Neuroscience最新文献_第6页

Exploring the cognitive effects of hearing loss in adult rats: Implications for visuospatial attention, social behavior, and prefrontal neural activity 探索听力损失对成年大鼠认知的影响：对视觉空间注意力、社交行为和前额叶神经活动的影响

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-08 DOI: 10.1016/j.neuroscience.2024.11.010

Mariele Stenzel , Mesbah Alam , Marla Witte , Jonas Jelinek , Nina Armbrecht , Adrian Armstrong , Andrej Kral , Joachim K. Krauss , Rüdiger Land , Kerstin Schwabe , Marie Johne

Age-related hearing loss in humans has been associated with cognitive decline, though the underlying mechanisms remain unknown. We investigated the long-term effects of hearing loss on attention, impulse control, social interaction, and neural activity within medial prefrontal cortex (mPFC) subregions.

Hearing loss was induced in adult rats via intracochlear neomycin injection (n = 13), with non-operated rats as controls (n = 10). Rats were tested for motor activity (open field), coordination (Rotarod), and social interaction (including ultrasonic vocalization, USV) before surgery and at weeks 1, 2, 4, 8, 16, and 24 post-surgery. From week 8 on, rats were trained in the five-choice serial reaction time task (5-CSRTT) to assess visuospatial attention and impulse control. Finally, oscillatory neuronal activity in mPFC subregions was recorded with multielectrode arrays during anesthesia, followed by immunohistological staining for NeuN⁺ and Parvalbumin⁺ cells.

Deafened rats were more active than controls, whereas social interaction and USV were temporarily reduced. They also had difficulties to learn the concept of the 5-CSRTT paradigm and made more incorrect responses. Electrophysiology showed decreased power in theta, alpha, and beta frequency, and enhanced high gamma band in the mPFC in deafened rats, which was most pronounced in the cingulate subregion (Cg1). The number of NeuN⁺ and Parvalbumin⁺ cells, however, did not differ between groups.

The behavioral deficits together with the altered neuronal activity found in the Cg1 subregion of the mPFC in adult deafened rats may be used as an endophenotype to elucidate the mechanisms behind the cognitive decline seen in older patients with hearing loss.

人类与年龄相关的听力损失与认知能力下降有关，但其潜在机制仍不清楚。我们研究了听力损失对注意力、冲动控制、社会交往和内侧前额叶皮质（mPFC）亚区神经活动的长期影响。通过耳蜗内注射新霉素诱导成年大鼠听力损失（n = 13），以未手术大鼠为对照组（n = 10）。在手术前和手术后第 1、2、4、8、16 和 24 周，对大鼠进行了运动活动（空场）、协调（旋转）和社会交往（包括超声发声）测试。从第8周开始，对大鼠进行五选一连续反应时间任务（5-CSRTT）训练，以评估视觉空间注意力和冲动控制能力。最后，在麻醉状态下使用多电极阵列记录 mPFC 亚区域的振荡神经元活动，然后对 NeuN+ 和 Parvalbumin+ 细胞进行免疫组织学染色。聋鼠比对照组更活跃，但社会交往和USV暂时减少。它们也很难学会5-CSRTT范式的概念，并做出更多错误的反应。电生理学研究显示，耳聋大鼠的 mPFC 中θ、α和β频率的功率下降，高γ波段增强，这在扣带回亚区（Cg1）最为明显。然而，NeuN+和Parvalbumin+细胞的数量在不同组间并无差异。在成年耳聋大鼠的 mPFC Cg1 亚区发现的行为缺陷和神经元活动改变可作为一种内表型，用于阐明老年听力损失患者认知能力下降的机制。

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引用次数: 0

Regulation of nerve cells and therapeutic potential in central nervous system injury using microglia-derived exosomes 利用小胶质细胞衍生的外泌体调节神经细胞并治疗中枢神经系统损伤的潜力。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-08 DOI: 10.1016/j.neuroscience.2024.11.011

Dongxiao Lu , Haohan Sun , Hao Fan , Nianlu Li , Yuming Li , Xianyong Yin , Yang Fan , Hao Sun , Shan Wang , Tao Xin

The intercellular communication within the central nervous system (CNS) is of great importance for in maintaining brain function, homeostasis, and CNS regulation. When the equilibrium of CNS is disrupted or injured, microglia are immediately activated and respond to CNS injury. Microglia-derived exosomes are capable of participating in intercellular communication within the CNS by transporting various bioactive substances, including nucleic acids, proteins, lipids, amino acids, and metabolites. Nevertheless, microglia activation is a double-edged sword. Activated microglia can coordinate the neural repair process and, conversely, can amplify tissue injury and impede CNS repair. This work reviewed the roles of exosomes derived from microglia stimulated by different environments (mainly lipopolysaccharide, interleukin-4, and other specific preconditioning) in CNS injury and their possible therapeutic potentials. This work focuses on the regulation of exosomes derived from microglia stimulated by different environments on nerve cells. Meanwhile, we summarized the molecular mechanisms by which the relevant exosomes exert regulatory effects. Exosomes, derived from microglia stimulated by different environments, regulate other nerve cells during the repair of CNS injury, having beneficial or detrimental effects on CNS repair. A comprehensive understanding of the molecular mechanisms underlying their role can provide a robust foundation for the clinical treatment of CNS injury.

