Cortical Areas Research Articles

Prediction Models Of The Aphasia Severity After Stroke By Lesion Load Of Cortical Language Areas and White Matter Tracts: An Atlas-based Study.

ObjectiveTo construct relatively objective, atlas-based multivariate models for predicting early aphasia severity after stroke, using structural magnetic resonance imaging. MethodsWe analyzed the clinical and imaging data of 46 patients with post-stroke aphasia. The aphasia severity was identified with a Western Aphasia Battery Aphasia Quotient. The assessments of stroke lesions were indicated by the lesion load of both the cortical language areas (Areas-LL) and four white matter tracts (i.e., the superior longitudinal fasciculus, SLF-LL; the inferior frontal occipital fasciculi, IFOF-LL; the inferior longitudinal, ILF-LL; and the uncinate fasciculi, UF-LL) extracted from human brain atlas. Correlation analyses and multiple linear regression analyses were conducted to evaluate the correlations between demographic, stroke- and lesion-related variables and aphasia severity. The predictive models were then established according to the identified significant variables. Finally, the receiver operating characteristic (ROC) curve was utilized to assess the accuracy of the predictive models. ResultsThe variables including Areas-LL, the SLF-LL, and the IFOF-LL were significantly negatively associated with aphasia severity (p < 0.05). In multiple linear regression analyses, these variables accounted for 59.4% of the variance (p < 0.05). The ROC curve analyses yielded the validated area under the curve (AUC) 0.84 both for Areas-LL and SLF-LL and 0.76 for IFOF-LL, indicating good predictive performance (p < 0.01). Adding the combination of SLF-LL and IFOF-LL to this model increased the explained variance to 62.6% and the AUC to 0.92. ConclusionsThe application of atlas-based multimodal lesion assessment may help predict the aphasia severity after stroke, which needs to be further validated and generalized for the prediction of more outcome measures in populations with various brain injuries.

An Audio-Visual Speech Separation Model Inspired by Cortico-Thalamo-Cortical Circuits.

Audio-visual approaches involving visual inputs have laid the foundation for recent progress in speech separation. However, the optimization of the concurrent usage of auditory and visual inputs is still an active research area. Inspired by the cortico-thalamo-cortical circuit, in which the sensory processing mechanisms of different modalities modulate one another via the non-lemniscal sensory thalamus, we propose a novel cortico-thalamo-cortical neural network (CTCNet) for audio-visual speech separation (AVSS). First, the CTCNet learns hierarchical auditory and visual representations in a bottom-up manner in separate auditory and visual subnetworks, mimicking the functions of the auditory and visual cortical areas. Then, inspired by the large number of connections between cortical regions and the thalamus, the model fuses the auditory and visual information in a thalamic subnetwork through top-down connections. Finally, the model transmits this fused information back to the auditory and visual subnetworks, and the above process is repeated several times. The results of experiments on three speech separation benchmark datasets show that CTCNet remarkably outperforms existing AVSS methods with considerably fewer parameters. These results suggest that mimicking the anatomical connectome of the mammalian brain has great potential for advancing the development of deep neural networks.

Interaction of motor behaviour, cortical oscillations and deep brain stimulation in Parkinson disease

Abstract Recent progress in the study of Parkinson's disease (PD) has highlighted the pivotal role of beta oscillations within the basal ganglia-thalamo-cortical network in modulating motor symptoms. Predominantly manifesting as transient bursts, these beta oscillations are central to the pathophysiology of PD motor symptoms, especially bradykinesia. Our central hypothesis is that increased bursting duration in cortex, coupled with kinematics of movement, disrupts the typical flow of neural information, leading to observable changes in motor behavior in PD. To explore this hypothesis, we employed an integrative approach, analyzing the interplay between moment-to-moment brain dynamics and movement kinematics, and the modulation of these relationships by therapeutic deep brain stimulation (DBS). Local field potentials were recorded from the hand motor (M1) and premotor cortical (PM) areas, and internal Globus Pallidus (GPi) in 26 PD patients undergoing DBS implantation surgery. Participants executed rapid alternating hand movements in 30-second blocks, both with and without therapeutic pallidal stimulation. Behaviorally, the analysis revealed bradykinesia, with hand movement cycle width increasing linearly over time during DBS-OFF blocks. Crucially, there was a moment-to-moment correlation between M1 low beta burst duration and movement cycle width, a relationship that dissipated with therapeutic DBS. Further analyses suggest that high gamma activity correlates with enhanced motor performance with DBS-ON. Regardless of the nature of coupling, DBS’s modulation of cortical bursting activity appeared to amplify the brain signals’ informational content regarding instantaneous movement changes. Our findings underscore that DBS significantly reshapes the interaction between motor behavior and neural signals in PD, not only modulating specific bands but also expanding the system's capability to process and relay information for motor control. These insights shed light on the possible network mechanisms underlying DBS therapeutic effects, suggesting a profound impact on both neural and motor domains.

