Neuroscience最新文献_第5页

Attentional management of cognitive-motor interference in adults during walking: Insights from an EEG study 成人在行走过程中对认知-运动干扰的注意力管理：脑电图研究的启示

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-16 DOI: 10.1016/j.neuroscience.2024.09.048

Dual-task paradigms, which involve performing cognitive and motor tasks simultaneously, are commonly used to study how attentional resources are allocated and managed under varying task demands. This study aimed to investigate cognitive-motor interferences (CMI) under different levels of cognitive and motor task difficulty without instruction on task prioritization. 17 healthy young adults performed an auditory oddball task with increasing cognitive and motor (walking vs. sitting) difficulty. Cognitive and motor performances, along with P3 (P3a and P3b) brainwave components, were analysed. Increasing cognitive difficulty resulted in more errors and increased P3a amplitude, reflecting enhanced attentional demand, while P3b remained unaffected. This suggests a threshold effect on attentional resources. Motor complexity lengthened P3a and P3b latencies without affecting amplitude, indicating delayed attentional resource recruitment. Additionally, walking with the most difficult cognitive task increased cognitive error, suggesting attentional resource limits. With increased motor and cognitive complexity, CMI emerged, leading to cognitive error increase and improved gait stability without amplitude changes in P3a and P3b. Two hypotheses were proposed: motor prioritization and motor facilitation. Our study suggests managing attentional resources to balance cognitive and motor tasks rather than linearly increasing task complexity. Viewing dual tasks as a new, integrated task is proposed, supported by previous neural network integration studies. Thus, understanding how the brain organizes tasks in response to constraints is crucial for comprehending complex task execution.

双任务范式涉及同时执行认知任务和运动任务，通常用于研究在不同任务需求下如何分配和管理注意力资源。本研究旨在调查在没有任务优先级指示的情况下，不同认知和运动任务难度下的认知-运动干扰（CMI）。17 名健康的年轻人在认知和运动（行走与坐姿）难度不断增加的情况下完成了听觉怪球任务。对认知和运动表现以及 P3（P3a 和 P3b）脑电波成分进行了分析。认知难度的增加导致更多的错误和 P3a 振幅的增加，反映出注意力需求的增强，而 P3b 则不受影响。这表明注意力资源存在阈值效应。运动复杂性会延长 P3a 和 P3b 的潜伏期，但不会影响其振幅，这表明注意力资源征用延迟。此外，在最困难的认知任务下行走会增加认知错误，这表明注意资源有限。随着运动和认知复杂性的增加，CMI出现，导致认知错误增加，步态稳定性提高，但P3a和P3b的振幅没有变化。我们提出了两个假设：运动优先化和运动促进。我们的研究建议管理注意力资源以平衡认知和运动任务，而不是线性增加任务复杂性。我们提出将双重任务视为一种新的综合任务，这也得到了之前神经网络整合研究的支持。因此，了解大脑如何组织任务以应对制约因素对于理解复杂任务的执行至关重要。

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引用次数: 0

Chronic pain-induced methylation in the prefrontal cortex targets gene networks associated with cognition and Alzheimer’s disease 慢性疼痛诱导的前额叶皮层甲基化针对与认知和阿尔茨海默病相关的基因网络。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-16 DOI: 10.1016/j.neuroscience.2024.10.015

Chronic pain is prevalent among aging adults. Epidemiologic evidence has demonstrated that individuals with chronic pain have accelerated memory decline and increased probability of dementia. Neurophysiologic, molecular, and pharmacologic hypotheses have been proposed to explain the relationship between chronic pain and cognitive decline, but there remains currently limited evidence supporting any of these. Here, we integrate multi-omic data across human cohorts and rodent species and demonstrate that methylation in the prefrontal cortex induced by chronic pain specifically targets transcriptional networks associated with cognitive ability, memory, and Alzheimer’s disease in humans. We validate this with multiple independent data sets and identify cortical microglia as a likely mechanism by which chronic pain can increase dementia risk. Our analyses support the molecular hypothesis for the role of chronic pain in cognitive decline and identifies several potential therapeutic targets.

