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Bastos, A. M.

Publications and source records attributed to Bastos, A. M..

At least 19 recordsLinked to original sources

Circuit and cell-type mechanisms of the spectrolaminar motif of cortical oscillations

Oscillations are a key feature of cortical activity, coordinating spike timing across areas, layers, and cell types. Recent work suggests these rhythms follow a stereotyped organization across cortical depth, the spectrolaminar (SL) motif, with higher-frequency gamma prominent in superficial layers and lower-frequency alpha/beta in deep layers, yet the mechanisms generating it remain poorly understood. Using a bio-realistic model of mouse primary visual cortex, we reproduced the SL motif and found it preserved across diverse visual stimuli. Systematic cell-type- and layer-resolved perturbations showed that the alpha/beta component was intrinsic to every layer, whereas the 50-80 Hz gamma component was predominantly generated within layer 4 (L4) and propagated network-wide through inter-laminar connections. Pvalb interneurons were the principal regulators of gamma, Sst cells shaped low-frequency power, and Vip cells controlled oscillation magnitude. The temporal properties of L4 Pvalb-to-excitatory synapses were especially influential in generating the SL motif. These models and simulation results thus offer a plausible description of circuit mechanisms underlying cortical oscillations and the SL motif and are publicly available to facilitate further studies.

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Human iEEG recordings during audiovisual speech violations support and extend predictive routing models

Rather than constantly reconstructing the world solely through sensory input, predictive processing theories posit that the brain utilizes predictions maintained as internal representations to guide sensory processing. An emerging model, predictive routing, proposes that an interplay between neuronal gamma (40-150 Hz) and alpha-beta (10-30 Hz) rhythms implements a dynamic mechanism for predictive processing. Namely, predictions enhance alpha-beta oscillations that suppress gamma activity during the processing of predicted inputs. While this model is supported by animal studies, its validity has not been fully explored within the human brain. The present study addresses this by leveraging human intracranial EEG (iEEG) recordings across superior temporal and prefrontal/premotor areas of seven presurgical epilepsy patients during an audiovisual speech paradigm. We calculated iEEG power in the theta, alpha-beta, and high gamma bands during simple auditory deviance, multisensory integration, and a condition where an incongruent visual cue (lip movements) clashed with an auditory stimulus (a syllable), creating audiovisual incongruence that can elicit the McGurk illusion. Results revealed increased high-gamma and decreased alpha-beta power in the superior temporal cortex in response to auditory deviance and the McGurk condition, while frontal areas, despite reflecting a similar decrease in alpha-beta power, did not present this high gamma prediction error signal. Instead, the theta band revealed a strong prediction error signal in the McGurk condition, consistent with theories on the role of theta in reorganizing cortical networks. These results both support and extend existing predictive routing models for human-specific forms of predictive processing.

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Disruption of interareal control during propofol anesthesia

Anesthetic-induced unconsciousness may arise partly from a change in how brain areas can manipulate each others activity. To quantify this change, we use control-theoretic tools that can precisely characterize how easily subsystems in complex networks can control each other. These tools rely on the Jacobian of the dynamics, an object that fully specifies how inputs to a function affect the outputs. We built on JacobianODE, a method for data-driven Jacobian learning, to enable its application to neural recordings. We developed a deep learning framework that recovers directional, nonlinear control from partially observed multi-area recordings by combining delay-coordinate embedding, a volume-preserving invertible encoder, and latent dynamics via JacobianODE. We validated our framework on the Lorenz system and a partially observed working-memory recurrent neural network. We then applied it to local field potential recordings from posterior parietal (PPC), superior temporal gyrus (STG), frontal eye fields (FEF), and ventrolateral prefrontal cortex (vlPFC) in two non-human primates, comparing wakefulness with propofol anesthesia. Anesthesia pervasively reduced the ability of areas to control each other, both in terms of driving towards novel states and stabilizing along existing trajectories. This change in ease of control was driven by a decrease in the magnitude of interareal coupling. Directional ease of driving control from PPC to vlPFC and FEF to vlPFC was increased under anesthesia, providing a potential mechanism for paradoxical excitation observed during propofol infusion. Together, these results recast anesthetic unconsciousness as a directional breakdown of cortical control.

