查看更多>>摘要：? 2021 IBROThe study of the effects of fear and disgust on the capture of automatic attention is gaining interest. Most findings reveal a more efficient capture of exogenous attention by disgust than by fear stimuli, although the underlying mechanisms are not completely understood. The manipulation of their spatial frequency may provide new insight that may contribute to clarify this issue. The present study aimed to explore differential processing of disgust and fear scenes containing only low spatial frequencies (LSF) or all spatial frequencies (intact) presented as distractors in an exogenous attention task. Event-related potentials (ERPs) and behavioral responses were recorded as dependent variables from forty participants (29 women). The results showed that disgust and fear distractors captured exogenous attention equally early, as indicated by the augmented amplitude of the N2p, and later disgust distractors are the ones eliciting the highest amplitude of the LPP component. While in an initial stage, both stimuli seem to have similar preferential access to further processing allowing fast responding in both cases, disgust is more deeply processed at a later stage probably facilitating its examination. These findings suggest that exploring the temporal course of processing is relevant for the understanding of the differential capture of exogenous attention by disgust and fear distractors.
查看更多>>摘要：? 2021 IBROProcrastination is generally recognized as a problematic behavior and the consequences of which spread to various aspects of an individual's life such as academic performance, social accomplishment, well-being, and health. Previous studies have indicated that neuroticism is positively correlated with procrastination; however, little is known about the neural substrates underlying the link between neuroticism and procrastination. To address this issue, we employed voxel‐based morphometry (VBM) and resting‐state functional connectivity (RSFC) methods to investigate the neural underpinning for their relationship in the present study (N = 153). Consistent with our hypothesis, the behavior results verified a positive correlation between neuroticism and procrastination (r = 0.47). The VBM analysis revealed that the gray matter (GM) volumes in the right middle temporal gyrus (RMTG) were positively correlated with neuroticism. Moreover, results from RSFC analysis suggested that the functional connectivity between RMTG and the right superior frontal gyrus (RSFG) was positively associated with neuroticism. More importantly, a mediation analysis demonstrated that neuroticism played a full mediating role in the impact of RMTG-RSFG functional connectivity on procrastination. Overall, the present study offered new insights into the relation between neuroticism and procrastination from a neural basis perspective, which also suggested the importance of emotional regulation with regard to the link between such an association.
查看更多>>摘要：? 2021 IBROThe primary sensory modality for probing spatial perception can vary among psychophysical paradigms. In the subjective visual vertical (SVV) task, the brain must account for the position of the eye within the orbit to generate an estimate of a visual line orientation, whereas in the subjective haptic vertical (SHV) task, the position of the hand is used to sense the orientation of a haptic bar. Here we investigated whether a hand sensory bias can affect SHV measurement. We measured SHV in 12 subjects (6 left-handed and 6 right-handed) with a forced-choice paradigm using their left and right hands separately. The SHV measurement was less accurate than the SVV measurements (?0.6 ± 0.7) and it was biased in the direction of the hand used in the task but was not affected by handedness; SHV left hand ?6.8 ± 2.1° (left-handed ?7.9 ± 3.6°, right-handed ?5.8 ± 2.5°) and right hand 9.8 ± 1.5° (left-handed 7.4 ± 2.2°, right-handed 12.3 ± 1.8°). SHV measurement with the same hand was also affected by the haptic bar placement on the left or right side versus midline, showing a side effect (left vs midline ?2.0 ± 1.3°, right vs midline 3.8 ± 1.7°). Midline SHV measures using the left and right hands were different, confirming a laterality effect (left hand ?4.5 ± 1.7°, right hand 6.4 ± 2.0°). These results demonstrate a sensory bias in SHV measurement related to the effects of both hand-in-body (i.e., right vs left hand) and hand-in-space positions. Such modality-specific bias may result in disparity between SHV and SVV measurements, and therefore cannot be generalized to vertical or spatial perception.
查看更多>>摘要：? 2021 IBROOrexin-producing cells in the lateral hypothalamic area have been shown to be involved in a wide variety of behavioral and cognitive functions, including the recall of appetitive associations and a variety of social behaviors. Here, we investigated the role of orexin in the acquisition and recall of socially transmitted food preferences in the rat. Rats were euthanized following either acquisition, short-term recall, or long-term recall of a socially transmitted food preference and their brains were processed for orexin-A and c-Fos expression. We found that while there were no significant differences in c-Fos expression between control and experimental subjects at any of the tested timepoints, females displayed significantly more activity in both orexinergic and non-orexinergic cells in the lateral hypothalamus. In the infralimbic cortex, we found that social behavior was significantly predictive of c-Fos expression, with social behaviors related to olfactory exploration appearing to be particularly influential. We additionally found that appetitive behavior was significantly predictive of orexin-A activity in a sex-dependent matter, with the total amount eaten correlating negatively with orexin-A/c-Fos colocalization in male rats but not female rats. These findings suggest a potential sex-specific role for the orexin system in balancing the stimulation of feeding behavior with the sleep/wake cycle.