慢性疼痛在老年人中十分普遍。流行病学证据表明，慢性疼痛患者的记忆力会加速衰退，患痴呆症的几率也会增加。人们提出了神经生理学、分子学和药理学假说来解释慢性疼痛与认知能力下降之间的关系，但目前支持这些假说的证据仍然有限。在这里，我们整合了人类队列和啮齿动物物种的多组数据，证明慢性疼痛诱导的前额叶皮层甲基化特异性地靶向与人类认知能力、记忆和阿尔茨海默病相关的转录网络。我们用多个独立数据集验证了这一点，并确定皮质小胶质细胞可能是慢性疼痛增加痴呆症风险的机制。我们的分析支持关于慢性疼痛在认知能力下降中作用的分子假说，并确定了几个潜在的治疗靶点。

引用次数: 0

The tryptophan catabolite or kynurenine pathway in Long COVID disease: A systematic review and meta-analysis. 长 COVID 疾病中的色氨酸代谢产物或犬尿氨酸途径：系统回顾和荟萃分析。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-16 DOI: 10.1016/j.neuroscience.2024.10.021

Abbas F Almulla, Yanin Thipakorn, Bo Zhou, Aristo Vojdani, Rossitsa Paunova, Michael Maes

Background: Recent studies confirm the involvement of activated immune-inflammatory responses and increased oxidative and nitrosative stress in Long COVID (LC) disease. However, the influence of these pathways on the metabolism of tryptophan (TRP) through the TRP catabolite (TRYCAT) pathway and their mediating effects on LC pathophysiology, has not been fully explored.

Objective: This meta-analysis investigates peripheral TRP and TRYCAT levels and the TRYCAT pathway in patients with LC disease.

Method: This review utilized systematic searches of PubMed, Google Scholar, and SciFinder, including 14 full-text articles and 1,167 participants, consisting of 480 patients with LC and 687 normal controls.

Results: The results indicated a significant increase in the kynurenine (KYN)/TRP ratio, with a large effect size (standardized mean difference, SMD = 0.755; confidence intervals, CI: 0.119;1.392), in LC patients compared to normal controls. Additionally, LC patients exhibited a significant decrease in TRP levels (SMD = -0.520, CI: -0.793; -0.246) and an increase in KYN levels after imputing missing studies (SMD = 1.176, CI: 0.474; 1.877), suggesting activation of the Indoleamine 2,3-dioxygenase (IDO) enzyme and upregulation of the TRYCAT pathway. No significant elevation in TRYCAT-related neurotoxicity, kynurenic acid (KA)/KYN and 3-hydroxykynurenine (3-HK)/KYN ratios were observed in LC patients compared to normal controls.

Conclusion: The current findings indicate that an activated TRYCAT pathway, characterized by decreased TRP levels and maybe elevated KYN levels, plays a significant role in the pathophysiology of LC.

背景：最近的研究证实，免疫炎症反应的激活以及氧化应激和亚硝基应激的增加参与了Long COVID（LC）疾病。然而，这些途径通过 TRP 分解物（TRYCAT）途径对色氨酸（TRP）代谢的影响及其对 LC 病理生理学的介导作用尚未得到充分探讨：本荟萃分析调查了 LC 患者的外周 TRP 和 TRYCAT 水平以及 TRYCAT 途径：本综述系统检索了 PubMed、Google Scholar 和 SciFinder，包括 14 篇全文文章和 1,167 名参与者，其中包括 480 名 LC 患者和 687 名正常对照者：结果表明，与正常对照组相比，LC 患者的犬尿氨酸（KYN）/TRP 比值明显增加，且影响范围较大（标准化平均差，SMD = 0.755；置信区间，CI：0.119;1.392）。此外，LC 患者的 TRP 水平显著下降（SMD = -0.520，CI：-0.793；-0.246），而在归因缺失研究后，KYN 水平上升（SMD = 1.176，CI：0.474；1.877），这表明吲哚胺 2,3-二氧化酶（IDO）被激活，TRYCAT 通路被上调。与正常对照组相比，LC 患者的 TRYCAT 相关神经毒性、犬尿氨酸（KA）/KYN 和 3-羟基犬尿氨酸（3-HK）/KYN 比率未见明显升高：目前的研究结果表明，激活的 TRYCAT 通路在 LC 的病理生理学中起着重要作用，其特点是 TRP 水平降低，KYN 水平可能升高。

