which were resolvable at the single-subject level.
Conclusions:
These results highlight the importance of considering individual behavioral and neural variation in response to ketamine. They also have implications for the development of individually precise pharmacological biomarkers for treatment selection in psychiatry.
Funding:
This study was supported by NIH grants DP5OD012109-01 (A.A.), 1U01MH121766 (A.A.), R01MH112746 (J.D.M.), 5R01MH112189 (A.A.), 5R01MH108590 (A.A.), NIAAA grant 2P50AA012870-11 (A.A.); NSF NeuroNex grant 2015276 (J.D.M.); Brain and Behavior Research Foundation Young Investigator Award (A.A.); SFARI Pilot Award (J.D.M., A.A.); Heffter Research Institute (Grant No. 1–190420) (FXV, KHP); Swiss Neuromatrix Foundation (Grant No. 2016–0111) (FXV, KHP); Swiss National Science Foundation under the framework of Neuron Cofund (Grant No. 01EW1908) (KHP); Usona Institute (2015 – 2056) (FXV).
Clinical trial number: