Neuroscience
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Individuals with pain report higher sensory disturbances during sensorimotor conflicts compared to pain-free individuals. In the pain field, it is frequently assumed that disturbances arise from a discordance between sensory and efference copies (defined as sensory-motor conflict), while in the sensorimotor control field they are considered to result from the incongruence between sensory modalities (defined as sensory-sensory conflict). The general aim of this study was to disentangle the relative contribution of motor efferences and sensory afferences to the increased sensitivity to sensorimotor conflicts in individual with fibromyalgia (n = 20) compared to controls (n = 20). ⋯ Moreover, the increase in conflict sensitivity from sensory-sensory to sensory-motor conflicts in fibromyalgia was related to conflict-induced motor disturbances (r = 0.57; p < 0.01), but did not result from a poorer proprioception (r = 0.12; p = 0.61). Therefore, it appears that higher conflict sensitivity in fibromyalgia is mainly explained by a sensory-motor conflict rather by a sensory-sensory conflict. We suggest this arises due to a deficit in updating predicted sensory feedback rather than in selecting appropriate motor commands.
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Motor imagery (MI) is the mental simulation of an action without any apparent muscular contraction. By means of transcranial magnetic stimulation (TMS), few studies revealed a decrease of short-interval intracortical inhibition (SICI) within the primary motor cortex. However, this decrease is ambiguous, as one would expect greater inhibition during MI to prevent overt motor output. ⋯ At the lowest CS intensities, a Task main effect revealed that SICI increased during MI (Exp.2). SICI modulation during MI depends critically on the CS intensity. By optimising CS intensity, we have shown that SICI circuits may increase during MI, revealing a potential mechanism to prevent the production of a movement while the motor system is activated.
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Emotion recognition reflects the psychological and physiological status of humans. Numerous studies have investigated the neural mechanisms of emotion recognition based on electroencephalography (EEG) features. In the previous study, emotion target was presented under a static or irregular background, which made the response highly time-locked. ⋯ The degree of alpha entrainment (valued as normalized Shannon entropy), SSVEP amplitude and recognition accuracy were calculated as response features. The results indicated that: SSVEP amplitude and recognition accuracy positively correlated with each other in frequency domain (7-15 Hz); alpha entrainment, and recognition accuracy had similar linear variation in intensity domain (level 1-4), and had a threshold around intensity 3; the three basic emotions had no clear relationship with each other in recognition. This study provided a new sight for neuroscience and would be an important reference to clinical psychology.
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In this study we focused on gene expression and behavioral differences in mice with brain-specific Commd1 knockout. Commd1 is an imprinted gene with preferential maternal expression, residing within a larger genomic region previously found to affect sensorimotor gating. In this study, individuals harboring a conditional Commd1 mutant allele were bred with Syn1-Cre animals, paying special attention to the parent of origin of the Commd1 mutation. ⋯ Interestingly, we found that maternal knockout animals exhibited decreased time swimming and increased time immobile when compared to maternal and paternal wild type, and paternal knockout animals. However, there were no differences in climbing behavior between genotypes. This study demonstrates an in vivo behavioral role for Commd1 for the first time and demonstrates the need for careful interpretation of experimental results involving Cre-based knockout systems.
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Noise-induced hidden hearing loss (NIHHL), one of the family of conditions described as noise-induced hearing loss (NIHL), is characterized by synaptopathy following moderate noise exposure that causes only temporary threshold elevation. Long noncoding RNAs (lncRNAs) mediate several essential regulatory functions in a wide range of biological processes and diseases, but their roles in NIHHL remain largely unknown. In order to determine the potential roles of these lncRNAs in the pathogenesis of NIHHL, we first evaluated their expression in NIHHL mice model and mapped possible regulatory functions and targets using RNA-sequencing (RNA-seq). ⋯ KEGG analysis was also used to identify the potential pathways being affected in NIHHL. These analyses allowed us to identify the guanine nucleotide binding protein alpha stimulating (GNAS) gene as a key transcription factor and the adrenergic signaling pathway as a key pathway in the regulation of NIHHL pathogenesis. Our study is the first, to our knowledge, to isolate a lncRNA mediated regulatory pathway associated with NIHHL pathogenesis; these observations may provide fresh insight into the pathogenesis of NIHHL and may pave the way for therapeutic intervention in the future.