查看更多>>摘要：study uses simple tasks to induce self-conscious emotions and event-related potentials to investigate the effects of pride, neutral, and shame emotions on cognitive flexibility. The behavior results revealed that the switching tasks had a longer reaction time and a lower accuracy rate than the repetitive tasks. Furthermore, the reaction time was longer, and the accuracy rate was lower for individuals in the shame and pride emotions group than the neutral group. ERP results revealed that the switching task induced a larger P3 wave amplitude than the repetitive task. In addition, the P3 difference wave for pride and shame emotions was significantly smaller than that of neutral emotions. However, there were no significant differences in N2 wave. These findings imply that pride and shame may inhibit conversion ability and consistently affect cognitive flexibility. This consistency may be manifested in late decision-making tasks. Our finds provide a theoretical basis for management of students' pride and shame. (c) 2021 Published by Elsevier Ltd on behalf of IBRO.
Zaback, MartinAdkin, Allan L.Chua, RomeoInglis, J. Timothy...
18页
查看更多>>摘要：to stability elicit context-specific changes in balance control; however, the underlying neural mechanisms are not fully understood. Previous work has speculated that a shift toward greater supraspinal control may contribute to threat-related balance changes. This study investigated how neural correlates of cortical and subcortical control of balance were affected by initial and repeated exposure to a height-related postural threat. Corticomuscular coherence (CMC) between EEG recorded over the sensorimotor cortex and EMG recorded from the soleus (SOL) provided an estimate of cortical control, while intermuscular coherence (IMC) between bilateral SOL provided estimates of both cortical and subcortical control. These outcomes, along with measures of psychological and arousal state and standing balance control, were examined in 28 healthy young adults during a series of 90-s quiet standing trials completed at LOW (0.8 m above ground; away from edge) and HIGH (3.2 m above ground, at edge) threat conditions. Initial exposure to threat significantly increased gamma-band CMC (31-40 Hz) and IMC at frequencies thought to be mediated by cortical (21-40 Hz) and subcortical (5-20 Hz) substrates. Following repeated threat exposure, only estimates of cortical control (gamma CMC and 21-40 Hz IMC) demonstrated significant habituation. Estimates of cortical control changed in parallel with high-frequency centre of pressure power (>0.5 Hz) and plantar-dorsiflexor coactivation, but not other threat related balance changes which did not habituate. These results support the hypothesis that postural threat induces a shift toward more supraspinal control of balance, and suggests this altered neural control may contribute to specific threat-related balance changes. (c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.
查看更多>>摘要：Visually guided equivalence learning is a special type of associative learning, which can be evaluated using the Rutgers Acquired Equivalence Test (RAET) among other tests. RAET applies complex stimuli (faces and colored fish) between which the test subjects build associations. The complexity of these stimuli offers the test subject several clues that might ease association learning. To reduce the number of such clues, we developed an equivalence learning test (Polygon), which is structured as RAET but uses simple grayscale geometric shapes instead of faces and colored fish. In this study, we compared the psychophysical performances of the same healthy volunteers in both RAET and Polygon test. Equivalence learning, which is a basal ganglia-associated form of learning, appears to be strongly influenced by the complexity of the visual stimuli. The simple geometric shapes were associated with poor performance as compared to faces and fish. However, the difference in stimulus complexity did not affect performance in the retrieval and transfer parts of the test phase, which are assumed to be mediated by the hippocampi.(c) 2022 The Authors. Published by Elsevier Ltd on behalf of IBRO. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
查看更多>>摘要：Optic neuritis and retinal damage are common manifestations of multiple sclerosis (MS). Pterostilbene (PT) has been used to treat multiple diseases for its anti-inflammatory, anti-apoptosis and neuroprotective activities. This study aimed to investigate whether PT exerts a therapeutic effect on optic neuritis and retinal damage triggered by MS. Here, experimental autoimmune encephalomyelitis (EAE), an experimental model for MS, was induced in female C57BL/6 mice by immunizing with MOG35-55 peptide and treating with pertussis toxin. The mice were intraperitoneally injected with 20 mg/kg and 40 mg/kg PT once daily for 25 days at 24 h post immunization. We found that PT alleviated EAE severity and delayed EAE onset. Moreover, PT mitigated EAE-induced optic nerves and retinal inflammation, as indicated by the decreased Iba-1(+) and GFAP+ cells and mRNA levels of interleukin-6, tumor necrosis factor -a and interleukin-1 beta and the increased Iba-1(+)sirtuin 1 (SIRT1)(+) and GFAP(+)- SIRT1(+) cells in the optic nerves and retina. PT also protected the optic nerves against demyelination and axonal loss and the retina against disorders in retinal morphology and apoptosis of retinal ganglion cells. High-dose PT had a more significant effect on protection of the optic nerves and retina in EAE than low-dose PT. In addition, PT activated SIRT1 signaling in the optic nerves and retina. Notably, EX-527, an inhibitor of SIRT1, reversed the effect of high-dose PT on the optic nerves and retina, indicating that PT exerted the protective effect via activating SIRT1 signaling. This study provides a potential candidate for treating MS. (C) 2022 Published by Elsevier Ltd on behalf of IBRO.