查看更多>>摘要：? 2021 IBROIt is well known that neuroinflammation plays a key role in neurodegenerative diseases. Hypoxia-inducible factor (HIF) and its hydroxylases-Prolyl-4-hydroxyases (PHDs) have been found to modulate the inflammatory processes. Here, the effects of PHDs enzyme onlipopolysaccharide-induced neuroinflammation and neurocognitive deficits were investigated. BV2 microglia cells were stimulated by LPS (1 μg/ml) as neuroinflammation model in vitro. Dimethyloxalylglycine (DMOG, 100 μM) and PHD3-siRNA were used to suppress the expression of PHD3. In vivo, mice received consecutive intraperitoneal injection of LPS (500 μg/kg) for 7 days, and intraperitoneal injection of DMOG (100 mg/kg) was applied 1 h before LPS at the same days. Several neurobehavioral tests (Open field, Novel object recognition and Morris water maze) were used to measure cognitive function. RT-qPCR and Western blotting were used to investigate the expression of inflammatory cytokines, HIF-PHDs protein. Metabolic reprogramming was measured by seahorse method. The results revealed that LPS induced neuroinflammation and PHD3 expression in vivo and vitro. DMOG and PHD3knockout decreased expression of inflammatory cytokines and improved the metabolic reprogramming caused by LPS treatment. Furthermore, pretreatment of DMOG reversed learning and memory deficits in systemic LPS-exposed mice through anti-neuroinflammation, which is independent of DMOG angiogenesis. These findings suggested that PHD3 may mediate LPS-induced microglial activation and neuroinflammation-associated neurobehavioral deficits.
查看更多>>摘要：? 2021 The Author(s)Central poststroke pain (CPSP) is a neuropathic pain syndrome that usually occurs after cerebrovascular accidents. Currently, the pathogenesis of CPSP is not fully understood. Purinergic P2X4 receptor (P2X4R) is implicated in neuropathic pain including CPSP. Herein, we demonstrated that the levels of microRNA-133b-3p (miR-133b-3p), which targets P2X4R transcripts, were significantly downregulated in the ventral posterolateral nucleus of the thalamus (VPL), cerebrospinal fluid (CSF), and plasma of CPSP rats. The expression levels of miR-133b-3p negatively correlated with the severity of allodynia. Genetic knockdown of P2X4R in the VPL protected CPSP rats against allodynia. Similarly, genetic overexpression of miR-133b-3p in the VPL reversed the allodynia established in CPSP rats via downregulation of P2X4R expression. Treatment using gabapentin in CPSP rats significantly restored the decreased miR-133b-3p expression in the VPL, CSF, and plasma and blocked allodynia in CPSP rats. The administration of an miR-133b-3p inhibitor into the VPL abolished the antiallodynic activity of gabapentin. This mechanism was associated with P2X4R expression and involved the endogenous opioid system. Human patients with CPSP showed decreased plasma levels of miR-133b-3p compared with those of control participants. Logistic regression analysis of our patient cohort showed that determining plasma levels of miR-133b-3p may be useful for CPSP diagnosis and treatment.
查看更多>>摘要：? 2021 IBROPresbycusis, or age-related hearing loss (ARHL), is primarily associated with sensory or transduction nerve cell degeneration in the peripheral and/or central auditory systems. During aging, the auditory system shows mitochondrial dysfunction and increased inflammatory responses. Mitochondrial dysfunction promotes leakage of mitochondrial DNA (mtDNA) into the cytosol, which activates the cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) pathway to induce type I interferon and inflammatory responses. However, whether this pathway is involved in the occurrence and development of ARHL is unknown. This study aimed to determine whether there are age-related changes in the levels of cytosolic mtDNA and cGAS–STING pathway activation in the auditory pathway and to explore their relationship with ARHL. The results showed that cGAS-positive immunoreactive cells were observed in the cochlea, inferior colliculus, and auditory cortex. Levels of cytosolic mtDNA, cGAS, STING, phosphorylated interferon regulatory factor 3, and cytokines were significantly increased in the cochlea, inferior colliculus, and auditory cortex of 6-, 9-, and 12-month-old mice compared with 3-month-old mice. These findings suggested that cytosolic mtDNA may play an important role in the pathogenesis of ARHL by activating cGAS–STING-mediated type I interferon and inflammatory responses.
