Somatosensory Cortex Research Articles

Endogenous opioid receptor system mediates costly altruism in the human brain

Functional neuroimaging studies suggest that a large-scale brain network transforms others’ pain into its vicarious representation in the observer, potentially modulating helping behavior. However, the neuromolecular basis of individual differences in vicarious pain and helping is poorly understood. We investigated the role of the endogenous μ-opioid receptor (MOR) system in altruistic costly helping. MOR density was measured using [11C]carfentanil. In a separate fMRI experiment, participants could donate money to reduce a confederate’s pain from electric shocks. Participants were generally willing to help, and brain activity was observed in amygdala, anterior insula, anterior cingulate cortex (ACC), striatum, primary motor cortex, primary somatosensory cortex and thalamus when witnessing others’ pain. Haemodynamic responses were negatively associated with MOR availability in emotion circuits. However, MOR availability positively associated with the ACC and hippocampus during helping. These findings suggest that the endogenous MOR system modulates altruism in the human brain.

Comparison of Subdural and Intracortical Recordings of Somatosensory Evoked Responses

Micro-electrocorticography (µECoG) electrodes have emerged to balance the trade-off between invasiveness and signal quality in brain recordings. However, its large-scale applicability is still hindered by a lack of comparative studies assessing the relationship between ECoG and traditional recording methods such as penetrating electrodes. This study aimed to compare somatosensory evoked potentials (SEPs) through the lenses of a µECoG and an intracortical microelectrode array (MEA). The electrodes were implanted in the pig’s primary somatosensory cortex, while SEPs were generated by applying electrical stimulation to the ulnar nerve. The SEP amplitude, signal-to-noise ratio (SNR), power spectral density (PSD), and correlation structure were analysed. Overall, SEPs resulting from MEA recordings had higher amplitudes and contained significantly more spectral power, especially at higher frequencies. However, the SNRs were similar between the interfaces. These results demonstrate the feasibility of using µECoG to decode SEPs with wide-range applications in physiology monitoring and brain–computer interfaces.

Dendritic spines of layer 5 pyramidal neurons of the aging somatosensory cortex exhibit reduced volumetric remodeling.

Impairments in synaptic dynamics and stability are observed both in neurodegenerative disorders and in the healthy aging cortex, which exhibits elevated dendritic spine turnover and decreased long-term stability of excitatory connections at baseline, as well as an altered response to plasticity induction. In addition to the discrete gain and loss of synapses, spines also change in size and strength both during learning and in the absence of neural activity, and synaptic volume has been associated with stability and incorporation into memory traces. Furthermore, intrinsic dynamics, an apparently stochastic component of spine volume changes, may serve as a homeostatic mechanism to prevent stabilization of superfluous connections. However, the effects of age on modulation of synaptic weights remain unknown. Using two-photon excitation (2PE) microscopy of spines during chemical plasticity induction in vitro and analyzing longitudinal in vivo 2PE images after a plasticity-inducing manipulation, we characterize the effects of age on volumetric changes of spines of the apical tuft of layer 5 pyramidal neurons of mouse primary somatosensory cortex. Aged mice exhibit decreased volumetric volatility and delayed rearrangement of synaptic weights of persistent connections, as well as greater susceptibility to spine shrinkage in response to chemical long-term depression. These results suggest a deficit in the aging brain's ability to fine-tune synaptic weights to properly incorporate and retain novel memories. This research provides the first evidence of alterations in spine volumetric dynamics in healthy aging and may support a model of impaired processing and learning in the aged somatosensory system.Significance Statement Aging is known to impact cognitive functions and sensory processing, yet the underlying mechanisms at the synaptic level remain unclear. This study investigates dendritic spine dynamics of layer 5 pyramidal neurons in the aging somatosensory cortex. By employing two-photon excitation microscopy and analyzing spine volume changes during plasticity induction, we reveal that aged mice exhibit decreased volumetric volatility and delayed synaptic weight rearrangement. These alterations may impair the brain's ability to fine-tune synaptic weights, which is crucial for incorporating and retaining new memories. This research provides the first evidence of altered spine volumetric dynamics in healthy aging, suggesting a potential mechanism for impaired processing and learning in the aged cortex. Understanding these changes could aid in mitigation of age-related cognitive decline.