MacKenzie, Jennifer L.Ivanova, NadezdaNell, Hayley J.Giordano, Courtney R....
19页
查看更多>>摘要：Ischemic stroke often co-occurs with Alzheimer's disease (AD) leading to a worsened clinical outcome. Neuroinflammation is a critical process implicated in AD and ischemic pathology, associated with cognitive decline. We sought to investigate the combined effects of ischemic stroke induced by endothelin-1 injection in two AD rat models, using motor function, memory and microglial inflammation in the basal forebrain and striatum as readouts. In addition, we sought to determine the effectiveness of the antioxidant biologic CAT-SKL in one of the models. The early AD model employed the bilateral intracerebroventricular injections of the toxic b-amyloid peptide Ab25-35, the prodromal AD model used the transgenic Fischer 344 rat overexpressing a pathological mutant human amyloid precursor protein. Motor function was assessed using a cylinder, modified sticky tape and beam-walk tasks; learning and memory were tested in the Morris water maze. Microglial activation was examined using immunohistochemistry. Ab25-35 toxicity and stroke combination greatly increased microglial inflammation in the basal forebrain. Prodromal AD-pathology coupled with ischemia in the transgenic rat resulted in a greater microgliosis in the striatum. Combined transgenic rats showed balance alterations, comorbid Ab25-35 rats showed a transient sensorimotor deficit, and both demonstrated spatial reference memory deficit. CAT-SKL treatment ameliorated memory impairment and basal forebrain microgliosis in Ab25-35 rats with stroke. Our results suggest that neuroinflammation could be one of the early processes underlying the interaction of AD with stroke and contributing to the cognitive impairment, and that therapies such as antioxidant CAT-SKL could be a potential therapeutic strategy. (C)& nbsp;2022 The Author(s). Published by Elsevier Ltd on behalf of IBRO.
Yu, Nan Chen HongyiLiu, SihanQian, MeiheZhang, Zhongling...
12页
查看更多>>摘要：ischemia/reperfusion injury is the main cause of neurological deficit following stroke. Pleckstrin homology-like domain, family A, member 1 (PHLDA1) is increasingly recognized as a critical determinant in immunological regulation and cell apoptosis, but its role in neuroinflammation during cerebral ischemia/reperfusion injury remains to be elucidated. In this study, middle cerebral artery occlusion/reperfusion (MCAO/R) in C57BL/6 mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in BV-2 cells were used as models in vivo and in vitro, respectively. MACO/R mice and OGD/R cells were treated with scramble or PHLDA1 small interfering RNAs (siRNAs) to achieve the goal of PHLDA1 knockdown. The results showed that the expression of PHLDA1 was significantly increased in MCAO/R mice and OGD/R cells compared to their normal controls, respectively. Mice treated with PHLDA1 siRNA exhibited a lower degree of infarct volume and brain water content compared to the NC siRNA-treated mice. Notably, PHLDA1 knockdown switched the M1 pro-inflammatory phenotype to the M2 anti-inflammatory phenotype by decreasing the expression of M1 markers (i.e., CD16, TNF-a, IL-6 and IFN-c, and iNOS) and elevating the expression of M2 markers (i.e., CD206, IL-4, IL-10, and Arg-1). Moreover, PHLDA1 knockdown suppressed the NLRP3 inflammasome activation by reducing NLRP3, ASC, cleaved caspase 1 and cleaved IL-1b expression. In summary, these results suggest that PHLDA1 blockade effectively alleviates the ischemia/reperfusion-induced cerebral injury by switching microglial M1/M2 polarization and inhibiting NLRP3 inflammasome activation. Targeting PHLDA1 could be considered as a novel strategy in the treatment against post-ischemic brain injury. (c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.
查看更多>>摘要：Although altered microstructure properties of white-matter tracts have been reported in children with attention-deficit/hyperactivity disorder (ADHD), findings from relatively few adult ADHD studies are inconsistent. This study aims to examine microstructural property over the whole brain in adults with ADHD and explore struc-tural connectivities. Sixty-four medication-nax3ca;ve adults with ADHD and 81 healthy adults received diffusion spec-trum imaging. Generalized fractional anisotropy (GFA), an index indicating microstructural property, was calculated stepwise among 76 white-matter tracts. With the threshold-free clustering weighted method, the seg-ments with the largest group difference were selected, and mean GFA (mGFA) values were calculated. Adults with ADHD had increased mGFA values in the segments located in the left frontal aslant tract, the right inferior longi-tudinal fasciculus, and the left perpendicular fasciculus, and reduced mGFA values in the segments located in the right superior longitudinal fasciculus (SLF) I, the left SLF II, the right frontostriatal tracts from dorsolateral pre -frontal cortex and the ventrolateral prefrontal cortex, the right medial lemniscus, the right inferior thalamic radi-ation to the auditory cortex, and the callosal fibers. Additionally, the mGFA value of the right SLF I segment was associated with hyperactivity-impulsivity symptoms. Our findings suggest that white-matter tracts with altered microstructure properties are located within the attention networks, fronto-striato-thalamocortical regions, and those associated with attention and visual perception in adults with ADHD. (c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.