Age-related differences in human cortical microstructure depend on the distance to the nearest vein

Abstract Age-related differences in cortical microstructure are used to understand the neuronal mechanisms that underlie human brain ageing. The cerebral vasculature contributes to cortical ageing, but its precise interaction with cortical microstructure is poorly understood. In a cross-sectional study, we combine venous imaging with vessel distance mapping to investigate the interaction between venous distances and age-related differences in the microstructural architecture of the primary somatosensory cortex, the primary motor cortex, and additional areas in frontal cortex as non-sensorimotor control regions. We scanned 18 younger adults and 17 older adults using 7 Tesla MRI to measure age-related changes in longitudinal relaxation time (T1) and quantitative susceptibility mapping (QSM) values at 0.5 millimetre isotropic resolution. We modelled different cortical depths using an equi-volume approach and assessed the distance of each voxel to its nearest vein using vessel distance mapping. Our data reveal a dependence of cortical quantitative T1 values and positive QSM values on venous distance. In addition, there is an interaction between venous distance and age on quantitative T1 values, driven by lower quantitative T1 values in older compared to younger adults in voxels that are closer to a vein. Together, our data show that the local venous architecture explains a significant amount of variance in standard measures of cortical microstructure and should be considered in neurobiological models of human brain organisation and cortical ageing.

Study of Eye Movements Abnormalities in Epilepsy

ABSTRACT Idiopathic epilepsy (IE), is a group of epileptic syndromes with no structural brain lesion, but with microstructural changes in neuronal networks leading to neuropsychological consequences. Therefore, the assessment of saccadic eye movements can provide insight into the integrity of cerebral networks as it involves large cortical and subcortical brain areas and circuitries. Describe saccadic eye movement abnormalities in patients with IE and correlate them with disease characteristics and antiseizure medication. Case–control study including IE patients followed in the Neurology Department of Razi University Hospital and healthy controls matched. Participants underwent a recording of saccadic eye movements. Pursuit, prosaccade, and anti-saccade tasks were performed. 115 patients and 98 matched healthy controls were included. The gender ratio (male to female) was 0.6. The mean age at onset was 16.3 ± 12 years. Diagnosed epileptic syndromes were juvenile myoclonic epilepsy (JME), epilepsy with generalized tonic-clonic seizures, childhood absence epilepsy, temporal lobe epilepsy, frontal lobe epilepsy, and rolandic epilepsy. Saccadic eye movements were impaired in 52.2% of our patients and significantly more altered in those with JME (p = .021). Prolonged horizontal saccades latencies were the most frequent eye movement abnormalities (32.1%), followed by altered horizontal smooth pursuit (22.6%). A positive correlation was found between age at eye movements recording, age at onset, disease duration, global cognitive impairment, and saccadic eye movements. However, no definite relationship was identified. Saccadic eye movement illustrates extending anatomic alterations in IE including frontal and temporoparietal cortical areas and cortico-subcortical circuits. Eye movement recording is a useful and reproducible tool in the assessment of epileptic patients and provides a better understanding of neuronal mechanisms in epilepsy.

Visually induced involuntary arm, head, and torso movements.