Latent dynamics of primary sensory cortical population activity structured by fluctuations in the local field potential

IntroductionAs emerging technologies enable measurement of precise details of the activity within microcircuits at ever-increasing scales, there is a growing need to identify the salient features and patterns within the neural populations that represent physiologically and behaviorally relevant aspects of the network. Accumulating evidence from recordings of large neural populations suggests that neural population activity frequently exhibits relatively low-dimensional structure, with a small number of variables explaining a substantial fraction of the structure of the activity. While such structure has been observed across the brain, it is not known how reduced-dimension representations of neural population activity relate to classical metrics of “brain state,” typically described in terms of fluctuations in the local field potential (LFP), single-cell activity, and behavioral metrics.MethodsHidden state models were fit to spontaneous spiking activity of populations of neurons, recorded in the whisker area of primary somatosensory cortex of awake mice. Classic measures of cortical state in S1, including the LFP and whisking activity, were compared to the dynamics of states inferred from spiking activity.ResultsA hidden Markov model fit the population spiking data well with a relatively small number of states, and putative inhibitory neurons played an outsize role in determining the latent state dynamics. Spiking states inferred from the model were more informative of the cortical state than a direct readout of the spiking activity of single neurons or of the population. Further, the spiking states predicted both the trial-by-trial variability in sensory responses and one aspect of behavior, whisking activity.DiscussionOur results show how classical measurements of brain state relate to neural population spiking dynamics at the scale of the microcircuit and provide an approach for quantitative mapping of brain state dynamics across brain areas.

Paclitaxel alters the microvascular network in the central and peripheral nervous system of rats with chemotherapy-induced painful peripheral neuropathy.

Chemotherapy-induced peripheral neurotoxicity (CIPN), with paraesthesia, numbness, dysesthesia and neuropathic pain ranks among the most common dose-limiting toxicity of several widely used anticancer drugs. Recent studies revealed the microvascular angiogenesis as a new important actor, beside peripheral neurons, in the neurotoxicity and neuropathic pain development and chronicisation. The aim of this work is to elucidate the role of vascular alterations in CIPN. We evaluated the severity of CIPN with neurophysiological, behavioural and neuropathological analysis together with the microvascular network in central and peripheral nervous systems of rats in order to correlate the features of the CIPN and the vascular abnormalities. The vascular network was quantitatively evaluated through synchrotron radiation-based X-ray phase-contrast micro-tomography imaging, measuring four specific parameters: vascular density, vessel diameter, vessel tortuosity and branching. Rats exposed to paclitaxel and affected by a severe painful sensory axonopathy showed an increased vascular density (putative sprouting angiogenesis) in the crucial districts of the central (somatosensory cortex and lumbar spinal cord) and peripheral nervous system (lumbar dorsal root ganglia). In addition, the complexity of the vascular network and the size of neo-formed vessels were significantly decreased in specific regions. On the other hand, less significant changes were observed in rats exposed to cisplatin, affected by a painless peripheral neuropathy, suggesting a specific involvement of neo-angiogenesis in the development of severe neurotoxicity and neuropathic pain. These new ground-breaking results can shed light on new pathogenetic mechanisms and potential novel therapeutic approaches for painful-CIPN.

High-resolution transcranial optical imaging of in vivo neural activity

Rapid sub-nanometer neuronal deformations have been shown to occur as a consequence of action potentials in vitro, allowing for optical registration of discrete axonal and synaptic depolarizations. Such optically-measured deformations are a novel signature for recording neural activity. We demonstrate this signature can be extended to in vivo measurements through recording of rapid neuronal deformations on the population level with holographic, optical phase-based recordings. Our system demonstrates, for the first time, non-invasive recordings of in vivo tissue deformation associated with population level neuronal activity, including through-skull. We confirmed this technique across a range of neural activation models, including direct epidural focal electrical stimulation, anesthetic-induced cortical deactivation, activation of primary somatosensory cortex via whisker barrel stimulation, and pharmacologically-induced seizures. Collectively, we show holographic imaging provides a pathway for high-resolution, label-free, non-invasive recording of transcranial in vivo neural activity at depth, making it highly advantageous for studying neural function and signaling.