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引用次数: 0

Dynamics of nitrergic system activation in the rat brain provoked by experimentally induced seizures. 实验性癫痫发作引起的大鼠大脑硝化系统激活的动态变化。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-16 DOI: 10.1016/j.neuroscience.2024.10.032

Szymon Kantor, Agnieszka Drzał, Zuzanna Setkowicz, Martyna Elas, Krzysztof Janeczko

Epilepsy is a pathophysiological condition displaying a highly diverse phenotype. Consequently, comprehending the mechanisms underlying seizures necessitates moving beyond a simplistic model focused on the imbalance between the classical excitatory and inhibitory neurotransmitter systems. Nitric oxide (NO), a nonclassical and multifunctional gaseous neurotransmitter, has the potential to exert a profound influence on epileptic reactivity. Unfortunately, numerous studies have not provided clear answers about its involvement in the pathophysiology of epilepsy. The objective of our study was to delineate the temporal dynamics of alterations in nitrergic system activation after experimentally induced seizures. Seizures were induced in 2-month-old male Wistar rats by an administration of pilocarpine. Over a 6-hour observation period, seizure behaviour intensity was continuously evaluated using a modified Racine scale. At intervals of 6, 12, 24, 48, or 96 h post-chemoconvulsant administration, NO spin trapping was conducted with ferrous-diethyldithiocarbamate complexes (Fe(DETC)₂). Electron paramagnetic resonance (EPR) spectroscopy was employed to quantify mononitrosyl iron complexes (NO-Fe(DETC)₂) in the brain. The temporal kinetic of NO release after seizures revealed a rise in NO synthesis during the initial 12 h. Subsequently, a sharp decline occurred, returning to baseline 96 h after pilocarpine injection. Notably, our research suggests that the level of NO synthesis does not interfere with the severity of the epileptic seizures that occur. In light of this, we propose that the nitrergic system is quickly activated in the epileptic brain as a compensatory mechanism of the central nervous system. However, under usual conditions, this activation is insufficient to effectively attenuate seizures.

癫痫是一种病理生理学疾病，其表型多种多样。因此，要理解癫痫发作的内在机制，就必须超越以经典兴奋性和抑制性神经递质系统失衡为重点的简单模式。一氧化氮（NO）是一种非经典的多功能气体神经递质，有可能对癫痫反应性产生深远影响。遗憾的是，关于一氧化氮在癫痫病理生理学中的参与，众多研究都没有给出明确的答案。我们的研究目的是在实验诱导癫痫发作后，对硝酸纤维素能系统激活的时间动态变化进行描述。给 2 个月大的雄性 Wistar 大鼠注射皮洛卡品诱发癫痫发作。在 6 小时的观察期内，使用改良的拉辛量表持续评估癫痫发作行为的强度。在给药后的 6、12、24、48 或 96 小时内，使用二乙基二硫代氨基甲酸铁络合物（Fe(DETC)2）进行 NO 自旋捕获。电子顺磁共振（EPR）光谱用于量化大脑中的单亚硝基铁复合物（NO-Fe(DETC)2）。癫痫发作后 NO 释放的时间动力学显示，在最初的 12 小时内，NO 合成量上升。随后，NO 合成量急剧下降，在注射皮洛卡品 96 小时后恢复到基线水平。值得注意的是，我们的研究表明，NO 的合成水平与癫痫发作的严重程度无关。有鉴于此，我们认为，作为中枢神经系统的一种补偿机制，能硝酸系统在癫痫患者大脑中被迅速激活。然而，在通常情况下，这种激活不足以有效减轻癫痫发作。

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引用次数: 0

Vocal communication in asocial BTBR mice is more malleable by a ketogenic diet in juveniles than adults 与成年小鼠相比，非社会性 BTBR 小鼠的发声交流更容易通过生酮饮食来改变。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-15 DOI: 10.1016/j.neuroscience.2024.10.001

Deficits in social communication and language development are a hallmark of autism spectrum disorder currently with no effective approaches to reduce the negative impact. Interventional studies using animal models have been very limited in demonstrating improved vocal communication. Autism has been proposed to involve metabolic dysregulation. Ketogenic diet (KD) is a metabolism-based therapy for medically intractable epilepsy, and its applications in other neurological conditions have been increasingly tested. However, how KD would affect vocal communication has not been explored. The BTBR mouse strain is widely used to model asocial phenotypes. They display robust and pronounced deficits in vocalization during social interaction, and have metabolic changes implicated in autism.

