Donner Lab

🧠✨ Exciting new research alert! ✨🧠

Did you know that catecholamines can reduce choice history biases in perceptual decision-making? 🧐🔍

Paper: journals.plos.org/plosbiology/...

With @donnerlab.bsky.social and @swammerdamuva.bsky.social

Experimental design and effects on peripheral arousal markers. Top left: Design was within-subject, double-blinded, randomized, and placebo-controlled (Materials and methods). Additionally, the stimulus-response mapping was counterbalanced within participants Bottom: Schematic sequence of events during the spatial contrast discrimination task (Materials and methods). Participants reported the location of the highest contrast Gabor patch (difference in contrast is high for illustration only). Top right: Heart rate and pupil size measured as the average across task blocks (Materials and methods), separately for placebo and atomoxetine sessions. Every connecting line is a participant; large data points in the middle are the group averages.

How do catecholamines like #noradrenaline influence perceptual #DecisionMaking? @degeelab.bsky.social @donnerlab.bsky.social &co show that higher #catecholamine levels reduce individual choice history biases by dampening bias in the accumulation of sensory evidence @plosbiology.org 🧪 plos.io/4mMmNNX

13/ This work was led by @ayeletarazi.bsky.social, with Alessandro Toso, and our collaborators Tineke Grent-‘t-Jong and Peter Uhlhaas.

12/ Our results are consistent with the notion that synaptic alterations underlying psychosis are widely distributed across the cerebral cortex. Our approach opens up new perspectives for a mechanistically informed stratification of patient cohorts in future psychosis research.

11/ We conclude that early-stage psychosis is associated with large-scale patterns of changes in cortical dynamics which result from alterations in GABA-A or NMDA receptor functions. Individual differences in those psychosis signatures relate to individual symptomatology.

10/ Individual similarities between psychosis signature and drug effects related to symptoms: Patients’ similarity to changes induced by NMDA-R blockade correlated with negative symptoms. Patients’ similarity to changes induced by GABA-A boost correlated with positive symptoms.

9/ These “large-scale psychosis signatures” resembled the patterns of changes induced by pharmacological manipulation of GABA-A and NMDA receptors.

8/ Spatial patterns of changes in dynamics parameters due to psychosis also varied across the cortex and were highly similar between at-risk participants and first-episode psychosis patients. These patterns did not reflect anatomical hierarchy but local GABA-A receptor densities.

7/ For each of 180 cortical regions, we extracted six parameters of cortical dynamics. As expected, these parameters varied across cortex in a manner that reflected the anatomical cortical hierarchy.

6/ The second was a pharmacological dataset, collected at University medical center Hamburg-Eppendorf, from healthy participants under placebo-controlled pharmacological manipulation of inhibitory GABA-A and excitatory NMDA-glutamate receptors.

5/ The first was a clinical dataset, collected at University of Glasgow, and included participants at high risk for developing psychosis, first episode psychosis patients, and healthy controls.

4/ Here, we mapped the spatial patterns of changes in spontaneous cortical dynamics in two resting-state MEG datasets.

3/ Properties of cortical circuits, such as the ratio between synaptic excitation and inhibition, vary across the cerebral cortex and are altered in psychosis. These properties are reflected in spontaneous neural population dynamics that can be mapped with high precision using MEG.

2/ Psychotic disorders, such as schizophrenia, present a major challenge for research and clinical practice: their pathogenesis is complex, the individual symptomatology is heterogenous, and there is a lack of biomarkers for early diagnosis.

Large-scale maps of altered cortical dynamics in early-stage psychosis are related to GABAergic and glutamatergic neurotransmission Cortex-wide changes in neural dynamics in early-stage psychosis relate to GABA-A or NMDA receptors and clinical symptoms.

1/ New paper on @ScienceAdvances: Large-Scale Maps of Altered Cortical Dynamics in Early-Stage Psychosis Are Related to GABAergic and Glutamatergic Neurotransmission (www.science.org/doi/10.1126/...).

Ayelet Arazi - 📍 Poster 3.5 | Wed (July 16th):
Cortex-wide changes in neural dynamics in early-stage psychosis relate to GABA-A or NMDA receptor expression and function, and to clinical symptoms.

Gina Monov - 📍 Poster 2.13 | Tue (July 15th):
Come explore our latest findings on cortical working memory dynamics in aging and MCI!

Alessandro Toso - 📍 Poster 1.4 | Mon (July 14th):
Through pharmacological manipulations in humans, we showed that GABA-A and NMDA receptors shape perceptual decision-making at distinct timescales — within-trial and across-trial, respectively.

Are you coming to #CPConf2025 next week?
📃Come check out some of our lab's work and meet Ayelet, Alessandro and Gina at their posters!

👀 sneak peeks below ⬇️

Are you at @assc28.bsky.social #ASSC28? On Wednesday I will present a poster on the causal relationship between choice history biases and catecholamines (noradrenaline / dopamine). With @donnerlab.bsky.social et al.

11/ Because information use is more susceptible to deliberative control, our results imply that confirmation bias may be malleable, contingent on appropriate feedback and incentives.

10/ We conclude that confirmation bias originates from the way in which decision-makers utilize information encoded in the brain, which sheds new light on an important cognitive phenomenon that has occupied scholars for centuries.

9/ By contrast, an information-theoretic measure of the use (“readout”) of encoded evidence for the final estimate (“intersection information”) in parietal and visual cortex was bigger for consistent than for inconsistent samples, in line with the selective use scenario.

8/ We also used MEG to measure cortical population dynamics in participants’ brains during the task. The evidence samples were precisely encoded in population activity in visual and parietal cortex, irrespective of their consistency with the previous choice.

7/ Interestingly, this consistency effect on behavioral evidence weighting was bigger when participants had to report their own categorical judgment of the evidence halfway through the trial, compared to when they instead received an external categorical cue.

6/ Participants’ final estimation reports were more strongly affected by evidence samples in the second half of the trial that were consistent (compared to inconsistent) with the previous left/right choice: a behavioral signature of confirmation bias.

5/ After viewing half of the samples, participants judged whether the mean of the source distribution was to the left or right from the vertical meridian. After viewing the rest of the samples, they reported a continuous estimation of the source with a joystick.

4/ To arbitrate between these scenarios, we asked participants to evaluate sequences of 12 noisy visual evidence samples: small discs with varying angles to the vertical meridian. Each sample was drawn from a hidden source: a probability distribution with constant mean per trial.

3/ We reasoned that such selective weighting of evidence could be brought about by two distinct neural mechanisms: (i) selective encoding of incoming evidence in the brain, or (ii) biased utilization of encoded evidence for reasoning and action.

2/ People often interpret information selectively, depending on whether that information aligns with their pre-existing beliefs: Consistent evidence has a strong impact on future judgments, while inconsistent evidence tends to be discarded. This is confirmation bias.