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Similar destabilization of neural dynamics under different general anesthetics

Different classes of anesthetics can induce unconsciousness despite acting through distinct biological mechanisms. This raises the possibility that they produce a convergent effect on the dynamics or temporal evolution of neural population activity. To explore this, we analyzed intracortical electrophysiological recordings during infusions of propofol, ketamine, and dexmedetomidine, using a rigorous method to estimate dynamical stability. We found that all three anesthetics, despite their molecular differences, similarly affect cortical states by destabilizing their dynamics. This destabilization matched the slower recovery from sensory perturbations and longer stimulus-induced autocorrelation times observed during the anesthetic infusions. The destabilization was also reflected predominantly in lower-frequency ranges, linking it to the well-known increase in low-frequency power during anesthesia. Finally, destabilization closely tracked real-time fluctuations in consciousness. Together, these findings suggest that cortical destabilization may be a shared neural correlate of anesthetic-induced unconsciousness, offering a mechanistic explanation for low-frequency oscillations observed during anesthesia.

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Ubiquitous predictive processing in the spectral domain of sensory cortex

The appearance at the anatomical level of a canonical laminar microcircuit suggests that each six-layer column of granular cortex may mediate a canonical computation. Hypotheses for such computations include predictive coding, predictive routing, efficient coding, and others. However, single-neuron recordings capture only the individual elements of the hypothesized laminar microcircuit, while local field potentials (LFPs) from a laminar probe offer insight into the broader population activity. Through the Allen Institutes OpenScope Brain Observatory, data in mice performing a visual oddball task during multi-area laminar recording was used to test predictive processing hypotheses in the spectral domain. Histological labeling of the cortical laminae enabled a fine-grained examination of their roles in the task, and frequency bands capturing both feedforward and feedback effects were analyzed. {gamma}-band local-field potential (LFP) oscillations conveyed feedforward prediction errors in lower sensory areas of cortex; /{beta}-band oscillations weakened in unpredictable conditions compared to predictable ones; and {theta}-band oscillations additionally signalled slower, longer-scale temporal prediction errors. In combination with the previous findings, predictive routing explains these experiments where neither ubiquitous predictive coding nor feedforward adaptation can. SignificanceCortical columns robustly signal perceptual features through the firing rates of spiking neurons. In accordance with this rate coding, predictive processing theories hypothesized that neuronal firing rates ubiquitously signal surprise. However, a recent large-scale study of spike rates did not support this conjecture. An alternate model, predictive routing, suggests that neuronal oscillations rather than spike rates could encode surprise. These neuronal oscillations, which can affect the timing but not rate of spiking, formed coherent {gamma} rhythms which consistently signaled both simpler and more complex forms of surprise in mouse visual cortex. Together with the findings on spike-rates in the same experiment, our findings suggest that cortical circuits encode surprise in the rhythmic timing of spikes rather than in their rate.

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Cell Density and mRNA Expression of Inhibitory Interneurons in Schizophrenia: A Meta-Analysis

Introduction GABAergic interneurons are implicated in the pathophysiology of schizophrenia, yet evidence regarding the nature of deficits across brain areas and interneuron subtypes remains conflicting. We adopted a meta-analytic, multi-level linear modeling approach to identify interneurons, cortical layers, and brain areas involved, and the implications for circuit functions in schizophrenia. Methods Following PRISMA guidelines, we conducted a systematic search and meta-analysis from inception to November 2025, for studies examining parvalbumin, somatostatin, calbindin, and calretinin interneuron density or mRNA expression in schizophrenia. We included data from 44 studies, comprising 736 individuals with schizophrenia and 814 healthy controls. Non-cell-specific, non-human, or indirect proxy studies were excluded. Linear mixed-effects models quantified deficits while accounting for cortical layer, cell-type, and brain area, providing a map of interneuron pathology. We further analyzed changes in GABAergic interneurons to determine whether deficits preferentially target cortical layers, cell-types, and brain areas more associated with top-down or bottom-up processing. Results Parvalbumin and somatostatin interneurons showed robust reductions, particularly in layers 3/4, whilst calbindin and calretinin interneurons were less affected. Deficits were widespread across cortical and subcortical regions. Contrasts revealed that schizophrenia is characterized by interneuron deficits preferentially affecting bottom-up signaling -- notably parvalbumin and somatostatin interneurons in layers 3/4, which are critical for gamma-band synchronization and feedforward sensory processing. Discussion These findings provide the most comprehensive meta-analysis on GABAergic interneurons in schizophrenia to-date, as well as a novel perspective on circuit dysfunctions, with implications for computational models. These results highlight the need for more widespread sampling across the brain using methodologies that can pinpoint deficits in molecularly more precise ways.

