rTMS affects EEG microstates dynamic during evoked activity

Cortex ◽  
2021 ◽  
Author(s):  
Pierpaolo Croce ◽  
Spadone Sara ◽  
Filippo Zappasodi ◽  
Antonello Baldassarre ◽  
Paolo Capotosto
Keyword(s):  
2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Michael Lohse ◽  
Johannes C. Dahmen ◽  
Victoria M. Bajo ◽  
Andrew J. King

AbstractIntegration of information across the senses is critical for perception and is a common property of neurons in the cerebral cortex, where it is thought to arise primarily from corticocortical connections. Much less is known about the role of subcortical circuits in shaping the multisensory properties of cortical neurons. We show that stimulation of the whiskers causes widespread suppression of sound-evoked activity in mouse primary auditory cortex (A1). This suppression depends on the primary somatosensory cortex (S1), and is implemented through a descending circuit that links S1, via the auditory midbrain, with thalamic neurons that project to A1. Furthermore, a direct pathway from S1 has a facilitatory effect on auditory responses in higher-order thalamic nuclei that project to other brain areas. Crossmodal corticofugal projections to the auditory midbrain and thalamus therefore play a pivotal role in integrating multisensory signals and in enabling communication between different sensory cortical areas.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Soren Wainio-Theberge ◽  
Annemarie Wolff ◽  
Georg Northoff

AbstractSpontaneous neural activity fluctuations have been shown to influence trial-by-trial variation in perceptual, cognitive, and behavioral outcomes. However, the complex electrophysiological mechanisms by which these fluctuations shape stimulus-evoked neural activity remain largely to be explored. Employing a large-scale magnetoencephalographic dataset and an electroencephalographic replication dataset, we investigate the relationship between spontaneous and evoked neural activity across a range of electrophysiological variables. We observe that for high-frequency activity, high pre-stimulus amplitudes lead to greater evoked desynchronization, while for low frequencies, high pre-stimulus amplitudes induce larger degrees of event-related synchronization. We further decompose electrophysiological power into oscillatory and scale-free components, demonstrating different patterns of spontaneous-evoked correlation for each component. Finally, we find correlations between spontaneous and evoked time-domain electrophysiological signals. Overall, we demonstrate that the dynamics of multiple electrophysiological variables exhibit distinct relationships between their spontaneous and evoked activity, a result which carries implications for experimental design and analysis in non-invasive electrophysiology.


2019 ◽  
Vol 29 (12) ◽  
pp. 5049-5060 ◽  
Author(s):  
Kainan S Wang ◽  
Mauricio R Delgado

AbstractThe ability to perceive and exercise control over an outcome is both desirable and beneficial to our well-being. It has been shown that animals and humans alike exhibit behavioral bias towards seeking control and that such bias recruits the ventromedial prefrontal cortex (vmPFC) and striatum. Yet, this bias remains to be quantitatively captured and studied neurally. Here, we employed a behavioral task to measure the preference for control and characterize its neural underpinnings. Participants made a series of binary choices between having control and no-control over a game for monetary reward. The mere presence of the control option evoked activity in the ventral striatum. Importantly, we manipulated the expected value (EV) of each choice pair to extract the pairing where participants were equally likely to choose either option. The difference in EV between the options at this point of equivalence was inferred as the subjective value of control. Strikingly, perceiving control inflated the reward value of the associated option by 30% and this value inflation was tracked by the vmPFC. Altogether, these results capture the subjective value of perceived control inherent in decision making and highlight the role of corticostriatal circuitry in the perception of control.


2012 ◽  
Vol 108 (2) ◽  
pp. 431-440 ◽  
Author(s):  
Oana Covasala ◽  
Sören L. Stirn ◽  
Stephanie Albrecht ◽  
Roberto De Col ◽  
Karl Messlinger

Calcitonin gene-related peptide (CGRP) is regarded as a key mediator in the generation of primary headaches. CGRP receptor antagonists reduce migraine pain in clinical trials and spinal trigeminal activity in animal experiments. The site of CGRP receptor inhibition causing these effects is debated. Activation and inhibition of CGRP receptors in the trigeminal ganglion may influence the activity of trigeminal afferents and hence of spinal trigeminal neurons. In anesthetized rats extracellular activity was recorded from neurons with meningeal afferent input in the spinal trigeminal nucleus caudalis. Mechanical stimuli were applied at regular intervals to receptive fields located in the exposed cranial dura mater. α-CGRP (10−5 M), the CGRP receptor antagonist olcegepant (10−3 M), or vehicle was injected through the infraorbital canal into the trigeminal ganglion. The injection of volumes caused transient discharges, but vehicle, CGRP, or olcegepant injection was not followed by significant changes in ongoing or mechanically evoked activity. In animals pretreated intravenously with the nitric oxide donor glyceryl trinitrate (GTN, 250 μg/kg) the mechanically evoked activity decreased after injection of CGRP and increased after injection of olcegepant. In conclusion, the activity of spinal trigeminal neurons with meningeal afferent input is normally not controlled by CGRP receptor activation or inhibition in the trigeminal ganglion. CGRP receptors in the trigeminal ganglion may influence neuronal activity evoked by mechanical stimulation of meningeal afferents only after pretreatment with GTN. Since it has previously been shown that olcegepant applied to the cranial dura mater is ineffective, trigeminal activity driven by meningeal afferent input is more likely to be controlled by CGRP receptors located centrally to the trigeminal ganglion.


2016 ◽  
Vol 124 (4) ◽  
pp. 766-778 ◽  
Author(s):  
Catherine Elizabeth Warnaby ◽  
Marta Seretny ◽  
Roísín Ní Mhuircheartaigh ◽  
Richard Rogers ◽  
Saad Jbabdi ◽  
...  

Abstract Background It has been postulated that a small cortical region could be responsible for the loss of behavioral responsiveness (LOBR) during general anesthesia. The authors hypothesize that any brain region demonstrating reduced activation to multisensory external stimuli around LOBR represents a key cortical gate underlying this transition. Furthermore, the authors hypothesize that this localized suppression is associated with breakdown in frontoparietal communication. Methods During both simultaneous electroencephalography and functional magnetic resonance imaging (FMRI) and electroencephalography data acquisition, 15 healthy volunteers experienced an ultraslow induction with propofol anesthesia while a paradigm of multisensory stimulation (i.e., auditory tones, words, and noxious pain stimuli) was presented. The authors performed separate analyses to identify changes in (1) stimulus-evoked activity, (2) functional connectivity, and (3) frontoparietal synchrony associated with LOBR. Results By using an FMRI conjunction analysis, the authors demonstrated that stimulus-evoked activity was suppressed in the right dorsal anterior insula cortex (dAIC) to all sensory modalities around LOBR. Furthermore, the authors found that the dAIC had reduced functional connectivity with the frontoparietal regions, specifically the dorsolateral prefrontal cortex and inferior parietal lobule, after LOBR. Finally, reductions in the electroencephalography power synchrony between electrodes located in these frontoparietal regions were observed in the same subjects after LOBR. Conclusions The authors conclude that the dAIC is a potential cortical gate responsible for LOBR. Suppression of dAIC activity around LOBR was associated with disruption in the frontoparietal networks that was measurable using both electroencephalography synchrony and FMRI connectivity analyses.


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