中枢神经系统（CNS）内的细胞间通信对维持大脑功能、平衡和中枢神经系统调节非常重要。当中枢神经系统的平衡被打破或受到损伤时，小胶质细胞会立即被激活并对中枢神经系统损伤做出反应。小胶质细胞衍生的外泌体能够通过运输各种生物活性物质（包括核酸、蛋白质、脂质、氨基酸和代谢物）参与中枢神经系统内的细胞间通信。然而，小胶质细胞的激活是一把双刃剑。活化的小胶质细胞可以协调神经修复过程，反之则会扩大组织损伤，阻碍中枢神经系统的修复。本研究综述了小胶质细胞在不同环境（主要是脂多糖、白细胞介素-4和其他特定预处理）刺激下产生的外泌体在中枢神经系统损伤中的作用及其可能的治疗潜力。这项研究的重点是小胶质细胞受不同环境刺激后产生的外泌体对神经细胞的调控。同时，我们总结了相关外泌体发挥调节作用的分子机制。小胶质细胞受不同环境刺激产生的外泌体在中枢神经系统损伤修复过程中会调控其他神经细胞，对中枢神经系统修复产生有利或不利的影响。全面了解其作用的分子机制可为中枢神经系统损伤的临床治疗奠定坚实的基础。

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引用次数: 0

Quantitative assessments of white matter hyperintensities and plasma biomarkers can predict cognitive impairment and cerebral microbleeds in cerebral small vessel disease patients 白质高密度和血浆生物标志物的定量评估可预测脑小血管疾病患者的认知障碍和脑微小出血。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-08 DOI: 10.1016/j.neuroscience.2024.11.014

Zhuo Fang , Xiaohan Chen , Yike Zhao , Xinrui Zhou , Xiao Cai , Jiale Deng , Wenbin Cheng , Wenjing Sun , Jianhua Zhuang , You Yin

The objective of this study is to examine the efficacy of magnetic resonance imaging (MRI) features and peripheral blood biomarkers in assessing cognitive function in patients with cerebral small vessel disease (CSVD). A total of 58 CSVD patients were recruited. Six features of white matter hyperintensities (WMHs) were derived from MRI scans. Additionally, five neurodegenerative biomarkers (Aβ40, Aβ42, t-tau, p-tau181, NfL) and 13 serum inflammatory cytokines (VILIP-1, CCL2, IL-6, IL-18, TNF-α, CX3CL, sTREM-1/2, VEGF, s-RAGE, BNDF, TGF-β1, β-NGF) were quantified. Cognitive assessments were conducted using standardized neuropsychological scales. Spearman analysis revealed that the volumetric characteristics (absolute area, upper area, bottom area, absolute area percentage, upper percentage, and bottom percentage) of WMHs were negatively correlated with performance on all cognitive scale measures except the verbal fluency test (VFT) (r < -0.3, p > 0.05), while they were positively correlated with plasma neurofilament light (NFL) levels (r > 0.4, p < 0.05). Additionally, serum tumor necrosis factor-α (TNF-α) and soluble receptor for advanced glycation end-products (s-RAGE) showed significant correlations with scales of speech function. An integrated model incorporating WMHs features, neurodegenerative biomarkers, and neuroinflammatory markers was developed, demonstrating high predictive accuracy for cognitive impairment with an area under the curve (AUC) of 0.95 (accuracy 0.88, sensitivity 0.87, specificity 0.89). Another integrated model that includes features of WMHs and inflammatory cytokines for predicting cerebral microbleeds (CMBs) achieved an AUC of 0.95 (accuracy 0.88, sensitivity 0.82, specificity 0.92). Our findings suggest that these markers have the potential to be used for the early detection of cognitive decline and CMBs in patients with CSVD.

本研究旨在探讨磁共振成像（MRI）特征和外周血生物标志物在评估脑小血管疾病（CSVD）患者认知功能方面的功效。共招募了 58 名 CSVD 患者。从核磁共振扫描中得出了六种白质高密度（WMH）特征。此外，还量化了五种神经退行性生物标记物（Aβ40、Aβ42、t-tau、p-tau181、NfL）和 13 种血清炎性细胞因子（VILIP-1、CCL2、IL-6、IL-18、TNF-α、CX3CL、sTREM-1/2、VEGF、s-RAGE、BNDF、TGF-β1、β-NGF）。认知评估采用标准化的神经心理学量表进行。斯皮尔曼分析表明，WMHs的体积特征（绝对面积、上部面积、底部面积、绝对面积百分比、上部百分比和底部百分比）与除语言流畅性测试（VFT）外的所有认知量表测试成绩呈负相关（r 0.05），而与血浆神经丝光（NFL）水平呈正相关（r > 0.4，p > 0.05）。

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引用次数: 0

Chronic stress disturbed the metabolism of homocysteine in mouse hippocampus and prefrontal cortex 慢性应激干扰了小鼠海马和前额叶皮层中同型半胱氨酸的代谢。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-07 DOI: 10.1016/j.neuroscience.2024.11.006