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A ubiquitous spectrolaminar motif across independent studies, including in the Mackey et al. dataset

Our study (Mendoza-Halliday et al., 2024) made two contributions: (1) discovery of a ubiquitous cortical motif and (2) a tool derived from it--the Frequency-based Layer Identification Procedure (FLIP and vFLIP). Mackey et al. critique the tool, questioning its advantage over classic current source density (CSD) analysis, and reason backwards to challenge the motifs ubiquity. In our rebuttal, we confirm the spectrolaminar motif in diverse cortical areas using data from multiple research groups (who joined us in this rebuttal) as well as Mackey et al.s own dataset. Additionally, we introduce vFLIP2, an improved version of our tool that addresses their comments. It reliably identified and localized the motif in our data and Mackey et al.s data. Our findings reaffirm the motifs ubiquity. We value Mackey et al.s comments, which helped refine our tool.

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Predictive routing emerges from self-supervised stochastic neural plasticity

Predictive processing theories propose that the brain builds internal models of its environment by reducing the discrepancy between internally generated predictions and external sensory signals. Prior work has linked these processes to oscillatory activity in gamma (40-100 Hz) and alpha/beta (10-30 Hz) frequency ranges. Current computational approaches face a trade-off: abstract predictive-processing models can implement self-supervised computations but often omit oscillatory spiking dynamics, whereas biophysically constrained spiking models can generate neural rhythms but often require extensive manual tuning. Here, we introduce the Genetic Stochastic Delta Rule (GSDR), an evolutionary optimization framework for fitting nonlinear neural models to electrophysiological objectives. We first evaluate GSDR in simplified optimization settings, then apply it to spiking-network objectives involving firing rates, beta/gamma spectral ratios, and empirical macaque stimulus-evoked gamma dynamics from visual cortex. We show that GSDR can search constrained synaptic parameter spaces, reduce reliance on manual tuning, and reproduce spectral and circuit-level phenotypes associated with predictive routing. We also used Izhikevich simulations as a model-class robustness analysis, showing that the approach is not limited to the original Hodgkin-Huxley-style implementation. These results position GSDR as a methodological framework for multi-objective exploration of oscillatory neural models. Author summaryIn predictive processing theories, the brain is hypothesized to build internal models of its environment. Empirical and theoretical studies suggest that neuronal oscillations are important components of this process, and abnormal oscillations are also linked to disorders such as schizophrenia. To study such mechanisms, computational neuroscience needs models that can express biologically meaningful spiking and oscillatory dynamics while also being trainable without extensive manual tuning. We developed the Genetic Stochastic Delta Rule (GSDR), a self-supervised evolutionary optimization framework for fitting nonlinear neural models to objectives. GSDR combines objective-guided search, stochastic exploration, genetic selection/deselection, and an activity-dependent MCDP update term. We show that GSDR can tune spiking networks toward beta/gamma spectral objectives and empirical stimulus-evoked gamma dynamics. The results do not prove predictive routing or identify a unique biological circuit; rather, they show that GSDR can identify candidate circuit configurations and can generalize beyond the original Hodgkin-Huxley-style model to Izhikevich simulations.

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Stimulus history, not expectation, drives sensory prediction errors in mammalian cortex

Hierarchical predictive coding (HPC) models have recently flourished in neuroscience1-9. Feedforward and feedback processing are at the heart of HPC models. Previous experimental studies using fMRI, EEG/MEG, and LFP9-11 do not reliably resolve feedback modulation from local computations and feedforward outputs. Here, using open-science8, multi-species, multi-area, high-density12, laminar neurophysiology13, we empirically test whether hierarchical predictive coding is a key component shaping cortical processing of visual stimuli. To isolate visual information processing and eliminate motor/reward confounders9-11, we use a no-report task. Our task leveraged so-called global oddballs (GO) as unpredictable, deviant stimuli that circumvent low-level adaptation. We examined their responses relative to local oddballs (LO) that we habituated into highly predictable priors. Four surprising findings in this dataset challenge many existing hierarchical predictive coding models. First, GO responses were exclusive to higher-order, more cognitive areas rather than early-to-mid visual cortex. Second, inhibitory interneuron-targeted optogenetics in primates and mice and waveform shape analysis in primates revealed no evidence that predictive suppression was implemented via these interneurons. Third, highly predictable LO responses dominated in over 50% of all neurons, including in higher-order cortex, which should have anticipated them, indicating limited evidence for predictive suppression. Lastly, prediction error responses evoked by GOs did not evoke feedforward processing. These results reveal circuit dynamics that govern how prediction shapes visual processing, motivating more neurally constrained predictive processing models.

