Understanding perceptual decision-making requires linking sensory neural responses to behavioral choices. In two-choice tasks, activity-choice covariations are commonly quantified with a single measure of choice probability (CP), without characterizing their changes across stimulus levels. We provide theoretical conditions for stimulus dependencies of activity-choice covariations. Assuming a general decision-threshold model, which comprises both feedforward and feedback processing and allows for a stimulus-modulated neural population covariance, we analytically predict a very general and previously unreported stimulus dependence of CPs. We develop new tools, including refined analyses of CPs and generalized linear models with stimulus-choice interactions, which accurately assess the stimulus- or choice-driven signals of each neuron, characterizing stimulus-dependent patterns of choice-related signals. With these tools, we analyze CPs of macaque MT neurons during a motion discrimination task. Our analysis provides preliminary empirical evidence for the promise of studying stimulus dependencies of choice-related signals, encouraging further assessment in wider data sets.
No data was collected as part of this study.
A relationship between behavioral choice and the visual responses of neurons in macaque MTData from the Vis Neurosci 1996 paper by these authors and with this title.
- Stefano Panzeri
- Stefano Panzeri
- Ralf M Haefner
- Daniel Chicharro
- Ralf M Haefner
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
- Kristine Krug, University of Oxford, United Kingdom
© 2021, Chicharro 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.
The presynaptic protein α-synuclein (αSyn) has been suggested to be involved in the pathogenesis of Parkinson’s disease (PD). In PD, the amygdala is prone to develop insoluble αSyn aggregates, and it has been suggested that circuit dysfunction involving the amygdala contributes to the psychiatric symptoms. Yet, how αSyn aggregates affect amygdala function is unknown. In this study, we examined αSyn in glutamatergic axon terminals and the impact of its aggregation on glutamatergic transmission in the basolateral amygdala (BLA). We found that αSyn is primarily present in the vesicular glutamate transporter 1-expressing (vGluT1+) terminals in mouse BLA, which is consistent with higher levels of αSyn expression in vGluT1+ glutamatergic neurons in the cerebral cortex relative to the vGluT2+ glutamatergic neurons in the thalamus. We found that αSyn aggregation selectively decreased the cortico-BLA, but not the thalamo-BLA, transmission; and that cortico-BLA synapses displayed enhanced short-term depression upon repetitive stimulation. In addition, using confocal microscopy, we found that vGluT1+ axon terminals exhibited decreased levels of soluble αSyn, which suggests that lower levels of soluble αSyn might underlie the enhanced short-term depression of cortico-BLA synapses. In agreement with this idea, we found that cortico-BLA synaptic depression was also enhanced in αSyn knockout mice. In conclusion, both basal and dynamic cortico-BLA transmission were disrupted by abnormal aggregation of αSyn and these changes might be relevant to the perturbed cortical control of the amygdala that has been suggested to play a role in psychiatric symptoms in PD.
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