Neuroscience
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Randomized Controlled Trial
The Role of Left Dorsolateral Prefrontal Cortex in Language Processing.
In addition to the role of left frontotemporal areas in language processing, there is increasing evidence that language comprehension and production require cognitive control and working memory resources involving the left dorsolateral prefrontal cortex (DLPFC). The aim of this study was to investigate the role of the left DLPFC in both language comprehension and production. ⋯ However, additional analyses revealed that the polarity of tDCS effects was highly correlated across tasks, implying differential individual susceptibility to the effect of tDCS within participants. Overall, our findings demonstrate that left DLPFC is part of the complex cortical network associated with language processing.
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Simple cells in the cat primary visual cortex usually have elongated receptive fields (RFs), and their orientation selectivity can be largely predicted by their RFs. As to the relay cells in cats' lateral geniculate nucleus (LGN), they also have weak but significant orientation bias (OB). It is thus of interest to investigate the fine spatiotemporal receptive field (STRF) properties in LGN, compare them with the dynamics of orientation tuning, and examine the dynamic relationship between STRF and orientation sensitivity in LGN. ⋯ Furthermore, biased orientation tuning emerged 20-30 ms earlier than those in the primary visual cortex. These data demonstrated that similar to the primary visual cortex, the orientation sensitivity was closely reflected by the RF properties in LGN. However, the elongated RF and OB in LGN did not originate from the primary visual cortex feedback.
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Phospholipase D2 (PLD2), an enzyme involved in vesicle trafficking and membrane signaling, interacts with α-synuclein, a protein known to contribute in the development of Parkinson disease (PD). We previously reported that PLD2 overexpression in rat substantia nigra pars compacta (SNc) causes a rapid neurodegeneration of dopamine neurons, and that α-synuclein suppresses PLD2-induced nigral degeneration (Gorbatyuk et al., 2010). Here, we report that PLD2 toxicity is due to its lipase activity. ⋯ These findings suggest that neither the interaction of PLD2 with dynamin, which has a role in vesicle trafficking, nor the PLD2 interaction with Grb2, which has multiple roles in cell cycle control, chemotaxis and activation of tyrosine kinase complexes, are the primary cause of neurodegeneration. Instead, the synthesis of phosphatidic acid (the product of PLD2), which is a second messenger in multiple cellular pathways, appears to be the key to PLD2 induced neurodegeneration. The fact that α-synuclein is a regulator of PLD2 activity suggests that regulation of PLD2 activity could be important in the progression of PD.
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Maintaining standing balance involves multisensory processing and integration to produce dynamic motor responses. Electrical vestibular stimulation (EVS) delivered over the mastoid processes can be used to explore the vestibular control of balance. The purpose of this study was to determine whether intrinsic foot muscles exhibit vestibular-evoked balance responses and to characterize the traits associated with these responses. ⋯ When vision was occluded, the EVS-EMG and EVS-AP forces coherence function amplitude increased at low frequencies (<2 Hz) and was accompanied by a heightened medium-latency peak amplitude for all muscles as well as the whole-body balance response (AP forces) compared to when static visual cues were present. The enhanced coherence amplitudes at lower frequencies may highlight a mechanism for the increase in postural sway from vision to occluded vision. The current findings indicate that the vestibular control of standing balance can be represented by the intrinsic foot muscles and implicate a postural role for these muscles in modulating quiet standing.
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Epigenetic modulation participates in the mechanism of multiple types of pathological pain, so targeting the involved regulators may be a promising strategy for pain treatment. Our previous research identified the analgesic effect of the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) on mechanical hyperalgesia in a rat model of bone cancer pain (BCP) via restoration of μ-opioid receptor (MOR) expression. However, the specific types of HDACs contributing to BCP have not been explored. ⋯ Notably, HDAC2 knock-down did not restore MOR expression, but it robustly reversed the down-regulation of potassium-chloride cotransporter 2 (KCC2). The impaired KCC2 expression is a vital mechanism of many types of pathological pain. Therefore, our results demonstrated that HDAC2 in spinal cord contributed to the mechanical hyperalgesia in BCP rats, and this effect may be associated with KCC2 modulation.