查看更多>>摘要：The experimental investigations on the pathogenesis of remifentanil-induced hyperalgesia (RIH) have been primarily conducted, but the effective treatment of RIH remains unclear. Recent reports highlight the neces-sity of ionotropic glutamate receptors in oxidative damage in spinal nociceptive transduction. Artesunate, the 1st-line anti-malaria drug, has been identified to be valid in removing superoxide in several pathological conditions. This study evaluated whether artesunate inhibits RIH via regulating metabotropic glutamate receptor 5 (mGluR5) and mitochondrial antioxidant enzyme peroxiredoxin-3 in rats. Artesunate was injected intrathecally 10 min before intravenous infusion of remifentanil (1 mu g.kg(-1).min(-1) for 60 min) in rats. The antinociception of artesunate was verified by assessment of paw withdrawal mechanical threshold and paw withdrawal thermal latency. Spinal mGluR5 expression and peroxiredoxin-3 hyperacetylation were examined. Also, both the mGluR5 agonist DHPG and antagonist MPEP were utilized to explore the involvement of mGluR5 in the anti-hyperalgesic property of arte-sunate. Here, we found that artesunate (10 lg and 100 lg but not 1 mu g) prevented RIH in a dose-dependent manner. Artesunate reduced remifentanil-related spinal over-expression of mGluR5 gene and protein, and hyperacetyla-tion of peroxiredoxin-3. Intrathecal application of MPEP (10 nmol and 100 nmol but not 1 nmol) inhibited behavioral RIH and peroxiredoxin-3 acetylation. Moreover, hyperalgesia and peroxiredoxin-3 hyperacetylation were attenuated after the combination of artesunate (1 mu g) and MPEP (1 nmol). Additionally, artesunate treatment reversed acute pain and peroxiredoxin-3 hyperacetylation following spinal exposure to DHPG. In conclusion, intrathecal injection of artesunate impairs RIH by down-regulating spinal mGluR5 expression and peroxiredoxin-3 hyperacetylation-mediated oxidative stress in rats.& nbsp; (C)& nbsp;2022 IBRO. Published by Elsevier Ltd. All rights reserved.
查看更多>>摘要：investigating motor learning in patients with multiple sclerosis (MS) disease highlighted that MS patients exhibit similar learning performance than healthy controls, but that learning can be hampered by the progression of MS eventually leading to impaired efficiency of subcortical-cortical networks. We aimed at investigating whether the long-term, overnight consolidation of sequential motor memories is preserved in MS disease. Thirty-one patients with MS and two healthy control groups (27 young and 14 middle age) were tested over two consecutive days using a serial reaction time task. Performance was tested (a) 20 min after the end of learning at Day 1 to monitor transient offline, short-term increase in motor and sequential performance and (b) after 24 h on Day 2 to quantify overnight delayed changes in performance reflecting memory consolidation. Besides a slower overall RT in patients with MS, motor performance similarly evolved in all groups. Sequence learning as assessed by interference effects was similar in patients with MS and both control groups on Day 1 (Learning and 20-min test). In contrast, while interference effects keep increasing on Day 2 after 24 h (Relearning) in healthy control groups, it reverted to levels reached at the end of learning for patients with MS. Long-term consolidation of sequential knowledge is impaired in patients with MS. At the motor level, learning and overnight consolidation abilities are preserved in MS disease. (c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.
查看更多>>摘要：G-coupled receptors (GPCRs) modulate brain function by signaling through heterotrimeric G(q/11), G(s), and G(i/o) protein subtypes. Researchers frequently study neuromodulation via these GPCR-subtypes on a 'cell-by-cell' basis. Although useful to explore a small number of interactions among neuromodulatory systems under controlled settings, this approach fails to account for a global organization of GPCRs in the brain. Furthermore, because multiple receptors and signal transduction pathways are present in single cells, neuromodulation is controlled by groups of GPCRs rather than by individual receptors. Using an integrative approach, the present study examined how large GPCR-subtype communities (ensembles) are expressed in different anatomical regions. Using the Allen Brain Atlas (http://www.brain-map.org/), we analyzed the mRNA expression energy of hundreds of GPCR-subtypes located in mouse, macaque, and human brains. We found that although there was a heterogeneous expression of GPCR-mRNA across all cortical regions, there were strong spatial correlations among congregated G(q/11)-, G(s)-, and G(i/o)-linked systems. Correlation strength increased with age but dropped when randomly removing genes from their corresponding groups. These findings suggest that the expression patterns of GPCR subtypes and receptor families are intricately intertwined. Well-orchestrated interactions by neuromodulatory-GPCR ensembles could be crucial for the brain to function as a highly integrated complex system. (C) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.
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