Transient CSF1R inhibition ameliorates behavioral deficits in Cntnap2 knockout and valproic acid-exposed mouse models of autism

Microglial abnormality and heterogeneity are observed in autism spectrum disorder (ASD) patients and animal models of ASD. Microglial depletion by colony stimulating factor 1-receptor (CSF1R) inhibition has been proved to improve autism-like behaviors in maternal immune activation mouse offspring. However, it is unclear whether CSF1R inhibition has extensive effectiveness and pharmacological heterogeneity in treating autism models caused by genetic and environmental risk factors. Here, we report pharmacological functions and cellular mechanisms of PLX5622, a small-molecule CSF1R inhibitor, in treating Cntnap2 knockout and valproic acid (VPA)-exposed autism model mice. For the Cntnap2 knockout mice, PLX5622 can improve their social ability and reciprocal social behavior, slow down their hyperactivity in open field and repetitive grooming behavior, and enhance their nesting ability. For the VPA model mice, PLX5622 can enhance their social ability and social novelty, and alleviate their anxiety behavior, repetitive and stereotyped autism-like behaviors such as grooming and marble burying. At the cellular level, PLX5622 restores the morphology and/or number of microglia in the somatosensory cortex, striatum, and hippocampal CA1 regions of the two models. Specially, PLX5622 corrects neurophysiological abnormalities in the striatum of the Cntnap2 knockout mice, and in the somatosensory cortex, striatum, and hippocampal CA1 regions of the VPA model mice. Incidentally, microglial dynamic changes in the VPA model mice are also reported. Our study demonstrates that microglial depletion and repopulation by transient CSF1R inhibition is effective, and however, has differential pharmacological functions and cellular mechanisms in rescuing behavioral deficits in the two autism models.

Developmental spike timing-dependent long-term depression requires astrocyte D-serine at L2/3-L2/3 synapses of the mouse somatosensory cortex.

Spike timing-dependent plasticity (STDP) is a learning rule important for synaptic refinement and for learning and memory during development. While different forms of presynaptic t-LTD have been deeply investigated, little is known about the mechanisms of somatosensory cortex postsynaptic t-LTD. In the present work, we investigated the requirements and mechanisms for induction of developmental spike timing-dependent long-term depression (t-LTD) at L2/3-L2/3 synapses in the juvenile mouse somatosensory cortex. We found that P13-21 mice of either sex show t-LTD at L2/3-L2/3 synapses induced by pairing single presynaptic activity with single postsynaptic action potentials at low stimulation frequency (0.2 Hz) is expressed postsynaptically, and requires the activation of ionotropic postsynaptic NMDA-type glutamate receptors containing GluN2B subunits. In addition, it requires postsynaptic Ca2+, Ca2+ release from internal stores, calcineurin, postsynaptic endocannabinoid (eCB) synthesis, activation of CB1 receptors and astrocytic signalling to release the gliotransmitter d-serine to activate postsynaptic NMDARs to induce t-LTD. These results show direct evidence of the mechanism involved in developmental postsynaptic t-LTD at L2/3-L2/3 synapses, revealing a central role of astrocytes and their release of D-serine in its induction.Significance statement We show here the mechanisms and role of astrocytes and gliotransmitters in a postsynaptic spike timing dependent long-term depression (t-LTD) form defined at layer (L)2/3-L2/3 synapses of the somatosensory cortex. We have discovered that this form of plasticity involves N-methyl D-aspartate receptors (NMDAR) containing the GluN2B subunit and requires astrocytes and the gliotransmitter D-serine to co-activate (together with glutamate) postsynaptic NMDAR to mediate LTD. This can be a general mechanism in the brain to define different forms of plasticity. Defining the mechanisms of synaptic plasticity may have important implications for brain repair, sensorial recovery, the treatment of neurodevelopmental disorders and even, for educational policy.

