468 research outputs found

    Different activation signatures in the primary sensorimotor and higher-level regions for haptic three-dimensional curved surface exploration

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    Haptic object perception begins with continuous exploratory contact, and the human brain needs to accumulate sensory information continuously over time. However, it is still unclear how the primary sensorimotor cortex (PSC) interacts with these higher-level regions during haptic exploration over time. This functional magnetic resonance imaging (fMRI) study investigates time-dependent haptic object processing by examining brain activity during haptic 3D curve and roughness estimations. For this experiment, we designed sixteen haptic stimuli (4 kinds of curves x 4 varieties of roughness) for the haptic curve and roughness estimation tasks. Twenty participants were asked to move their right index and middle fingers along the surface twice and to estimate one of the two features -roughness or curvature -depending on the task instruction. We found that the brain activity in several higher-level regions (e.g., the bilateral posterior parietal cortex) linearly increased as the number of curves increased during the haptic exploration phase. Surprisingly, we found that the contralateral PSC was parametrically modulated by the number of curves only during the late exploration phase but not during the early exploration phase. In contrast, we found no similar parametric modulation activity patterns during the haptic roughness estimation task in either the contralateral PSC or in higher-level regions. Thus, our findings suggest that haptic 3D object perception is processed across the cortical hierarchy, whereas the contralateral PSC interacts with other higher-level regions across time in a manner that is dependent upon the features of the object

    A review of fMRI simulation studies

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    Simulation studies that validate statistical techniques for fMRI data are challenging due to the complexity of the data. Therefore, it is not surprising that no common data generating process is available (i.e. several models can be found to model BOLD activation and noise). Based on a literature search, a database of simulation studies was compiled. The information in this database was analysed and critically evaluated focusing on the parameters in the simulation design, the adopted model to generate fMRI data, and on how the simulation studies are reported. Our literature analysis demonstrates that many fMRI simulation studies do not report a thorough experimental design and almost consistently ignore crucial knowledge on how fMRI data are acquired. Advice is provided on how the quality of fMRI simulation studies can be improved

    Layer-specific activation of sensory input and predictive feedback in the human primary somatosensory cortex

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    When humans perceive a sensation, their brains integrate inputs from sensory receptors and process them based on their expectations. The mechanisms of this predictive coding in the human somatosensory system are not fully understood. We fill a basic gap in our understanding of the predictive processing of somatosensation by examining the layer-specific activity in sensory input and predictive feedback in the human primary somatosensory cortex (S1). We acquired submillimeter functional magnetic resonance imaging data at 7T (n = 10) during a task of perceived, predictable, and unpredictable touching sequences. We demonstrate that the sensory input from thalamic projects preferentially activates the middle layer, while the superficial and deep layers in S1 are more engaged for cortico-cortical predictive feedback input. These findings are pivotal to understanding the mechanisms of tactile prediction processing in the human somatosensory cortex

    Hemodynamic-informed parcellation of fMRI data in a Joint Detection Estimation framework

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    International audienceIdentifying brain hemodynamics in event-related functional MRI (fMRI) data is a crucial issue to disentangle the vascular response from the neuronal activity in the BOLD signal. This question is usually addressed by estimating the so-called Hemodynamic Response Function (HRF). Voxelwise or region-/parcelwise inference schemes have been proposed to achieve this goal but so far all known contributions commit to pre-specified spatial supports for the hemodynamic territories by defining these supports either as individual voxels or a priori fixed brain parcels. In this paper, we introduce a Joint Parcellation-Detection-Estimation (JPDE) procedure that incorporates an adaptive parcel identification step based upon local hemodynamic properties. Efficient inference of both evoked activity, HRF shapes and supports is then achieved using variational approximations. Validation on synthetic and real fMRI data demonstrate the JPDE performance over standard detection estimation schemes and suggest it as a new brain exploration tool

    Glycine receptor in rat hippocampal and spinal cord neurons as a molecular target for rapid actions of 17-β-estradiol

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    Glycine receptors (GlyRs) play important roles in regulating hippocampal neural network activity and spinal nociception. Here we show that, in cultured rat hippocampal (HIP) and spinal dorsal horn (SDH) neurons, 17-β-estradiol (E2) rapidly and reversibly reduced the peak amplitude of whole-cell glycine-activated currents (IGly). In outside-out membrane patches from HIP neurons devoid of nuclei, E2 similarly inhibited IGly, suggesting a non-genomic characteristic. Moreover, the E2 effect on IGly persisted in the presence of the calcium chelator BAPTA, the protein kinase inhibitor staurosporine, the classical ER (i.e. ERα and ERβ) antagonist tamoxifen, or the G-protein modulators, favoring a direct action of E2 on GlyRs. In HEK293 cells expressing various combinations of GlyR subunits, E2 only affected the IGly in cells expressing α2, α2β or α3β subunits, suggesting that either α2-containing or α3β-GlyRs mediate the E2 effect observed in neurons. Furthermore, E2 inhibited the GlyR-mediated tonic current in pyramidal neurons of HIP CA1 region, where abundant GlyR α2 subunit is expressed. We suggest that the neuronal GlyR is a novel molecular target of E2 which directly inhibits the function of GlyRs in the HIP and SDH regions. This finding may shed new light on premenstrual dysphoric disorder and the gender differences in pain sensation at the CNS level

    Attention-dependent modulation of cortical taste circuits revealed by granger causality with signal-dependent noise

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    We show, for the first time, that in cortical areas, for example the insular, orbitofrontal, and lateral prefrontal cortex, there is signal-dependent noise in the fMRI blood-oxygen level dependent (BOLD) time series, with the variance of the noise increasing approximately linearly with the square of the signal. Classical Granger causal models are based on autoregressive models with time invariant covariance structure, and thus do not take this signal-dependent noise into account. To address this limitation, here we describe a Granger causal model with signal-dependent noise, and a novel, likelihood ratio test for causal inferences. We apply this approach to the data from an fMRI study to investigate the source of the top-down attentional control of taste intensity and taste pleasantness processing. The Granger causality with signal-dependent noise analysis reveals effects not identified by classical Granger causal analysis. In particular, there is a top-down effect from the posterior lateral prefrontal cortex to the insular taste cortex during attention to intensity but not to pleasantness, and there is a top-down effect from the anterior and posterior lateral prefrontal cortex to the orbitofrontal cortex during attention to pleasantness but not to intensity. In addition, there is stronger forward effective connectivity from the insular taste cortex to the orbitofrontal cortex during attention to pleasantness than during attention to intensity. These findings indicate the importance of explicitly modeling signal-dependent noise in functional neuroimaging, and reveal some of the processes involved in a biased activation theory of selective attention
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