Neuroscience
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Studies using the flanker task have reported that response conflict is detected by the medial frontal cortex (MFC). As a conflict alert system, the MFC shows enhanced functional communication with task-related regions. Previous studies have revealed individual differences in functional connectivity during cognitive task performance. ⋯ However, these findings were only found in the right hemisphere, which may be related to the asymmetrical role of the bilateral PPC in response conflict processing. Furthermore, hierarchical regression analyses revealed that 44% of individual variability in FCz-P4 conflict-induced theta phase synchronization could be explained by variations in axial diffusivity (AD) in the genu of the corpus callosum (gCC). These results demonstrated that structural integrity in the gCC predicts conflict-induced functional connectivity between the MFC and right PPC.
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The aim of this study is to investigate the effect of ketogenic metabolism, induced by different diet interventions, on histone acetylation and its potential antioxidant capacity to injured spinal cord tissue in rats. 72 male Sprague-Dawley rats were randomly divided into 4 groups, fed with ketogenic diet (KD), every other day fasting (EODF), every other day ketogenic diet (EODKD) and standard diet (SD) respectively for 2 weeks. β-Hydroxybutyrate (βOHB) concentration was measured both in serum and cerebrospinal fluid (CSF). C5 spinal cord tissue was harvested before, at 3 h and 24 h after injury for analysis of HDAC activity, histone acetylation and oxidative makers. All three dietary interventions resulted in a significant increase of βOHB level in both serum and CSF, and inhibited HDAC activity by 31-43% in spinal cord. ⋯ Anti-oxidative stress genes Foxo3a and Mt2 and related proteins, such as mitochondrial superoxide dismutase (SOD), FOXO3a, catalase were increased in dietary intervention groups. After SCI, high ketogenic metabolism demonstrated significant reduction of the expression of lipid peroxidation factors malondialdehyde (MDA), and this might contribute to the reported neuroprotection of the spinal cord from oxidative damage possibly mediated by increasing SOD. The result of this study suggested that by inhibiting HDAC activity and modifying related gene transcription, ketogenic metabolism, induced by KD, EODF or EODKD, might reduce oxidative damage in the spinal cord tissue after acute injury.
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According to the theories of neural plasticity and neural efficiency, professional skill training improves performance by strengthening the underlying neural mechanisms. Therefore, subjects trained professionally may exhibit changes in resting-state neurophysiological characteristics closely related to performance. ⋯ There was also a significant linear correlation between the characteristic path length of the resting-state theta band brain network and shooting performance (r = 0.56, P < 0.0005). This study identifies potential neural mechanisms underlying successful shooting and a new method for predicting and evaluating performance based on EEG characteristics.
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Neuroglobin (Ngb) is a member of the globin family of respiratory proteins, which was recently observed in many neurons of the auditory pathways. Up to now, however, nothing was known about the role of Ngb in hearing processes. We therefore studied auditory function by recording distortion-product otoacoustic emissions (DPOAE) and auditory brainstem responses (ABRs) in wild-type (C57BL/6N) and Ngb-knockout mice. ⋯ While ABR amplitudes were similar in both groups before noise overexposure, four weeks after trauma a moderate but statistically significant decrease of the latest peak-to-peak response amplitude (originating in the inferior colliculus) was observed in KO mice. Our results suggest that the lack of Ngb, at least in the model used in the present study, results in only marginal deficits in hearing ability. A putative functional role of Ngb in the efferent system warrants further studies.
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Oxytocin (OT) administration in the ventromedial hypothalamic nucleus (VMH) reduces chow intake. The nature of VMH OT's anorexigenic action remains unclear. Here we provide insight into neural mechanisms underlying VMH OT-driven anorexia by (a) identifying feeding-related brain sites activated by VMH OT injection; (b) measuring VMH OT receptor (OTr) mRNA changes in response to hunger and palatability; and (c) examining how VMH OT affects episodic sweet solution intake in sated and hungry rats. ⋯ OT acting in the VMH decreases intake driven by energy not by palatability, and it stimulates activity of hypothalamic sites controlling energy balance.