Intracortical microstimulation of human somatosensory cortex induces natural perceptual biases

Time-order error, a psychophysical phenomenon in which the duration in between successive stimuli alters perception, has been studied for decades by neuroscientists and psychologists. To date, however, the locus of these effects is unknown. We use intracortical microstimulation of somatosensory cortex in three humans with spinal cord injury as a tool to bypass initial stages of processing and restrict the possible locations that signals could be modified. Using a 2-interval forced choice amplitude discrimination paradigm, we first assessed the extent to which order effects are observed. Comparing trials where the standard stimulus was in the first or second interval, we found that systematic biases are exhibited, typically causing the intensity of the second stimulus to be overestimated The degree of this overestimation for individual electrodes was dependent on the perceptual sensitivity to changes in stimulus amplitude. To investigate the role of memory on this phenomenon, we implemented a 2-interval magnitude estimation task in which participants were instructed to ignore the first stimulus and again found that the perceptual intensity of the second stimulus tended to be enhanced by the first in a manner that depended on the amplitude and duration of the first stimulus. Finally, we repeated both paradigms while varying the inter-stimulus interval to examine the timescale over which these effects occur and found that longer inter-stimulus intervals reduced the effect size. These results show that direct activation of primary somatosensory cortex is sufficient to induce time-order errors.

Processing the fine-grained features of tactile textures involves the primary somatosensory cortex

Abstract Dynamic tactile perception and discrimination of textures require the ability to encode and differentiate complex vibration patterns elicited at the level of the skin when sliding against a surface. Whether the primary somatosensory cortex (S1) can encode the fine-grained spectrotemporal features distinguishing textures remains debated. To address this question, EEG frequency-tagging was used to characterize responses to vibrotactile oddball contrasts between two textures. In a first session designed to identify the topographical distribution of responses originating from the hand and foot representations in S1, standard and deviant stimuli were pure sinusoidal vibrations differing in frequency and intensity. In a second session, standard and deviant stimuli were two different snippets of bandpass-filtered white noise matched in terms of intensity and average frequency content, but differing in terms of their complex spectrotemporal content. Using the S1 functional localizer, we showed that oddball responses to a spectrotemporal contrast follow the somatotopical organization of S1. Our results suggest that the encoding of fine-grained spectrotemporal features associated with different vibration patterns involves S1.

Pain Catastrophizing and Functional Activation During Occlusion in TMD Patients-An Interventional Study.

In temporomandibular disorder (TMD), the effects of standard interventions such as using an occlusal splint and its impact on pain relief and pain catastrophizing are poorly understood. Earlier work pointed to a crucial role of insula activation with changes in pain relief by occlusal splint treatment. We performed a functional imaging study using specially developed splint systems to allow for a placebo-controlled longitudinal design. Using functional MRI we examined 20 TMD patients during repetitive occlusal movements at baseline and over the course of splint therapy and also collected self-reported pain catastrophizing. For balancing performance between baseline and after intervention we used occlusion force measures in an individualized fMRI-splint system. Splint therapy lasted for approximately 7 weeks with one group selected by randomization wearing a palatine placebo splint over the first 3 weeks (delayed start; 11 individuals). As expected, fMRI activation in areas involved in pain processing (insula, primary and secondary somatosensory cortex) decreased with intervention. At baseline a positive correlation between activation of the left anterior insula and pain catastrophizing was present. Both parameters decreased over intervention while associations were primarily observable for patients with rather mild TMD.

Somatosensory migraine auras evoked by bihemispheric cortical spreading depression events in human parietal cortex.