We investigated the effects of KD on ultrasonic vocalizations (USVs) in juvenile and adult BTBR mice during male–female social encounters.

After a brief treatment with KD, the number, spectral bandwidth, and much of the temporal structure of USVs were robustly closer to control levels in both juvenile and adult BTBR mice. Composition of call categories and transitioning between individual call subtypes were more effectively altered to more closely align with the control group in juvenile BTBR mice.

Together, our data provide further support to the hypothesis that metabolism-based dietary intervention could modify disease expression, including core symptoms, in autism. Future studies should tease apart the molecular mechanisms of KD’s effects on vocalization.

社交沟通和语言发育障碍是自闭症谱系障碍的一大特征，目前还没有有效的方法来减少其负面影响。使用动物模型进行的干预研究在改善发声交流方面效果非常有限。自闭症被认为与新陈代谢失调有关。生酮饮食（KD）是一种基于新陈代谢的疗法，可用于治疗医学上难治的癫痫，其在其他神经系统疾病中的应用也得到了越来越多的测试。然而，生酮饮食会如何影响发声交流还没有进行过研究。BTBR 小鼠品系被广泛用于模拟非社会表型。它们在社会交往过程中表现出强烈而明显的发声缺陷，并出现与自闭症有关的代谢变化。我们研究了KD对幼年和成年BTBR小鼠在雌雄社交相遇时的超声发声（USVs）的影响。经过短暂的KD处理后，幼年和成年BTBR小鼠的USV数量、频谱带宽和大部分时间结构都明显接近对照组水平。在幼年 BTBR 小鼠中，呼叫类别的组成和各个呼叫亚型之间的转换得到了更有效的改变，从而更接近对照组。总之，我们的数据进一步支持了基于代谢的饮食干预可以改变自闭症疾病表达（包括核心症状）的假设。未来的研究应深入探讨 KD 对发声影响的分子机制。

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引用次数: 0

Unraveling the neuroprotective potential of scalp electroacupuncture in ischemic stroke: A key role for electrical stimulation 揭示头皮电针在缺血性中风中的神经保护潜力：电刺激的关键作用

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-12 DOI: 10.1016/j.neuroscience.2024.10.019

This study aims to explore the neuroprotective effects of scalp Electroacupuncture (EA) on ischemic stroke, with a specific focus on the role of electrical stimulation (ES). Employing a rat model of middle cerebral artery occlusion (MCAO), we used methods such as Triphenyl tetrazolium chloride staining, micro-CT scanning, Enzyme linked immunosorbent assay (ELISA), and immunofluorescence to assess the impacts of EA. We further conducted RNA-seq analysis and in vitro experiments with organotypic brain slices and cerebral organoids to explore the underlying mechanisms. Our research revealed that EA notably reduced cerebral infarct volume and improved regional cerebral blood flow in rats following MCAO. Micro-CT imaging showed improved vascular integrity in EA-treated groups. Histological analyses, including HE staining, indicated reduced brain tissue damage. ELISA demonstrated a decrease in pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, suggesting improved blood–brain barrier function. Immunofluorescence and Western blot analyses revealed that EA treatment significantly inhibited microglial and astrocytic overactivation. RNA-seq analysis of brain tissues highlighted a downregulation of immune pathways and inflammatory responses, confirming the neuroprotective role of EA. This was further corroborated by in vitro experiments using organotypic brain slices and cerebral organoids, which showcased the efficacy of electrical stimulation in reducing neuroinflammation and protecting neuronal cells. The study highlights the potential of scalp EA, particularly its ES component, in treating ischemic stroke. It provides new insights into the mechanisms of EA, emphasizing its efficacy in neuroprotection and modulation of neuroinflammation, and suggests avenues for optimized treatment strategies in stroke therapy.

