Brain Research Bulletin最新文献

A zoonotic disease called brucellosis can cause flu-like symptoms and heart inflammation. The bacteria responsible for this disease can also enter the brain, causing a condition called neurobrucellosis that can result in long-term neurological problems. In this study, researchers aimed to determine the changes in the hippocampal cells of rats infected with Brucella. For the study, 24 adult male albino rats were inoculated with 1 × 10⁶ CFU Brucella abortus 544. The rats were then deeply anesthetized, and their hippocampus samples were taken for stereological, histological, and molecular studies. The results showed that the infected rats had increased microgliosis and astrogliosis. Furthermore, a high level of caspase-3 in their hippocampal tissue indicated their susceptibility to apoptosis. Additionally, there was a decrease in expression of Ki67, which further supported this. Sholl's analysis confirmed a significant failure in glial morphology. The study demonstrated that the pathogen has the ability to destroy the hippocampus and potentially affect its normal physiology. However, more research is needed to clarify various aspects of neurobrucellosis.

Motion sickness (MS) is caused by exposure to unfamiliar movements. The theory is that MS is due to a conflict between information perceived by the vestibular, visual, and somatosensory systems. This study examines the role of vision in MS by comparing MS susceptibility among individuals with varying degrees of visual impairments to sighted individuals. We hypothesized that subjects with no perception of light would be less susceptible to MS than less impaired subjects, who would themselves be less susceptible than sighted subjects. To address these, the Motion Sickness Susceptibility Questionnaire (MSSQ¹) was administered to 340 subjects (170 visually impaired paired with 170 sighted subjects) to assess their susceptibility to various modes of transport under real conditions. Visually impaired subjects were divided into subgroups according to the presence (partially sighted) or absence (totally blind) of light perception, as well as the period of onset of impairment (congenital or acquired). Totally blind individuals are significantly less susceptible to MS than partially sighted (p = 0.001), and sighted (p < 0.001) subjects, with no difference between partially sighted and sighted subjects (p = 0.526). Additionally, acquired totally blind subjects are less susceptible to MS than congenitally blind subjects (p = 0.038). Thus, despite a lower susceptibility totally blind subjects may still be susceptible to MS. The absence of vision reduces MS susceptibility but does not completely prevent it. This suggests that vision is more a mediator, than an essential condition for MS appearance.

Background

Cognitive dysfunction, encompassing perioperative psychological distress and cognitive impairment, is a prevalent postoperative complication within the elderly population, and in severe cases, it may lead to dementia. Building upon our prior research that unveiled a connection between postoperative mood fluctuations and cognitive dysfunction with the phosphorylation of P38, this present investigation aims to delve deeper into the involvement of the P38 MAPK/NLRP3 pathway in perioperative neurocognitive disorders (PND) in an abdominal exploratory laparotomy (AEL) aged mice model.

Methods

C57BL/6 mice (male, 18-month-old) underwent AEL with 3 % anesthesia. Then, inhibitors targeting P38 MAPK (SB202190, 1 mg/kg) and GSK3β (TWS119, 10 mg/kg) were administered multiple times daily for 7 days post-surgery. The NLRP3-cKO AEL and WT AEL groups only underwent the AEL procedure. Behavioral assessments, including the open field test (OFT), novel object recognition (NOR), force swimming test (FST), and fear conditioning (FC), were initiated on postoperative day 14. Additionally, mice designated for neuroelectrophysiological monitoring had electrodes implanted on day 14 before surgery and underwent novel object recognition while their local field potential (LFP) was concurrently recorded on postoperative day 14. Lastly, after they were euthanasized, pathological analysis and western blot were performed.

Results

SB202190, TWS119, and astrocyte-conditional knockout NLRP3 all ameliorated the cognitive impairment behaviors induced by AEL in mice and increased mean theta power during novel location exploration. However, it is worth noting that SB202190 may exacerbate postoperative depressive and anxiety-like behaviors in mice, while TWS119 may induce impulsive behaviors.

