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Schallmo, M.-P.

Publications and source records attributed to Schallmo, M.-P..

9 recordsLinked to original sources

Aperiodic slope reflects glutamatergic tone in the human brain

Excitatory and inhibitory neural processes are essential for every aspect of brain function, but current non-invasive neuroimaging methods to study these in the human brain are limited. Recent studies which separate oscillatory and aperiodic components of electrophysiological power spectra have highlighted a relationship between aperiodic activity and functional brain states. Studies in both animal models and humans suggest that the aperiodic slope of electrophysiological power spectra reflects the local balance of excitatory:inhibitory (E:I) synaptic transmission. Aperiodic slope varies across individuals, brain states, and clinical populations, which may reflect important differences in E:I balance. However, there is currently a lack of evidence linking aperiodic slope to other measures of excitation and inhibition in the human brain. Here, we show that flatter (less steep) aperiodic slopes from human electroencephalography (EEG) are associated with higher concentrations of the excitatory neurotransmitter glutamate measured with 7 tesla magnetic resonance spectroscopy (MRS) in the occipital lobe at rest. This suggests that individual differences in aperiodic neural activity reflect cortical glutamate concentrations, providing important insight for understanding changes in neural excitation across brain states and neuropsychiatric populations (e.g., schizophrenia) where glutamatergic function may differ. Our results support the use of aperiodic slope as a non-invasive marker for excitatory tone in the human brain.

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Assessing methods for geometric distortion compensation in 7T gradient echo fMRI data

Echo planar imaging (EPI) is widely used in functional and diffusion-weighted MRI, but suffers from significant geometric distortions in the phase encoding direction caused by inhomogeneities in the static magnetic field (B0). This is a particular challenge for EPI at very high field ([≥] 7T), as distortion increases with higher field strength. A number of techniques for distortion correction exist, including those based on B0 field mapping and acquiring EPI scans with opposite phase encoding directions. However, few quantitative comparisons of distortion compensation methods have been performed using human EPI data, especially at very high field. Here, we compared distortion compensation using B0 field maps and opposite phase encoding scans in two different software packages (FSL and AFNI) applied to 7T gradient echo (GE) EPI data from 31 human participants. We assessed distortion compensation quality by quantifying alignment to anatomical reference scans using Dice coefficients and mutual information. Performance between FSL and AFNI was equivalent. In our whole-brain analyses, we found superior distortion compensation using GE scans with opposite phase encoding directions, versus B0 field maps or spin echo (SE) opposite phase encoding scans. However, SE performed better when analyses were limited to ventromedial prefrontal cortex, a region with substantial dropout. Matching the type of opposite phase encoding scans to the EPI data being corrected (e.g., SE-to-SE) also yielded better distortion correction. While the ideal distortion compensation approach likely varies depending on methodological differences across experiments, this study provides a framework for quantitative comparison of different distortion compensation methods.

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Reduced Influence of Perceptual Context in Schizophrenia: Behavioral and Neurophysiological Evidence

BackgroundAccurate perception of visual contours is essential for seeing and differentiating objects in the environment. Both the ability to detect visual contours and the influence of perceptual context created by surrounding stimuli are diminished in people with schizophrenia. The central aim of the present study was to better understand the biological underpinnings of impaired contour integration and weakened effects of perceptual context. Additionally, we sought to determine whether visual perceptual abnormalities reflect genetic factors in schizophrenia and are present in other severe mental disorders. MethodsWe examined behavioral data and event-related potentials (ERPs) collected during the perception of simple linear contours embedded in similar background stimuli in 27 patients with schizophrenia (SCZ), 23 patients with bipolar disorder, 23 first-degree relatives of SCZ and 37 controls. ResultsSCZ exhibited impaired visual contour detection while patients with bipolar disorder exhibited intermediate performance. The orientation of neighboring stimuli (i.e., flankers) relative to the contour modulated perception across all groups, but SCZ exhibited weakened suppression by the perceptual context created by flankers. Late visual (occipital P2) and cognitive (centroparietal P3) neural responses showed group differences and flanker orientation effects, unlike earlier ERPs (occipital P1 and N1). Moreover, behavioral effects of flanker context on contour perception were correlated with modulation in P2/P3 amplitudes. ConclusionIn addition to replicating and extending findings of abnormal contour integration and visual context modulation in SCZ, we provide novel evidence that abnormal use of perceptual context is associated with higher-order sensory and cognitive processes.

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Weaker neural suppression in autism

Increased neural excitation resulting from weakened inhibition is a leading hypothesis for the pathophysiology of autism. However, experimental support in humans remains equivocal. Alternatively, modulatory processes that suppress neural responses but do not specifically rely on inhibition may be impacted in ASD. Leveraging well-characterized suppressive neural circuits in the visual system, we used behavioral and fMRI tasks to demonstrate a significant reduction in neural suppression in young adults with ASD compared to neurotypical controls. We further tested the mechanism of this suppression by measuring levels of the inhibitory neurotransmitter GABA, and found no differences in GABA between groups. We show how a computational model that incorporates divisive normalization, as well as narrower top-down gain (that could result, for example, from a narrower window of attention), can explain our observations and divergent previous findings. Thus, weaker neural suppression in ASD may be attributable to differences in top-down processing, but not to differences in GABA levels.