本研究旨在探讨头皮电针（EA）对缺血性中风的神经保护作用，尤其关注电刺激（ES）的作用。我们采用大脑中动脉闭塞（MCAO）大鼠模型，使用三苯基氯化四氮唑染色、显微 CT 扫描、酶联免疫吸附试验（ELISA）和免疫荧光等方法来评估 EA 的影响。我们进一步进行了RNA-seq分析以及有机脑切片和脑有机体的体外实验，以探索其潜在机制。我们的研究发现，EA能显著减少大鼠MCAO后的脑梗死体积，改善区域脑血流量。显微 CT 成像显示，EA 治疗组的血管完整性有所改善。包括 HE 染色在内的组织学分析表明脑组织损伤减轻。酶联免疫吸附试验表明，促炎细胞因子 TNF-α、IL-1β 和 IL-6 有所减少，表明血脑屏障功能有所改善。免疫荧光和 Western 印迹分析显示，EA 能显著抑制小胶质细胞和星形胶质细胞的过度激活。脑组织的 RNA-seq 分析强调了免疫通路和炎症反应的下调，证实了 EA 的神经保护作用。使用有机脑切片和脑有机体进行的体外实验进一步证实了这一点，这些实验展示了电刺激在减少神经炎症和保护神经细胞方面的功效。该研究强调了头皮 EA（尤其是其 ES 成分）在治疗缺血性中风方面的潜力。它为 EA 的机制提供了新的见解，强调了 EA 在神经保护和神经炎症调节方面的功效，并为中风治疗中的优化治疗策略提出了建议。

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引用次数: 0

Simultaneous EEG recording of cortical tracking of speech and movement kinematics 同步脑电图记录大脑皮层对语音和运动运动学的追踪

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-11 DOI: 10.1016/j.neuroscience.2024.10.013

Rationale: Cortical activity is coupled with streams of sensory stimulation. The coupling with the temporal envelope of heard speech is known as the cortical tracking of speech (CTS), and that with movement kinematics is known as the corticokinematic coupling (CKC). Simultaneous measurement of both couplings is desirable in clinical settings, but it is unknown whether the inherent dual-tasking condition has an impact on CTS or CKC.

Aim

We aim to determine whether and how CTS and CKC levels are affected when recorded simultaneously.

Methods

Twenty-three healthy young adults underwent 64-channel EEG recordings while listening to stories and while performing repetitive finger-tapping movements in 3 conditions: separately (audio- or tapping-only) or simultaneously (audio-tapping). CTS and CKC values were estimated using coherence analysis between each EEG signal and speech temporal envelope (CTS) or finger acceleration (CKC). CTS was also estimated as the reconstruction accuracy of a decoding model.

Results

Across recordings, CTS assessed with reconstruction accuracy was significant in 85 % of the subjects at phrasal frequency (0.5 Hz) and in 68 % at syllabic frequencies (4–8 Hz), and CKC was significant in over 85 % of the subjects at movement frequency and its first harmonic. Comparing CTS and CKC values evaluated in separate recordings to those in simultaneous recordings revealed no significant difference and moderate-to-high levels of correlation.

Conclusion.

Despite the subtle behavioral effects, CTS and CKC are not evidently altered by the dual-task setting inherent to recording them simultaneously and can be evaluated simultaneously using EEG in clinical settings.

理由皮层活动与感觉刺激流相关联。与听到的语音的时间包络的耦合称为皮质语音跟踪（CTS），与运动运动学的耦合称为皮质运动学耦合（CKC）。我们的目的是确定在同时记录时，CTS 和 CKC 水平是否会受到影响，以及会受到怎样的影响。方法23 名健康的年轻人在听故事和做重复性手指敲击动作时接受了 64 通道脑电图记录，记录分为三种情况：分别记录（仅音频或敲击）或同时记录（音频-敲击）。通过分析每个脑电信号与语音时间包络（CTS）或手指加速度（CKC）之间的相干性，估算 CTS 和 CKC 值。结果在所有录音中，85% 的受试者在短语频率（0.5 Hz）和 68% 的受试者在音节频率（4-8 Hz）上用重建准确性评估的 CTS 显著，85% 以上的受试者在运动频率及其第一次谐波上用 CKC 评估的 CTS 显著。结论：尽管存在微妙的行为影响，但同时记录 CTS 和 CKC 的双任务设置并未明显改变 CTS 和 CKC，在临床环境中可使用脑电图同时进行评估。