We explored in 75s long trials the effects of visually induced self-rotation and displacement (SR&D) on the horizontally extended right arm of standing subjects (N = 12). A "tool condition" was included in which subjects held a long rod. The extent of arm movement was contingent on whether the arm was extended out Freely or Pointing at a briefly proprioceptively specified target position. The results were nearly identical when subjects held the rod. Subjects in the Free conditions showed significant unintentional arm deviations, averaging 55° in the direction opposite the induced illusory self-motion. Deviations in the Pointing conditions were on average a fifth of those in the Free condition. Deviations of head and torso positions also occurred in all conditions. Total arm and head deviations were the sum of deviations of the arm and head with respect to the torso and deviations of the torso with respect to space. Pointing subjects were able to detect and correct for arm and head deviations with respect to the torso but not for the arm and head deviations with respect to space due to deviations of the torso. In all conditions, arm, head, and torso deviations began before subjects experienced SR&D. We relate our findings to being an extension of the manual following response (MFR) mechanism to influence passive arm control and arm target maintenance as well. Visual-vestibular convergence at vestibular nuclei cells and multiple cortical movement related areas can explain our results, MFR results, and classical Pass Pointing. We distinguish two Phases in the induction of SR&D. In Phase 1, the visual stimulation period prior to SR&D onset, the arm, head, and torso deviations are first apparent, circa < 1 s after stimulus begins. They are augmented at the onset of Phase 2 that starts when SR&D is first sensed. In Phase 2, reaching movements first show curved paths that are compensatory for the Coriolis forces that would be generated on the reaching arm were subjects actually physically rotating. These movement deviations are in the opposite direction to the MFR and the arm, head, and torso deviations reported here. Our results have implications for vehicle control in environments that can induce illusory self motion and displacement.

Claustrum and dorsal endopiriform cortex complex cell-identity is determined by Nurr1 and regulates hallucinogenic-like states in mice

The Claustrum/dorsal endopiriform cortex complex (CLA) is an enigmatic brain region with extensive glutamatergic projections to multiple cortical areas. The transcription factor Nurr1 is highly expressed in the CLA, but its role in this region is not understood. By using conditional gene-targeted mice, we show that Nurr1 is a crucial regulator of CLA neuron identity. Although CLA neurons remain intact in the absence of Nurr1, the distinctive gene expression pattern in the CLA is abolished. CLA has been hypothesized to control hallucinations, but little is known of how the CLA responds to hallucinogens. After the deletion of Nurr1 in the CLA, both hallucinogen receptor expression and signaling are lost. Furthermore, functional ultrasound and Neuropixel electrophysiological recordings revealed that the hallucinogenic-receptor agonists’ effects on functional connectivity between prefrontal and sensorimotor cortices are altered in Nurr1-ablated mice. Our findings suggest that Nurr1-targeted strategies provide additional avenues for functional studies of the CLA.

Children born very preterm experience altered cortical expansion over the first decade of life

Abstract The brain develops rapidly from the final trimester of gestation through childhood, with cortical surface area expanding greatly in the first decade of life. However, it is unclear exactly where and how cortical surface area changes after birth, or how prematurity affects these developmental trajectories. Fifty-two very preterm (gestational age at birth = 26 ± 1.6 weeks) and forty-one full term (gestational age at birth = 39 ± 1.2 weeks) infants were scanned using structural magnetic resonance imaging at term-equivalent age and again at 9/10 years of age. Individual cortical surface reconstructions were extracted for each scan. Infant and 9/10 cortical surfaces were aligned using anatomically constrained Multimodal Surface Matching (aMSM), a technique that allows calculation of local expansion gradients across the cortical surface for each individual subject. At the neonatal time point, very preterm infants had significantly smaller surface area than their full-term peers (P &amp;lt; 0.001), but at the age 9/10-year time point, very preterm and full-term children had comparable surface area (P &amp;gt; 0.05). Across all subjects, cortical expansion by age 9/10 years was most pronounced in frontal, temporal, and supramarginal/inferior parietal junction areas, which are key association cortices (PSpin&amp;lt; 0.001). Very preterm children showed greater cortical surface area expansion between term-equivalent age and age 9/10 compared to their full-term peers in the medial and lateral frontal areas, precuneus, and middle temporal/banks of the superior sulcus junction (P &amp;lt; 0.05). Furthermore, within the very preterm group, expansion was highly variable within the orbitofrontal cortex and posterior regions of the brain. By mapping these patterns across the cortex, we identify differences in association cortices that are known to be important for executive functioning, emotion processing, and social cognition. Additional longitudinal work will be needed to understand if increased expansion in very preterm children is adaptive, or if differences persist into adulthood.