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The laminar organization of cell types in macaque cortex and its relationship to neuronal oscillations

The canonical microcircuit (CMC) has been hypothesized to be the fundamental unit of information processing in cortex. Each CMC unit is thought to be an interconnected column of neurons with specific connections between excitatory and inhibitory neurons across layers. Recently, we identified a conserved spectrolaminar motif of oscillatory activity across the primate cortex that may be the physiological consequence of the CMC. The spectrolaminar motif consists of local field potential (LFP) gamma-band power (40-150 Hz) peaking in superficial layers 2 and 3 and alpha/beta-band power (8-30 Hz) peaking in deep layers 5 and 6. Here, we investigate whether specific conserved cell types may produce the spectrolaminar motif. We collected laminar histological and electrophysiological data in 11 distinct cortical areas spanning the visual hierarchy: V1, V2, V3, V4, TEO, MT, MST, LIP, 8A/FEF, PMD, and LPFC (area 46), and anatomical data in DP and 7A. We stained representative slices for the three main inhibitory subtypes, Parvalbumin (PV), Calbindin (CB), and Calretinin (CR) positive neurons, as well as pyramidal cells marked with Neurogranin (NRGN). We found a conserved laminar structure of PV, CB, CR, and pyramidal cells. We also found a consistent relationship between the laminar distribution of inhibitory subtypes with power in the local field potential. PV interneuron density positively correlated with gamma (40-150 Hz) power. CR and CB density negatively correlated with alpha (8-12 Hz) and beta (13-30 Hz) oscillations. The conserved, layer-specific pattern of inhibition and excitation across layers is therefore likely the anatomical substrate of the spectrolaminar motif. Significance StatementNeuronal oscillations emerge as an interplay between excitatory and inhibitory neurons and underlie cognitive functions and conscious states. These oscillations have distinct expression patterns across cortical layers. Does cellular anatomy enable these oscillations to emerge in specific cortical layers? We present a comprehensive analysis of the laminar distribution of the three main inhibitory cell types in primate cortex (Parvalbumin, Calbindin, and Calretinin positive) and excitatory pyramidal cells. We found a canonical relationship between the laminar anatomy and electrophysiology in 11 distinct primate areas spanning from primary visual to prefrontal cortex. The laminar anatomy explained the expression patterns of neuronal oscillations in different frequencies. Our work provides insight into the cortex-wide cellular mechanisms that generate neuronal oscillations in primates.

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Propofol anesthesia destabilizes neural dynamics across cortex

Every day, hundreds of thousands of people undergo general anesthesia. One hypothesis is that anesthesia disrupts dynamic stability, the ability of the brain to balance excitability with the need to be stable and thus controllable. We tested this hypothesis using a new method for quantifying population-level dynamic stability in complex systems, Delayed Linear Analysis for Stability Estimation (DeLASE). Propofol was used to transition animals between the awake state and anesthetized unconsciousness. DeLASE was applied to macaque cortex local field potentials (LFPs). We found that neural dynamics were more unstable in unconsciousness compared to the awake state. Cortical trajectories mirrored predictions from destabilized linear systems. We mimicked the effect of propofol in simulated neural networks by increasing inhibitory tone. Paradoxically, increased inhibition also destabilized the networks. Our results suggest that anesthesia disrupts dynamical stability that is required for consciousness.

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Propofol-mediated loss of consciousness disrupts predictive routing and local field phase modulation of neural activity