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引用次数: 0

Neurological effects of carbon quantum dots on zebrafish: A review 碳量子点对斑马鱼神经系统的影响：综述。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-09 DOI: 10.1016/j.neuroscience.2024.10.016

Fluorescent carbon dots have emerged as promising nanomaterials for various applications, including bioimaging, food safety detection and drug delivery. However, their potential impact on neurological systems, especially in-vivo models, remains a critical area of investigation. This review focuses on the neurological effects of carbon dots and carbon quantum dots on zebrafish, an established vertebrate model with a conserved central nervous system. Recent studies have demonstrated the efficient uptake and distribution of carbon dots in zebrafish tissues, with a particular affinity for neural tissues. The intricate neural architecture of zebrafish allows for the precise examination of behavioral changes and neurodevelopmental alterations induced by fluorescent carbon dots. Neurotoxicity assessments reveal both short-term and long-term effects, ranging from immediate behavioral alterations to subtle changes in neuronal morphology. The review discusses potential mechanisms underlying these effects highlights the need for standardized methodologies in assessing neurological outcomes and emphasizes the importance of ethical considerations in nanomaterial research. As the field of nanotechnology continues to advance, a comprehensive understanding of the impact of fluorescent carbon dots on neurological function in zebrafish is crucial for informing safe and sustainable applications in medicine and beyond.

荧光碳点是一种前景广阔的纳米材料，可用于生物成像、食品安全检测和药物输送等多种应用领域。然而，它们对神经系统（尤其是体内模型）的潜在影响仍然是一个关键的研究领域。本综述重点探讨碳点和碳量子点对斑马鱼神经系统的影响，斑马鱼是一种具有保守中枢神经系统的成熟脊椎动物模型。最近的研究表明，碳点在斑马鱼组织中的吸收和分布效率很高，对神经组织尤其亲和。斑马鱼错综复杂的神经结构允许对荧光碳点诱导的行为变化和神经发育改变进行精确检查。神经毒性评估揭示了短期和长期影响，从直接的行为改变到神经元形态的微妙变化。综述讨论了这些影响的潜在机制，强调了评估神经系统结果的标准化方法的必要性，并强调了纳米材料研究中伦理考虑的重要性。随着纳米技术领域的不断进步，全面了解荧光碳点对斑马鱼神经功能的影响对于安全、可持续地应用于医学及其他领域至关重要。

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引用次数: 0

Neuron-glia crosstalk and inflammatory mediators in migraine pathophysiology 偏头痛病理生理学中的神经元-胶质细胞串扰和炎症介质。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-09 DOI: 10.1016/j.neuroscience.2024.10.006

Migraine is a complex neurological disorder with neuroinflammation playing a crucial role in its pathogenesis. This review provides an overview of the neuroinflammation mechanisms in migraine, focusing on both cellular and molecular aspects. At the cellular level, we examine the role of glial cells, including astrocytes, microglia, oligodendrocytes in the central nervous system, and Schwann cells and satellite glial cells in the peripheral nervous system. On the molecular level, we explore the signaling pathways, including IL-1β, TNF-α, IL-6, and non-coding RNAs, that mediate cell interactions or independent actions. Some of the molecular signaling pathways mentioned, such as TNF-α and IL-1β, have been investigated as druggable targets. Recent advancements, such as ^[11C] PBR28-targeted imaging for visualizing astrocyte activation and single-cell sequencing for exploring cellular heterogeneity, represent breakthroughs in understanding the mechanisms of neuroinflammation in migraine. By considering factors for personalized treatments, estrogen and TRPM8 emerge as promising therapeutic targets regarding sexual dimorphism. These advancements may help bridge the gap between preclinical findings and clinical applications, ultimately leading to more precise and personalized options for migraine patients.