Cortical sites critical to language function act as connectors between language subnetworks

Historically, eloquent functions have been viewed as localized to focal areas of human cerebral cortex, while more recent studies suggest they are encoded by distributed networks. We examined the network properties of cortical sites defined by stimulation to be critical for speech and language, using electrocorticography from sixteen participants during word-reading. We discovered distinct network signatures for sites where stimulation caused speech arrest and language errors. Both demonstrated lower local and global connectivity, whereas sites causing language errors exhibited higher inter-community connectivity, identifying them as connectors between modules in the language network. We used machine learning to classify these site types with reasonably high accuracy, even across participants, suggesting that a site’s pattern of connections within the task-activated language network helps determine its importance to function. These findings help to bridge the gap in our understanding of how focal cortical stimulation interacts with complex brain networks to elicit language deficits.

A comparative study of simulated electric fields of transcranial magnetic stimulation targeting different cortical motor regions.

This computational simulation study investigates the strength of transcranial magnetic stimulation (TMS)-induced electric fields (EF) in primary motor cortex (M1) and secondary motor areas. Our results reveal high interindividual variability in the strength of TMS-induced EF responses in secondary motor areas, relative to the stimulation threshold in M1. Notably, the activation of the supplementary motor area requires high-intensity stimulation, which could be attributed to the greater scalp-to-cortex distance observed over this area. These findings emphasize the importance of individualized planning using computational simulation for optimizing neuromodulation strategies targeting the cortical motor system.

Alterations in cortical and subcortical neuroanatomy and associations with behavior in females with fragile X syndrome.

To address substantial gaps in the literature on neuroanatomical variations in females with fragile X syndrome (FXS). Surface-based modeling techniques were applied to the magnetic resonance imaging of 45 females with FXS (mean age = 10 years 9 months, range 6 years-16 years 4 months, SD = 2 years 9 months) and 33 age-matched and developmentally matched females without FXS to elucidate differences in cortical gray matter volume, surface area, and thickness. Gray matter volumes in subcortical regions were examined to ascertain differences in subcortical volume. In females with FXS, cortical volume was greater bilaterally in the occipital pole and smaller in the right postcentral gyrus. Seven regions demonstrated lower surface area in participants with FXS, while cortical thickness was significantly greater over the posterior and medial surfaces in the group with FXS. Subcortical region of interest analyses demonstrated greater volume in the caudate nucleus, globus pallidus, and nucleus accumbens in the group with FXS. Global gray matter volume, pial thickness, and surface area were associated with behavioral outcomes in the group with FXS but not in the comparison group. Females with FXS demonstrated unique cortical and subcortical gray matter anatomy relative to a matched comparison group. These findings may be relevant to the pathogenesis of the FXS behavioral phenotype and provide insights into behavioral interventions targeted to this population.

Biofabricated adipose-derived mesenchymal cell sheets recover cryo-injured kidneys in rats.