Cortical spreading depression (CSD) is associated with pronounced alterations in cerebral blood flow. These alterations can be captured using high-field functional magnetic resonance imaging (fMRI). While compelling clinical and experimental data suggest that CSD is involved in the pathogenesis of migraine aura, the mechanistic intricacies remain poorly understood. Here, we use visual stimulus-induced blood oxygen level-dependent (BOLD) fMRI responses to characterize spatiotemporal alterations in cerebral blood flow during spontaneous attacks with migraine aura. Six adult participants diagnosed with migraine with aura underwent BOLD fMRI scans with a visual stimulation paradigm, consisting of flickering checkerboard stimulation. Our results revealed that auras with somatosensory symptoms corresponded with bilateral alterations of stimulus-induced BOLD responses in the somatosensory cortex, exhibiting anterior-to-posterior propagation and absence of antecedent occipital abnormalities. These altered stimulus-induced BOLD responses were bilateral, despite a unilateral manifestation of aura symptoms, and had no relationship with positive or negative aura symptoms. The bilateral abnormalities in stimulus-induced BOLD responses completes our current knowledge on migraine aura.

Integration of distinct cortical inputs to primary and higher order inhibitory cells of the thalamus.

The necortex regulates its own sensory input in part through top-down inhibitory mechanisms. Descending corticothalamic projections drive GABAergic neurons of the thalamic reticular nucleus (TRN), which then control thalamocortical cells via inhibition. Neurons in sensory TRN are organized into primary and higher order (HO) subpopulations, with separate intrathalamic connections and distinct genetic and functional properties. Here, we investigated top-down neocortical control over primary and HO neurons of somatosensory TRN. Projections from layer 6 of somatosensory cortex evoked stronger and more state-dependent activity in primary than in HO TRN, driven by more robust synaptic inputs and potent T-type calcium currents. However, HO TRN received additional, physiologically distinct, inputs from layer 5 of S1 and motor cortex. Thus, in a departure from the canonical focused sensory layer 6 innervation characteristic of primary TRN, HO TRN integrates broadly from multiple corticothalamic systems, with unique state-dependence, extending the range of mechanisms for top-down control.

Cell class-specific long-range axonal projections of neurons in mouse whisker-related somatosensory cortices.

Long-range axonal projections of diverse classes of neocortical excitatory neurons likely contribute to brain-wide interactions processing sensory, cognitive and motor signals. Here, we performed light-sheet imaging of fluorescently labeled axons from genetically defined neurons located in posterior primary somatosensory barrel cortex and supplemental somatosensory cortex. We used convolutional networks to segment axon-containing voxels and quantified their distribution within the Allen Mouse Brain Atlas Common Coordinate Framework. Axonal density was analyzed for different classes of glutamatergic neurons using transgenic mouse lines selectively expressing Cre recombinase in layer 2/3 intratelencephalic projection neurons (Rasgrf2-dCre), layer 4 intratelencephalic projection neurons (Scnn1a-Cre), layer 5 intratelencephalic projection neurons (Tlx3-Cre), layer 5 pyramidal tract projection neurons (Sim1-Cre), layer 5 projection neurons (Rbp4-Cre), and layer 6 corticothalamic neurons (Ntsr1-Cre). We found distinct axonal projections from the different neuronal classes to many downstream brain areas, which were largely similar for primary and supplementary somatosensory cortices. Functional connectivity maps obtained from optogenetic activation of sensory cortex and wide-field imaging revealed topographically organized evoked activity in frontal cortex with neurons located more laterally in somatosensory cortex signaling to more anteriorly located regions in motor cortex, consistent with the anatomical projections. The current methodology therefore appears to quantify brain-wide axonal innervation patterns supporting brain-wide signaling.