Predictive coding is a fundamental function of the cortex. The predictive routing model proposes a neurophysiological implementation for predictive coding. Predictions are fed back from deep-layer cortex via alpha/beta (8-30Hz) oscillations. They inhibit the gamma (40-100Hz) and spiking that feed sensory inputs forward. Unpredicted inputs arrive in circuits unprepared by alpha/beta, resulting in enhanced gamma and spiking. To test the predictive routing model and its role in consciousness, we collected data from intracranial recordings of macaque monkeys during passive presentation of auditory oddballs (e.g., AAAAB) before and after propofol-mediated loss of consciousness (LOC). In line with the predictive routing model, alpha/beta oscillations in the awake state served to inhibit the processing of predictable stimuli. Propofol-mediated LOC eliminated alpha/beta modulation by a predictable stimulus in sensory cortex and alpha/beta coherence between sensory and frontal areas. As a result, oddball stimuli evoked enhanced gamma power, late (> 200 ms from stimulus onset) period spiking, and superficial layer sinks in sensory cortex. Therefore, auditory cortex was in a disinhibited state during propofol-mediated LOC. However, despite these enhanced feedforward responses in auditory cortex, there was a loss of differential spiking to oddballs in higher order cortex. This may be a consequence of a loss of within-area and inter-area spike-field coupling in the alpha/beta and gamma frequency bands. These results provide strong constraints for current theories of consciousness. Significance statementNeurophysiology studies have found alpha/beta oscillations (8-30Hz), gamma oscillations (40-100Hz), and spiking activity during cognition. Alpha/beta power has an inverse relationship with gamma power/spiking. This inverse relationship suggests that gamma/spiking are under the inhibitory control of alpha/beta. The predictive routing model hypothesizes that alpha/beta oscillations selectively inhibit (and thereby control) cortical activity that is predictable. We tested whether this inhibitory control is a signature of consciousness. We used multi-area neurophysiology recordings in monkeys presented with tone sequences that varied in predictability. We recorded brain activity as the anesthetic propofol was administered to manipulate consciousness. Compared to conscious processing, propofol-mediated unconsciousness disrupted alpha/beta inhibitory control during predictive processing. This led to a disinhibition of gamma/spiking, consistent with the predictive routing model.

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Near-field potentials index local neural computations more accurately than population spiking

Local field potentials (LFP) are low-frequency extracellular voltage fluctuations thought to primarily arise from synaptic activity. However, unlike highly localized neuronal spiking, LFP is spatially less specific. LFP measured at one location is not entirely generated there due to far-field contributions that are passively conducted across volumes of neural tissue. We sought to quantify how much information within the locally generated, near-field low-frequency activity (nfLFP) is masked by volume-conducted far-field signals. To do so, we measured laminar neural activity in primary visual cortex (V1) of monkeys viewing sequences of multifeatured stimuli. We compared information content of regular LFP and nfLFP that was mathematically stripped of volume-conducted far-field contributions. Information content was estimated by decoding stimulus properties from neural responses via spatiotemporal multivariate pattern analysis. Volume-conducted information differed from locally generated information in two important ways: (1) for stimulus features relevant to V1 processing (orientation and eye-of-origin), nfLFP contained more information. (2) in contrast, the volume-conducted signal was more informative regarding temporal context (relative stimulus position in a sequence), a signal likely to be coming from elsewhere. Moreover, LFP and nfLFP differed both spectrally as well as spatially, urging caution regarding the interpretations of individual frequency bands and/or laminar patterns of LFP. Most importantly, we found that population spiking of local neurons was less informative than either the LFP or nfLFP, with nfLFP containing most of the relevant information regarding local stimulus processing. These findings suggest that the optimal way to read out local computational processing from neural activity is to decode the local contributions to LFP, with significant information loss hampering both regular LFP and local spiking. Authors ContributionsConceptualization, D.A.T., J.A.W, and A.M.; Data Collection, J.A.W., M.A.C., K.D.; Formal Analysis, D.A.T. and J.A.W.; Data Visualization, D.A.T. and J.A.W.; Original Draft, D.A.T., J.A.W., and A.M.; Revisions and Final Draft, D.A.T., J.A.W., M.A.C., K.D., M.T.W., A.M.B., and A.M. Competing InterestsThe authors declare no conflicts of interest.

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Measurable fields to spikes causality and its dependence on cortical layer and area.

Distinct dynamics in different cortical layers are apparent in neuronal and local field potential (LFP) patterns, yet their associations in the context of laminar processing have been sparingly analyzed. Here, we study the laminar organization of spike-field causal flow within and across visual (V4) and frontal areas (PFC) of monkeys performing a visual task. Using an event-based quantification of LFPs and a directed information estimator, we found area and frequency specificity in the laminar organization of spike-field causal connectivity. Gamma bursts (40-80 Hz) in the superficial layers of V4 largely drove intralaminar spiking. These gamma influences also fed forward up the cortical hierarchy to modulate laminar spiking in PFC. In PFC, the direction of intralaminar information flow was from spikes [->] fields where these influences dually controlled top-down and bottom-up processing. Our results, enabled by innovative methodologies, emphasize the complexities of spike-field causal interactions amongst multiple brain areas and behavior.