This study aimed to develop a treatment for chronic kidney disease (CKD) by investigating whether transplantation of biofabricated adipose-derived mesenchymal cell (AMC) sheets could improve renal tissue and function. Thirty-nine 10-week-old male Sprague-Dawley rats underwent the harvesting of adipose tissues and right nephrectomy. AMCs that were collected from adipose tissues were labeled and cultured on temperature-responsive dishes, and applied to a gelatin hydrogel sheet. Subsequently, two identical AMC-gelatin sheets were attached together to biofabricate a bilayered AMC-gelatin sheet. Further, 3 weeks after nephrectomy, the renal artery and vein of the left kidney were clamped, and the kidney was sprayed with liquid nitrogen for 60 seconds. The biofabricated AMC sheet was autologously transplanted into the renal capsule of the cryo-injured region (n = 14). Control rats were given acellular sheet (n = 25). One day before and four weeks after transplantation, blood and 24-hour urinary specimens were collected. Histological analysis of the experimental kidneys was performed four weeks after transplantation. Four weeks after transplantation, in the acellular control-transplanted rats, creatinine clearance levels tended to increase, while serum creatinine levels significantly increased. However, in the biofabricated AMC sheet-transplanted rats, creatinine clearance levels significantly increased, and serum creatinine levels remained unchanged and were significantly lower than that of the control rats. The ratio of damaged to undamaged renal tubules in the AMC sheet-transplanted rats was lower than that in the control rats. In addition, the occupancy rate of fibrotic areas in the renal cortex under the AMC sheet-transplanted regions was significantly lower than that in the control regions. After transplantation, while the expressions of transforming growth factor-beta 1 and hypoxia-inducible factor-1 alpha were observed in both the control- and AMC sheet-transplanted regions, these expressions tended to be lower in the AMC sheet-transplanted rats than in the control rats. The labeled transplanted AMCs were detected in the transplanted regions, with some of them also showing positive staining for the vascular endothelial growth factor antibody. In conclusion, the biofabricated AMC sheets improved renal functions by ameliorating renal tubule disorders and renal fibrosis. Therefore, biofabricated AMC sheets would serve as a potential treatment for CKD.

Effects of gait retraining in knee joint position sense

BackgroundJoint position sense (JPS) is crucial for maintaining posture, protecting joints, and carrying out daily activities such as walking. Studies show that exercises to strengthen muscles and improve proprioception can positively impact JPS during passive and less complex activities. Evidence suggests that motor training can effectively enhance sensory function, including JPS, due to the extensive connections between the motor cortex and somatosensory areas. Gait retraining using real-time feedback has improved outcomes among patients with musculoskeletal disorders. The effect of gait retraining on JPS has not been investigated. This study assessed the effects of gait retraining to reduce knee extension in joint position sense in individuals with knee hyperextension walking patterns. MethodsTen women with asymptomatic knee hyperextension (KH) >5° during overground walking participated in this study. Sagittal-plane kinematics were assessed using a three-dimensional (3D) motion analysis system. The JPS was assessed using the Knee Position Active Reproduction Test. The knee with the highest hyperextension was the focus of the gait retraining intervention, which consisted of six 1-h sessions using verbal instructions and visual kinematic feedback. Comparisons of peak knee extension during walking and knee JPS overall error (RMSE) were made using a paired t-test. ResultsGait retraining intervention significantly reduced knee extension angle during walking (83.8 % change; p < 0.001; Cohen's d = −1.6) and improved knee JPS (62 % change; p = 0.023; Cohen's d = 0.8) post-training. In addition, the improvements in joint kinematics (36.7 % change; p = 0.005; Cohen's d = −1.2) and JPS (52.6 % change; p = 0.015; Cohen's d = 0.9) were observed in the untrained knee. SignificanceGait retraining can improve joint position sense. This study addresses a gap in our understanding of how gait retraining can influence JPS. Our results corroborate that gait retraining is an evolving and promising strategy for improving gait outcomes, particularly in individuals with KH walking patterns.

Neuroanatomical and functional correlates in tic disorders and Tourette's syndrome: A narrative review

AbstractTic disorders represent a developmental neuropsychiatric condition whose causes can be attributed to a variety of environmental, neurobiological, and genetic factors. From a neurophysiological perspective, the disorder has classically been associated with neurochemical imbalances (particularly dopamine and serotonin) and structural and functional alterations affecting, in particular, brain areas and circuits involved in the processing and coordination of movements: the basal ganglia, thalamus, motor cortical area, and cingulate cortex; however, more recent research is demonstrating the involvement of many more brain regions and neurotransmission systems than previously observed, such as the prefrontal cortex and cerebellum. In this paper, therefore, we summarize the evidence to date on these abnormalities with the intent to illustrate and clarify the main neuroanatomical differences between patients with tic disorders and healthy individuals.