Cell class-specific long-range axonal projections of neurons in mouse whisker-related somatosensory cortices

Long-range axonal projections of diverse classes of neocortical excitatory neurons likely contribute to brain-wide interactions processing sensory, cognitive and motor signals. Here, we performed light-sheet imaging of fluorescently labeled axons from genetically defined neurons located in posterior primary somatosensory barrel cortex and supplemental somatosensory cortex. We used convolutional networks to segment axon-containing voxels and quantified their distribution within the Allen Mouse Brain Atlas Common Coordinate Framework. Axonal density was analyzed for different classes of glutamatergic neurons using transgenic mouse lines selectively expressing Cre recombinase in layer 2/3 intratelencephalic projection neurons (Rasgrf2-dCre), layer 4 intratelencephalic projection neurons (Scnn1a-Cre), layer 5 intratelencephalic projection neurons (Tlx3-Cre), layer 5 pyramidal tract projection neurons (Sim1-Cre), layer 5 projection neurons (Rbp4-Cre), and layer 6 corticothalamic neurons (Ntsr1-Cre). We found distinct axonal projections from the different neuronal classes to many downstream brain areas, which were largely similar for primary and supplementary somatosensory cortices. Functional connectivity maps obtained from optogenetic activation of sensory cortex and wide-field imaging revealed topographically organized evoked activity in frontal cortex with neurons located more laterally in somatosensory cortex signaling to more anteriorly located regions in motor cortex, consistent with the anatomical projections. The current methodology therefore appears to quantify brain-wide axonal innervation patterns supporting brain-wide signaling.

Somatosensory temporal discrimination analysis reveals impaired processing in amyotrophic lateral sclerosis.

While amyotrophic lateral sclerosis (ALS) is primarily characterized as a motor system disorder, there is a growing body of evidence indicating sensory involvement. This study aimed to examine the hypothesis that somatosensory processing is impaired in ALS. Study participants were ALS patients followed at the Neuromuscular Outpatient Unit, as well as healthy volunteers, from March 2021 to July 2023. The Medical Research Council (MRC) sum score was calculated for nine muscle groups bilaterally. The clinical status of patients was evaluated with the ALS Functional Rating Scale-Revised (ALSFRS-R) and the Penn Upper Motor Neuron core. Somatosensory temporal discrimination thresholds (STDTs) were recorded on the medial and lateral parts of both hands. Somatosensory cortex excitability was investigated with the paired somatosensory evoked potentials (SEP) paradigm in a subgroup. Increased STD values were detected in ALS patients compared to controls in both medial (107.66 ± 35 ms vs. 82.7 ± 32.5 ms, p = .001) and lateral (106.5 ± 34.5 ms vs. 82.9 ± 31.3 ms, p = .002) hands. There were no significant differences in STDTs among ALS patients across four regions (medial and lateral parts of the right and left hands). Amplitude ratios obtained from the paired-pulse SEP paradigm were approximately 1 for all interstimulus intervals (ISIs). STDTs did not show any correlations with motor findings or scales. Somatosensory processing appears to be compromised among ALS patients. The lack of correlation between impaired STDT and motor findings implies that it is a purely sensory deficit in ALS.

Imaging the large-scale and cellular response to focal traumatic brain injury in mouse neocortex.

Traumatic brain injury (TBI) affects neural function at the local injury site and also at distant, connected brain areas. However, the real-time neural dynamics in response to injury and subsequent effects on sensory processing and behavior are not fully resolved, especially across a range of spatial scales. We used in vivo calcium imaging in awake, head-restrained male and female mice to measure large-scale and cellular resolution neuronal activation, respectively, in response to a mild/moderate TBI induced by focal controlled cortical impact (CCI) injury of the motor cortex (M1). Widefield imaging revealed an immediate CCI-induced activation at the injury site, followed by a massive slow wave of calcium signal activation that traveled across the majority of the dorsal cortex within approximately 30 s. Correspondingly, two-photon calcium imaging in primary somatosensory cortex (S1) found strong activation of neuropil and neuronal populations during the CCI-induced traveling wave. A depression of calcium signals followed the wave, during which we observed atypical activity of a sparse population of S1 neurons. Longitudinal imaging in the hours and days after CCI revealed increases in the area of whisker-evoked sensory maps at early time points, in parallel to decreases in cortical functional connectivity and behavioral measures. Neural and behavioral changes mostly recovered over hours to days in our M1-TBI model, with a more lasting decrease in the number of active S1 neurons. Our results in unanesthetized mice describe novel spatial and temporal neural adaptations that occur at cortical sites remote to a focal brain injury.