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A ubiquitous spectrolaminar motif of local field potential power across the primate cortex

The mammalian cerebral cortex is anatomically organized into a six-layer motif. It is currently unknown whether a corresponding laminar motif of neuronal activity exists across the cortex. Here, we report such a motif in the power of local field potentials (LFP). We implanted multicontact laminar probes in five macaque monkeys and recorded activity across layers in 14 cortical areas at various hierarchical processing stages in all cortical lobes. The anatomical laminar locations of recordings were histologically identified via electrolytic lesions. In all areas, we found a common spectrolaminar pattern characterized by an increasing deep-to-superficial layer gradient of gamma frequency LFP power peaking in layers 2/3, and an increasing superficial-to-deep gradient of alpha-beta power peaking in layers 5/6. Our results show an electrophysiological dissociation between superficial and deep layers that is preserved across the cortex, suggesting a ubiquitous layer and frequency-based mechanism for cortical computation.

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Selective V1-to-V4 communication of attended stimuli mediated by attentional effects in V1

Selective attention implements preferential routing of attended stimuli, likely through increasing the influence of the respective synaptic inputs on higher-area neurons. As the inputs of competing stimuli converge onto postsynaptic neurons, presynaptic circuits might offer the best target for attentional top-down influences. If those influences enabled presynaptic circuits to selectively entrain postsynaptic neurons, this might explain selective routing. Indeed, when two visual stimuli induce two gamma rhythms in V1, only the gamma induced by the attended stimulus entrains gamma in V4. Here, we modeled induced responses with a Dynamic Causal Model for Cross-Spectral Densities and found that selective entrainment can be explained by attentional modulation of intrinsic V1 connections. Specifically, local inhibition was decreased in the granular input layer and increased in the supragranular output layer of the V1 circuit that processed the attended stimulus. Thus, presynaptic attentional influences and ensuing entrainment were sufficient to mediate selective routing. HIGHLIGHTSO_LIWe model selective visual attention in macaques using Dynamic Causal Modeling. C_LIO_LIIntrinsic V1 modulation can explain attention effects in V1-V4 communication. C_LIO_LIModulation of superficial and granular inhibition is key to induce the effects. C_LIO_LIThose modulations increase V1-V4 communication in a feedforward manner. C_LI GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=97 SRC="FIGDIR/small/484223v2_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1cc79a7org.highwire.dtl.DTLVardef@146e6bdorg.highwire.dtl.DTLVardef@1d6bd6borg.highwire.dtl.DTLVardef@12dd663_HPS_FORMAT_FIGEXP M_FIG C_FIG

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The role of anatomical connection strength for interareal communication in macaque cortex

What is the relationship between anatomical connection strength and rhythmic synchronization? Simultaneous recordings of 15 cortical areas in two macaque monkeys show that interareal networks are functionally organized in spatially distinct modules with specific synchronization frequencies, i.e. frequency-specific functional connectomes. We relate the functional interactions between 91 area pairs to their anatomical connection strength defined in a separate cohort of twenty six subjects. This reveals that anatomical connection strength predicts rhythmic synchronization and vice-versa, in a manner that is specific for frequency bands and for the feedforward versus feedback direction, even if interareal distances are taken into account. These results further our understanding of structure-function relationships in large-scale networks covering different modality-specific brain regions and provide strong constraints on mechanistic models of brain function. Because this approach can be adapted to non-invasive techniques, it promises to open new perspectives on the functional organization of the human brain.

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Neural effects of propofol-induced unconsciousness and its reversal using thalamic stimulation

The specific circuit mechanisms through which anesthetics induce unconsciousness have not been completely characterized. We recorded neural activity from the frontal, parietal, and temporal cortices and thalamus while maintaining unconsciousness in non-human primates (NHPs) with the anesthetic propofol. Unconsciousness was marked by slow frequency (~1 Hz) oscillations in local field potentials, entrainment of local spiking to Up states alternating with Down states of little spiking, and decreased coherence in frequencies above 4 Hz. Thalamic stimulation "awakened" anesthetized NHPs and reversed the electrophysiologic features of unconsciousness. Unconsciousness is linked to cortical and thalamic slow frequency synchrony coupled with decreased spiking, and loss of higher-frequency dynamics. This may disrupt cortical communication/integration.

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