Confidence and second-order errors in cortical circuits

Abstract Minimization of cortical prediction errors has been considered a key computational goal of the cerebral cortex underlying perception, action and learning. However, it is still unclear how the cortex should form and use information about uncertainty in this process. Here, we formally derive neural dynamics that minimize prediction errors under the assumption that cortical areas must not only predict the activity in other areas and sensory streams but also jointly project their confidence (inverse expected uncertainty) in their predictions. In the resulting neuronal dynamics, the integration of bottom-up and top-down cortical streams is dynamically modulated based on confidence in accordance with the Bayesian principle. Moreover, the theory predicts the existence of cortical second-order errors, comparing confidence and actual performance. These errors are propagated through the cortical hierarchy alongside classical prediction errors and are used to learn the weights of synapses responsible for formulating confidence. We propose a detailed mapping of the theory to cortical circuitry, discuss entailed functional interpretations and provide potential directions for experimental work.

The importance of timing of socioeconomic disadvantage throughout development for depressive symptoms and brain structure

Prior studies have reported associations between socioeconomic disadvantage, brain structure and mental health outcomes, but the timing of these relations is not well understood. Using prospective longitudinal data from the Avon Longitudinal Study of Parents and Children (ALSPAC), this preregistered study examined whether socioeconomic disadvantage related differentially to depressive symptoms (n=3012–3530) and cortical and subcortical structures (n=460–733) in emerging adults, depending on the timing of exposure to socioeconomic disadvantage. Family income in early childhood and own income measured concurrently were both significantly related to depressive symptoms in emerging adulthood. Similar results were observed for perceived financial strain. In contrast, only family income in early childhood was associated with brain structure in emerging adulthood, with positive associations with intracranial volume and total and regional cortical surface area. The findings suggest that both objective and subjective aspects of one’s financial standing throughout development relate to depressive symptoms in adulthood, but that specifically early life family income is related to brain structural features in emerging adulthood. This suggests that associations between socioeconomic disadvantage and brain structure originate early in neurodevelopment, highlighting the role of timing of socioeconomic disadvantage.

Anatomo-functional changes in neural substrates of cognitive memory in developmental amnesia: Insights from automated and manual Magnetic Resonance Imaging examinations.

Despite bilateral hippocampal damage dating to the perinatal or early childhood period and severely impaired episodic memory, patients with developmental amnesia continue to exhibit well-developed semantic memory across the developmental trajectory. Detailed information on the extent and focality of brain damage in these patients is needed to hypothesize about the neural substrate that supports their remarkable capacity for encoding and retrieval of semantic memory. In particular, we need to assess whether the residual hippocampal tissue is involved in this preservation, or whether the surrounding cortical areas reorganize to rescue aspects of these critical cognitive memory processes after early injury. We used voxel-based morphometry (VBM) analysis, automatic (FreeSurfer) and manual segmentation to characterize structural changes in the brain of an exceptionally large cohort of 23 patients with developmental amnesia in comparison with 32 control subjects. Both the VBM and the FreeSurfer analyses revealed severe structural alterations in the hippocampus and thalamus of patients with developmental amnesia. Milder damage was found in the amygdala, caudate, and parahippocampal gyrus. Manual segmentation demonstrated differences in the degree of atrophy of the hippocampal subregions in patients. The level of atrophy in CA-DG subregions and subicular complex was more than 40%, while the atrophy of the uncus was moderate (-24%). Anatomo-functional correlations were observed between the volumes of residual hippocampal subregions in patients and selective aspects of their cognitive performance, viz, intelligence, working memory, and verbal and visuospatial recall. Our findings suggest that in patients with developmental amnesia, cognitive processing is compromised as a function of the extent of atrophy in hippocampal subregions. More severe hippocampal damage may be more likely to promote structural and/or functional reorganization in areas connected to the hippocampus. In this hypothesis, different levels of hippocampal function may be rescued following this variable reorganization. Our findings document not only the extent, but also the limits of circuit reorganization occurring in the young brain after early bilateral hippocampal damage.

Not All Stroop-Type Tasks Are Alike: Assessing the Impact of Stimulus Material, Task Design, and Cognitive Demand via Meta-analyses Across Neuroimaging Studies.