查看更多>>摘要：? 2021 IBROAstrocytes experience significant metabolic shifts in the “sensitive period” of neurological function recovery following cerebral ischemia. However, the changes in astrocyte lipid metabolism and their implications for neurological recovery remain unknown. In the present study, we employed a mouse middle cerebral artery occlusion model to investigate the changes in de novo lipogenesis and interleukin-33 (IL-33) production in astrocytes and elucidate their role in blood–brain barrier (BBB) repair in the subacute phase of cerebral ischemia. Neurological behavior evaluation was used to assess functional changes in mice. Pharmacological inhibition and astrocyte-specific downregulation of fatty acid synthase (FASN) were used to evaluate the role of de novo lipogenesis in brain injury. Intracerebroventricular administration of recombinant IL-33 was performed to study the contribution of IL-33 to BBB disruption. Extravasation of Evans blue dye, dextran and IgG were used to assess BBB integrity. Western blotting of tight junction proteins ZO-1, Occludin, and Claudin-5 were performed at defined time points to evaluate changes in BBB. It was found that de novo lipogenesis was activated, and IL-33 production increased in astrocytes at the subacute stage of cerebral ischemia injury. Inhibition of lipogenesis in astrocytes decreased IL-33 production in the peri-infarct area, deteriorated BBB damage and interfered with neurological recovery. In addition, supplementation of IL-33 alleviated BBB destruction and improved neurological recovery worsened by lipogenesis inhibition. These findings indicate that astrocyte lipogenesis increases the production of IL-33 in the peri-infarct area, which promotes BBB repair in the subacute phase of cerebral ischemia injury and improves long-term functional recovery.
查看更多>>摘要：? 2021 IBROThe widespread application of ionizing radiation in industrial and medical fields leads to the increased brain exposure to X-rays. Radiation brain injury (RBI) seriously affects health of patients by causing cognitive dysfunction and neuroinflammation. However, the link between X-ray exposure and depressive symptoms and their detailed underlying mechanisms have not been well studied. Herein, we investigated the potential depression-like behaviors in mice exposed to X-rays and then explored the role of HMGB1 in this injury. We found that X-ray stimulation induced the generation of reactive oxygen species (ROS) in the prefrontal cortex in a dose-dependent manner, leading to the occurrence of depression-like behaviors of the mice. Moreover, X-ray exposure increased the expression of HMGB1, activated NLRP3 inflammasome signaling pathway and microglial cells, and then facilitated the release of pro-inflammatory cytokines, resulting in the pyroptosis and neuron loss both in vivo and in vitro. Additionally, glycyrrhizin (Gly), which is a HMGB1 inhibitor, reversed X-ray-induced behavioral changes and neuronal damage. Our findings indicated that HMGB1-mediated pyroptosis was involved in radiation-induced depression.
查看更多>>摘要：? 2021 IBROFragmentation of the daily sleep-wake rhythm with increased nighttime awakenings and more daytime naps is correlated with the risk of development of Alzheimer's disease (AD). To explore whether a causal relationship underlies this correlation, the present study tested the hypothesis that chronic fragmentation of the daily sleep-wake rhythm stimulates brain amyloid-beta (Aβ) levels and neuroinflammation in the 3xTg-AD mouse model of AD. Female 3xTg-AD mice were allowed to sleep undisturbed or were subjected to chronic sleep fragmentation consisting of four daily sessions of enforced wakefulness (one hour each) evenly distributed during the light phase, five days a week for four weeks. Piezoelectric sleep recording revealed that sleep fragmentation altered the daily sleep-wake rhythm to resemble the pattern observed in AD. Levels of amyloid-beta (Aβ40 and Aβ42) determined by ELISA were higher in hippocampal tissue collected from sleep-fragmented mice than from undisturbed controls. In contrast, hippocampal levels of tau and phospho-tau differed minimally between sleep fragmented and undisturbed control mice. Sleep fragmentation also stimulated neuroinflammation as shown by increased expression of markers of microglial activation and proinflammatory cytokines measured by q-RT-PCR analysis of hippocampal samples. No significant effects of sleep fragmentation on Aβ, tau, or neuroinflammation were observed in the cerebral cortex. These studies support the concept that improving sleep consolidation in individuals at risk for AD may be beneficial for slowing the onset or progression of this devastating neurodegenerative disease.
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Elsevier