Mental rotation-related neural interactions between gender and cognitive strategy

Abstract A long-standing history of research has focused on the differences between men and women in cognitive tasks, including that men would be more accurate and faster than women in mental rotation (MR). This advantage suggests that men would use an object-based cognitive strategy (OBS) to perform MR, whereas women would rely more on an effector-based cognitive strategy (EBS). To test this hypothesis, participants in the present study performed MR using OBS and EBS (plus a control condition) while their brain activity was recorded using fMRI. As sex hormones have often been reported to influence spatial ability, we also assessed the relationship between MR and testosterone levels and digit ratio. Behavioral results showed that (1) men performed faster MR than women in the OBS and control conditions, (2) men were more accurate than women in the OBS condition, and (3) women performed better in OBS than the other two conditions. No relationship was found between MR and testosterone or digit ratio. fMRI data showed that women in the OBS condition had greater activation than men in the inferior frontal and somatosensory cortices. Salivary testosterone levels had no effect on whole-brain activity. Combining behavioral and brain imaging data, these findings suggest that the additional somatosensory activation found in women during OBS somehow affects their MR, preventing the use of a purely spatial strategy and promoting the use of body-based sensorimotor processing, which would result in lower accuracy. These results support that gender differences in MR would be better explained by considering their relationship with the cognitive strategies used to perform MR.

Functional Roles of Sensorimotor Alpha and Beta Oscillations in Overt Speech Production.

Power decreases, or desynchronization, of sensorimotor alpha and beta oscillations (i.e., alpha and beta ERD) have long been considered as indices of sensorimotor control in overt speech production. However, their specific functional roles are not well understood. Hence, we first conducted a systematic review to investigate how these two oscillations are modulated by speech motor tasks in typically fluent speakers (TFS) and in persons who stutter (PWS). Eleven EEG/MEG papers with source localization were included in our systematic review. The results revealed consistent alpha and beta ERD in the sensorimotor cortex of TFS and PWS. Furthermore, the results suggested that sensorimotor alpha and beta ERD may be functionally dissociable, with alpha related to (somato-)sensory feedback processing during articulation and beta related to motor processes throughout planning and articulation. To (partly) test this hypothesis of a potential functional dissociation between alpha and beta ERD, we then analyzed existing intracranial electroencephalography (iEEG) data from the primary somatosensory cortex (S1) of picture naming. We found moderate evidence for alpha, but not beta, ERD's sensitivity to speech movements in S1, lending supporting evidence for the functional dissociation hypothesis identified by the systematic review.

Layer-specific BOLD effects in gradient and spin-echo acquisitions in somatosensory cortex.

Previous studies have shown varied BOLD signals with gradient echo (GE) across cortical depth. To interpret these variations, and understand the effects of vascular geometry and size, the magnitudes and layer distributions of GE and spin-echo (SE) BOLD functional MRI signals were compared in the somatosensory cortex of squirrel monkeys during tactile stimulation and in a resting state at high spatial resolution and high field. A block-design stimulation was used to identify tactile-evoked activation signals in somatosensory Areas 3b and 1. Layer-specific connectivities were calculated using resting-state data. Signal power spectra were compared by depth and pulse sequence. The measured ratios of transverse relaxation rate changes were compared with Anderson and Weiss's model. SE signals showed a 26% lower percentage signal change during tactile stimulation compared with GE, along with a slower time course. SE signals remained consistent but weaker in lower layers, whereas GE signals decreased with cortical depth. This pattern extended to resting-state power spectra. Resting-state functional connectivity indicated larger connectivity between the top layers of Area 3b and Area 1 for GE, with minimal changes for SE. Comparisons with theory suggest vessel diameters ranging from 19.4 to 9 microns are responsible for BOLD effects across cortical layers at 9.4 T. These results provide further evidence that at high field, SE BOLD signals are relatively free of contributions from sources other than microvascular changes in response to neural activity, whereas GE signals, even in the superficial layers, are not dominated by very large vessels.