Neuroscience
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Numerous clinical investigations have reported that children with cerebral palsy (CP) have tactile discrimination deficits that likely limit their ability to plan and manipulate objects. Despite this clinical awareness, we still have a substantial knowledge gap in our understanding of the neurological basis for these tactile discrimination deficits. Previously, we have shown that children with CP have aberrant theta-alpha (4-14 Hz) oscillations in the somatosensory cortices following tactile stimulation of the foot. ⋯ This inference is plausible since the participating children with CP had Manual Ability Classification System (MACS) levels between I and II. In contrast to the theta-alpha results, children with CP did exhibit a sharp increase in beta activity during the same time period, which was not observed in TD children. This suggests that children with CP still have deficits in the computational aspect of somatosensory processing.
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Rapid automatized naming (RAN) has been established to be a strong predictor of reading. Yet, the neural correlates underlying the RAN-reading relationship remain unknown. Thus, the purpose of this study was to determine: (a) the extent to which RAN and reading activate similar brain regions (within subjects), (b) whether RAN and reading are directly related in the shared activity network outlined in (a), and (c) to what extent RAN neural activation predicts behavioral reading performance. ⋯ Further, we found a unique relationship between in-scanner reading response time and RAN PSC in the left inferior frontal gyrus. Taken together, these findings support the notion that RAN and reading activate similar neural networks. However, the relationship between RAN and reading is primarily driven by commonalities in the motor-sequencing/articulatory processes.
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The neural substrates of fatigue induced by muscular activity have been addressed in depth in relation to isometric tasks. For these activities, when fatigue develops, it has been noted that the duration of the silent periods (SPs) increases in response to both transcranial magnetic stimulation (TMS) of primary motor cortex or electric cervicomedullary stimulation (CMS). However, fatigue is known to be task-dependent and the mechanisms giving rise to a decrease in motor performance during brief, fast repetitive tasks have been less studied. ⋯ They increased TMS-SPs, but not CMS-SPs. On the other hand, isometric contraction had a clear impact on spinal circuits. The consideration of these differences might help to optimize the study of fatigue in physiological conditions and neurological disorders.
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Two event-related potential (ERP) experiments were conducted to investigate whether Cantonese lexical tones are processed with general auditory perception mechanisms and/or a special speech module. Two tonal features (f0 direction and f0 height deviation) were manipulated to reflect acoustic processing, and the contrast between syllables and hums was used to reveal the involvement of a speech module. Experiment 1 adopted a passive oddball paradigm to study a relatively early stage of tonal processing. ⋯ Moreover, detecting tonal deviants of syllables elicited N1 and P2 that were not found in hum detection. Together, these findings suggest that the processing of lexical tone relies on both acoustic and linguistic processes from the early stage. Another noteworthy finding is the absence of brain lateralization in both experiments, which challenges the use of a lateralization pattern as evidence for processing lexical tones through a special speech module.
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The development of a hyperexcitable neuronal network is thought to be a critical event in epilepsy. Thrombospondins (TSPs) regulate synaptogenesis by binding the neuronal α2δ subunit of the voltage-gated calcium channel. TSPs regulate synapse formation during development and in the mature brain following injury. ⋯ Here we report similar findings, TSP1, and TSP1/2 KO mice have low levels of CACNA2D2 mRNA expression and α2δ-1/2 receptor level in the cortex, and are more susceptible to seizures. CACNA2D2 mutations in mice and humans can cause epilepsy. Our data suggest TSP1 in particular may control CACNA2D2 levels and could be a modifier of seizure susceptibility.