偏头痛是一种复杂的神经系统疾病，神经炎症在其发病机制中起着至关重要的作用。本综述概述了偏头痛的神经炎症机制，重点关注细胞和分子两个方面。在细胞层面，我们研究了胶质细胞的作用，包括中枢神经系统中的星形胶质细胞、小胶质细胞和少突胶质细胞，以及周围神经系统中的许旺细胞和卫星胶质细胞。在分子水平上，我们探讨了介导细胞相互作用或独立作用的信号通路，包括 IL-1β、TNF-α、IL-6 和非编码 RNA。提到的一些分子信号通路，如 TNF-α 和 IL-1β，已被研究为药物靶点。最近取得的进展，如用于观察星形胶质细胞活化的[11C] PBR28靶向成像技术和用于探索细胞异质性的单细胞测序技术，代表着在了解偏头痛的神经炎症机制方面取得了突破性进展。考虑到个性化治疗的因素，雌激素和TRPM8成为有关性二态性的有希望的治疗靶点。这些进展可能有助于缩小临床前研究结果与临床应用之间的差距，最终为偏头痛患者提供更精确、更个性化的选择。

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引用次数: 0

Hypercorticosteronemia induces hyperphagia and obesity in human growth hormone transgenic rats 高皮质酮血症会诱发人类生长激素转基因大鼠食欲亢进和肥胖。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-10-09 DOI: 10.1016/j.neuroscience.2024.10.012

Hyperphagia and subsequent obesity are important public health issues due to the associated risks of developing serious diseases. Certain stressors play a major role in the development of hyperphagia. In previous studies, we established a line of human growth hormone transgenic (TG) rats that exhibit hyperphagia and obesity from a young age. We recently demonstrated that voluntary running on a running wheel alleviates hyperphagia in TG rats. Wheel running provides environmental enrichment for rodents and plays a role in relieving stress. These results suggested that stress is the major factor inducing hyperphagia in TG rats. Thus, in the present study, we evaluated activation of the hypothalamus–pituitary–adrenal axis. TG rats showed bilateral enlargement of adrenal glands and hypercorticosteronemia, although their hypothalamic CRH level was comparable to that of wild-type (WT) rats. The ACTH-immunoreactive area was larger and the serum ACTH level in the dark phase was higher in TG rats than in WT rats. Adrenalectomy reduced the food intake of TG rats to a level comparable to that in WT rats, and supplying glucocorticoids recurred hyperphagia in TG rats. These treatments did not affect the food intake of WT rats. Rearing TG rats under group housing prevented hyperphagia and hypercorticosteronemia. These results suggest that glucocorticoids are appetite stimulants, and that TG rats exhibit increased sensitivity to the appetite-stimulating effect of glucocorticoids.

多食症和随后的肥胖症是重要的公共卫生问题，因为它们有可能引发严重的疾病。某些压力因素在多食症的发生中起着重要作用。在以前的研究中，我们建立了一个人类生长激素转基因（TG）大鼠品系，这种大鼠从幼年起就表现出多食和肥胖。我们最近证明，在跑步轮上自主跑步可以缓解 TG 大鼠的多食症状。跑轮为啮齿动物提供了丰富的环境，并在缓解压力方面发挥了作用。这些结果表明，压力是诱发 TG 大鼠多食的主要因素。因此，在本研究中，我们评估了下丘脑-垂体-肾上腺轴的激活情况。尽管 TG 大鼠的下丘脑 CRH 水平与野生型（WT）大鼠相当，但它们表现出双侧肾上腺增大和高皮质酮血症。与 WT 大鼠相比，TG 大鼠的促肾上腺皮质激素免疫反应区更大，暗期血清促肾上腺皮质激素水平更高。肾上腺切除术使TG大鼠的食物摄入量降低到与WT大鼠相当的水平，而糖皮质激素的供应又使TG大鼠的食欲亢进复发。这些处理并不影响 WT 大鼠的食物摄入量。分组饲养 TG 大鼠可防止吞食过多和高皮质酮血症。这些结果表明，糖皮质激素是食欲刺激剂，而TG大鼠对糖皮质激素的食欲刺激作用表现出更高的敏感性。

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引用次数: 0