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Concerning suppression and facilitation of motion perception in humans

Here we consider some topics from a commentary by Tzvetanov (2018) on our article entitled \"Suppression and facilitation of human neural responses\" (Schallmo et al., 2018). The author raises two main points of criticism, which we will summarize thus: 1) psychophysical response bias is not adequately modeled, and 2) other computational models may be better suited to describe the psychophysical motion discrimination data. Both of these points are reasonable in principle, but we disagree with the author in a few areas. We provide some discussion of both issues in order to further elevate the scientific dialogue.

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The time course of different surround suppression mechanisms

What we see depends on the spatial context in which it appears. Previous work has linked the reduction of perceived stimulus contrast in the presence of surrounding stimuli to the suppression of neural responses in early visual cortex. It has also been suggested that this surround suppression depends on at least two separable neural mechanisms, one low-level and one higher-level, which can be differentiated by their response characteristics. In a recent study, we found evidence consistent with these two suppression mechanisms using psychophysical measurements of perceived contrast. Here, we used EEG to demonstrate for the first time that neural responses in the human occipital lobe also show evidence of two separable suppression mechanisms. Eighteen adults (10 female and 8 male) each participated in a total of 3 experimental sessions, in which they viewed visual stimuli through a mirror stereoscope. The first session was used to definitively identify the C1 component, while the second and third comprised the main experiment. ERPs were measured in response to center gratings either with no surround, or with surrounding gratings oriented parallel or orthogonal, and presented either in the same eye (monoptic) or opposite eye (dichoptic). We found that the earliest ERP component (C1; [~]60 ms) was suppressed in the presence of surrounding stimuli, but that this suppression did not depend on surround configuration, suggesting a low-level suppression mechanism which is not tuned for relative orientation. A later response component (N1; [~]160 ms) showed stronger surround suppression for parallel and monoptic stimulus configurations, consistent with our earlier psychophysical results and a higher-level, binocular, orientation-tuned suppression mechanism. We conclude that these two surround suppression mechanisms have distinct response time courses in the human visual system, which can be differentiated using electrophysiology.

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Disrupted neural adaptation in autism spectrum disorder

There has been long-standing speculation that autism spectrum disorder (ASD) involves an increase in excitation relative to inhibition. However, there is little direct evidence of increased neural excitation in humans with ASD. Here we provide a potential explanation for this discrepancy: we show that increased neural excitation emerges only after repeated stimulation, manifesting as a deficit in neural adaptation. We measured fMRI responses induced by repeated audio-visual stimulation and button presses in early sensory-motor cortical areas. Across all cortical areas we show reduced adaptation in individuals with ASD compared to neurotypical individuals. The degree of adaptation is correlated between cortical areas and with button-press reaction times across subjects. These findings suggest that increased neural excitation in ASD, manifesting as dysregulated neural adaptation, is domain-general and behaviorally-relevant.

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Glutamatergic facilitation of neural responses in MT enhances motion perception in humans

There is large individual variability in human neural responses and perceptual abilities. The factors that give rise to these individual differences, however, remain largely unknown. To examine these factors, we separately measured fMRI responses to moving gratings in the motion-selective region MT, and perceptual duration thresholds for motion direction discrimination within the same group of male and female subjects. Further, we acquired MR spectroscopy data that allowed us to quantify an index of neurotransmitter levels in the region surrounding MT. We show that individual differences in the Glx (glutamate + glutamine) signal in the MT region are associated with both higher fMRI responses and improved psychophysical task performance. Our results suggest that individual differences in baseline levels of glutamate within MT contribute to motion perception by increasing neural responses in this region.\n\nSignificanceWhat factors govern the relationship between neural activity and behavior? Our results suggest that one such factor is the level of glutamate, an excitatory neurotransmitter, within a particular region of cortex. By measuring an index of glutamate in vivo using magnetic resonance spectroscopy, we show that human subjects with more glutamate in the visual motion area known as MT also have larger fMRI responses (an index of neural activity) in this region. Further, people with more glutamate in MT can accurately perceive moving images presented more briefly within a behavioral task. Our findings point to an important role for glutamate levels in determining the relationship between neural responses and behavior during visual motion perception.

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Suppression and facilitation of human neural responses

Efficient neural processing depends on regulating responses through suppression and facilitation of neural activity. Utilizing a well-known visual motion paradigm that evokes behavioral suppression and facilitation, and combining 5 different methodologies (behavioral psychophysics, computational modeling, functional MRI, pharmacology, and magnetic resonance spectroscopy), we provide evidence that challenges commonly held assumptions about the neural processes underlying suppression and facilitation. We show that: 1) both suppression and facilitation can emerge from a single, computational principle - divisive normalization; there is no need to invoke separate neural mechanisms, 2) neural suppression and facilitation in the motion-selective area MT mirror perception, but strong suppression also occurs in earlier visual areas, and 3) suppression is not driven by GABA-mediated inhibition. Thus, while commonly used spatial suppression paradigms may provide insight into neural response magnitudes in visual areas, they cannot be used to infer neural inhibition.

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