Conclusions

Our study suggests that anesthesia and surgical procedures induce alterations in mood and cognition, which may be intricately linked to the P38 MAPK/NLRP3 pathway.

Epilepsy with recurrent seizures is characterized by neuronal damage and glial proliferation induced by brain inflammation. Recurrent seizures can lead to changes in the microRNA (miRNA) spectrum, significantly influencing the inflammatory response of microglia. MiR-155–5p, as a pro-inflammatory miRNA, is increased in the epileptic brain. However, its specific role in acute seizures remains unknown. The study aimed to develop a new strategy for treating epilepsy by investigating how silencing of miR-155–5p initiated its anticonvulsive mechanism. The level of miR-155–5p was up-regulated in the hippocampus of epileptic immature rats induced by kainic acid (KA). The use of antago-miR-155–5p exerted significant beneficial effects on the seizure scores, brain discharges and cognition in immature rats following KA-induced epilepsy. Antago-miR-155–5p also inhibited neuron damage and microglial activation. Moreover, the silencing of miR-155–5p significantly inhibited the Dual-specificity phosphatase 14 (Dusp14)/ mitogen-activated protein kinase (MAPK) axis in vivo. MiR-155–5p interacted with dusp14 to regulate MAPK signaling way expression, verified by a dual-luciferase reporter assay. The results suggested that the silencing of miR-155–5p might reduce hippocampal damage in epileptic immature rats induced by KA via Dusp14/MAPK signaling way. This implied that miR-155–5p could serve as a therapeutic tool to prevent the development of epilepsy.

The establishment of positive early parent–infant relationships provide essential nourishment and social stimulation for newborns. During the early stages of postnatal brain development, events such as synaptogenesis, neuronal maturation and glial differentiation occur in a highly coordinated manner. Maternal separation, as an early-life stress introducer, can disrupt the formation of parent–child bonds and exert long-term adverse effects throughout life. When offspring are exposed to maternal separation, the body regulates the stress of maternal separation through multiple mechanisms, including neuroinflammatory responses, neuroendocrinology, and neuronal electrical activity. In adulthood, early maternal separation has long-term effects, such as the induction of neuropsychiatric disorders such as anxiety, depression, and cognitive dysfunction. This review summarized the application of maternal separation models and the mechanisms of stress system response in neuropsychiatric disorders, serving as both a reminder and inspiration for approaches to improve neonatal care, “from bench to bedside”.

The intricate interplay existing between gut microbiota and homeostasis extends to the realm of the brain, where emerging research underscores the significant impact of the microbiota on mood regulation and overall neurological well-being and vice-versa, with inflammation playing a pivotal role in mediating these complex interactions. This comprehensive review explores the complex interplay between inflammation, alterations in gut microbiota, and their impact on major depressive disorder (MDD). It provides a cohesive framework for the puzzle pieces of this triad, emphasizing recent advancements in understanding the gut microbiota and inflammatory states' contribution to the depressive features. Two directions of communication between the gut and the brain in depression are discussed, with inflammation serving as a potential modulator. Therapeutic implications were discussed as well, drawing insights from interventional studies on the effects of probiotics on gut bacterial composition and depressive symptoms. Ultimately, this review will attempt to provide a complete and valuable framework for future research and therapeutic interventions in MDD.