The Stroop effect is one of the most often studied examples of cognitive conflict processing. Over time, many variants of the classic Stroop task were used, including versions with different stimulus material, control conditions, presentation design, and combinations with additional cognitive demands. The neural and behavioral impact of this experimental variety, however, has never been systematically assessed. We used activation likelihood meta-analysis to summarize neuroimaging findings with Stroop-type tasks and to investigate whether involvement of the multiple-demand network (anterior insula, lateral frontal cortex, intraparietal sulcus, superior/inferior parietal lobules, midcingulate cortex, and pre-supplementary motor area) can be attributed to resolving some higher-order conflict that all of the tasks have in common, or if aspects that vary between task versions lead to specialization within this network. Across 133 neuroimaging experiments, incongruence processing in the color-word Stroop variant consistently recruited regions of the multiple-demand network, with modulation of spatial convergence by task variants. In addition, the neural patterns related to solving Stroop-like interference differed between versions of the task that use different stimulus material, with the only overlap between color-word, emotional picture-word, and other types of stimulus material in the posterior medial frontal cortex and right anterior insula. Follow-up analyses on behavior reported in these studies (in total 164 effect sizes) revealed only little impact of task variations on the mean effect size of reaction time. These results suggest qualitative processing differences among the family of Stroop variants, despite similar task difficulty levels, and should carefully be considered when planning or interpreting Stroop-type neuroimaging experiments.

Neuroelectrophysiology-compatible electrolytic lesioning.

Lesion studies have historically been instrumental for establishing causal connections between brain and behavior. They stand to provide additional insight if integrated with multielectrode techniques common in systems neuroscience. Here, we present and test a platform for creating electrolytic lesions through chronically implanted, intracortical multielectrode probes without compromising the ability to acquire neuroelectrophysiology. A custom-built current source provides stable current and allows for controlled, repeatable lesions in awake-behaving animals. Performance of this novel lesioning technique was validated using histology from ex vivo and in vivo testing, current and voltage traces from the device, and measurements of spiking activity before and after lesioning. This electrolytic lesioning method avoids disruptive procedures, provides millimeter precision over the extent and submillimeter precision over the location of the injury, and permits electrophysiological recording of single-unit activity from the remaining neuronal population after lesioning. This technique can be used in many areas of cortex, in several species, and theoretically with any multielectrode probe. The low-cost, external lesioning device can also easily be adopted into an existing electrophysiology recording setup. This technique is expected to enable future causal investigations of the recorded neuronal population's role in neuronal circuit function, while simultaneously providing new insight into local reorganization after neuron loss.

The neural and computational architecture of feedback dynamics in mouse cortex during stimulus report.

Conscious reportability of visual input is associated with a bimodal neural response in primary visual cortex (V1): an early-latency response coupled to stimulus features and a late-latency response coupled to stimulus report or detection. This late wave of activity, central to major theories of consciousness, is thought to be driven by prefrontal cortex (PFC), responsible for "igniting" it. Here we analyzed two electrophysiological studies in mice performing different stimulus detection tasks, and characterize neural activity profiles in three key cortical regions: V1, posterior parietal cortex (PPC) and PFC. We then developed a minimal network model, constrained by known connectivity between these regions, reproducing the spatio-temporal propagation of visual- and report-related activity. Remarkably, while PFC was indeed necessary to generate report-related activity in V1, this occurred only through the mediation of PPC. PPC, and not PFC, had the final veto in enabling the report-related late wave of V1 activity.Significance statement A long-standing objective in the study of consciousness is to characterize the neural signatures of perceived compared to non-perceived sensory stimuli. In particular, the role of different cortical areas in the generation of consciousness is actively debate. Here we combined electrophysiological and modeling studies to investigate the mechanistic role of individual connections between brain regions in the generation of the activity patterns observed during conscious report. We found that, while frontal areas initiate report-related activity, parietal cortex acts as a gate to determine whether such activity will propagate back to visual cortex. This division of labor between prefrontal and parietal cortices is unexplained by current theoretical models of consciousness and therefore should strongly impact mechanistic neural models of conscious report.