Intermittent hypoxia (IH) in patients with obstructive sleep apnea (OSA) syndrome elicited neuron injury (especially in the hippocampus and cortex), contributing to cognitive dysfunction. This study investigated the effects and clarified the mechanisms of ETS domain-containing protein Elk-4 (ELK4) on the cognitive function and neuroinflammation of mice with IH. Mouse microglia BV2 cells were induced with IH by exposure to fluctuating O₂ concentrations (alternating from 5 % to 21 % every 30 min), and mice with OSA were developed and subjected to lentivirus-mediated gene intervention. ELK4 expression was significantly reduced in IH-induced microglia and brain tissues of mice with OSA. Overexpression of ELK4 attenuated oxidative stress, decreased the pro-inflammatory factors IL-1β, IL-6, and TNF-α, and increased the level of the anti-inflammatory factors IL-10 and TGF-β1, as well as the neuroprotective factor BDNF. ELK4 promoted the transcription of fibronectin type III domain-containing protein 5 (FNDC5) by binding to the promoter of FNDC5. Knockdown of FNDC5 in IH-induced microglia and animals reversed the protective effects of ELK4 on OSA-associated neuroinflammation and cognitive dysfunction. Overall, the results demonstrated that ELK4 overexpression repressed microglial activation by inducing the transcription of FNDC5, thus attenuating neuroinflammation and cognitive dysfunction induced by OSA.

The present study aims to investigate the unknown relationship between inhibitory control and repetitive subconcussion induced by the indirect brain impacts. We enrolled 28 parachuters exposed to repetitive subconcussion (SC) and 27 matched health controls (HC). Parachuters who have completed at least 70 actual parachuting (71–112 times) and at least 1500 simulated platform jumps (1500–4500 times) were included in the SC group. The SC group had a reduced accuracy rate in both the Stroop congruent and incongruent conditions. Larger N2 and N450 amplitudes were elicited in the frontal regions of the SC group, which indicate compensatory adaptations to the deficit in conflict monitoring. The reduced frontal resting-state EEG complexity in full-band (1–40 Hz) may demonstrate the frontal structural damage following the indirect brain impacts of repetitive subconcussion. Pearson correlation analysis showed that in the SC group, the frontal beta-band sample entropy values are positively correlated with the accuracy rate of the Stroop incongruent condition, suggesting the frontal beta-band sample entropy values may serve as potential electrophysiological markers of impaired inhibitory control after indirectly repetitive brain impacts. This study provides the robust evidence that repetitive subconcussion resulting from indirect brain impacts may lead to impairment of inhibitory control.

Background

Internet gaming disorder (IGD) is mainly characterized by its core dysfunction in higher-order brain cortices involved in inhibitory control, whose neurobiological basis remains unclear. Then, we will investigate local intrinsic neural activity (INA) alterations in IGD, ascertain whether these potential alterations are related to clinical characteristics, and further explore the underlying molecular architecture.

Method

In this study, we performed the fractional amplitude of low-frequency fluctuation (fALFF) and regional homogeneity (ReHo) derived from resting-state functional magnetic resonance imaging (rs-fMRI) to explore the impact of IGD on local INA. Correlation analysis revealed the relationship between ReHo and fALFF in terms of group differences and clinical characteristics. Moreover, correlations between fALFF, ReHo, and PET- and SPECT-driven maps were investigated to elucidate the specific molecular architecture alternations in IGD. Finally, receiver operating characteristic curve (ROC) analysis was used to show the potential abilities of fALFF and ReHo in distinguishing individuals with IGD (IGDs) from healthy controls (HCs).

Result

Compared with HCs, IGDs revealed increased ReHo and fALFF in the prefrontal cortex. Significantly decreased ReHo was observed in the temporal lobe, occipital lobe, and cerebellum. In addition, the ReHo values in the cerebellum_7b_R were positively correlated with internet addiction severity. ROC curve analysis showed that ReHo and fALFF-altered brain regions could effectively distinguish IGDs from HCs. More importantly, cross-modal correlations revealed local INA changes in brain regions associated with the monoamine neurotransmitter system and the less studied cholinergic/GABAergic system.

Conclusion

These results suggest that local functional impairments are shown in the audiovisual and inhibitory control circuits in IGDs. This may be associated with underlying neurotransmitter system alterations. Therefore, this study provides the possibility of GABAergic receptor agonists and cholinergic receptor inhibitors for the treatment of IGD.