Cong Xue , Bing Liu , Yun Zhao , Xue Wang , Zhao-Wei Sun , Fang Xie , Ling-Jia Qian

Stress is an independent risk factor for cognitive impairment, with elevated plasma homocysteine (HCY) levels playing a crucial role in stress-induced cognitive decline. While the rise in plasma HCY levels is linked to abnormal peripheral catabolism, the impact of stress on HCY catabolism in the brain remains unclear. This study investigated the effect of stress on HCY metabolism in the brain by analyzing HCY and its metabolic enzymes in the hippocampus and prefrontal cortex. The results showed a significant decrease in enzymes MS (methionine-synthase), CBS (cystathionineβ-synthase), and CSE (cystathionine γ-lyase) in these brain regions of mice subjected to 3 weeks of restraint stress, leading to HCY accumulation. Additionally, the enzyme MTHFR (methylenetetrahydrofolate reductase) remained unchanged. Immunofluorescence double-labeling revealed the downregulation of HCY metabolic enzymes in neurons of stressed mice. The transcription factor KLF4 (Kruppel-like factor 4), known for its inhibitory role, increased after stress or glucocorticoid treatment and suppressed the expression of MS, CBS, and CSE, contributing to elevated HCY levels in the brain. These findings offer new insights into the impairment of HCY catabolism in the stressed brain, suggesting that the downregulation of HCY metabolic enzymes may underlie HCY accumulation and exacerbate stress-induced cognitive dysfunction.

压力是认知障碍的一个独立风险因素，而血浆同型半胱氨酸（HCY）水平的升高在压力导致的认知能力下降中起着至关重要的作用。虽然血浆中 HCY 水平的升高与外周分解代谢异常有关，但压力对大脑中 HCY 分解代谢的影响仍不清楚。本研究通过分析海马和前额叶皮层中的HCY及其代谢酶，研究了压力对大脑中HCY代谢的影响。结果表明，在受到3周束缚应激的小鼠的这些脑区，酶MS（蛋氨酸合成酶）、CBS（胱硫醚β合成酶）和CSE（胱硫醚γ-赖氨酸酶）明显减少，导致HCY积累。此外，MTHFR（亚甲基四氢叶酸还原酶）也没有发生变化。免疫荧光双标记显示应激小鼠神经元中的 HCY 代谢酶下调。转录因子 KLF4（Kruppel-likefactor4）以其抑制作用而著称，它在应激或糖皮质激素治疗后增加，并抑制了 MS、CBS 和 CSE 的表达，导致大脑中 HCY 水平升高。这些发现为了解应激状态下大脑中HCY分解代谢的障碍提供了新的视角，表明HCY代谢酶的下调可能是HCY积累和加剧应激诱导的认知功能障碍的基础。

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引用次数: 0

Scalp acupuncture alleviates remote hippocampal damage in MCAO rats by inhibiting neuroinflammation: A TMT-based proteomics analysis 头皮针通过抑制神经炎症减轻MCAO大鼠海马远端损伤：基于TMT的蛋白质组学分析

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-07 DOI: 10.1016/j.neuroscience.2024.11.008

Huacong Liu , Weijia Huang , Qian Ding , Yumeng Huang , Zhenyi Lai , Zhaoxing Liu , Shaoxiong Li , Xinyi Peng , Zhenhong Wu , Liangbin Deng , Yong Huang , Junqi Chen

While mounting evidence suggests that scalp acupuncture (SA) may be effective in alleviating neurological deficits in patients with acute ischemic stroke (IS), its effect on remote hippocampal damage in acute IS and the underlying mechanisms remain elusive. Thus, proteomics analysis was conducted to identify potential targets of SA therapy in acute IS. SA significantly reduced cerebral infarct volume and attenuated neuronal damage in the ischemic penumbra and hippocampus, as well as alleviated neurological deficits in rats with middle cerebral artery occlusion (MCAO). Moreover, 74 upregulated and 50 downregulated proteins were identified in the MCAO group compared to the sham group, whilst 52 up-regulated and 50 down-regulated proteins were identified in the SA group compared to the MCAO group. Bioinformatics analysis indicated that SA may exert neuroprotective effects by modulating the acute inflammatory response and microglial activation. Additionally, SA down-regulated the expression levels of Iba-1, TNF-α, IL-1β, and IL-6, while up-regulating those of IL-4 and IL-10. Likewise, it downregulated the expression levels of three key proteins identified via proteomics analysis (Kng1, Brd9, and Magl) that may mediate the anti-inflammatory effects of SA. Overall, these results indicate that SA attenuates neuronal damage in the hippocampus and ischemic penumbra and ameliorates neurological deficits. Proteomic analysis suggested that this effect is related to the modulation of the acute inflammatory response. SA attenuated remote hippocampal damage after IS by inhibiting microglia activation and neuroinflammation. Lastly, Kng1, Brd9, and Magl were identified as potential targets that mediate the anti-inflammatory effects of SA.

越来越多的证据表明，头皮针灸（SA）可有效缓解急性缺血性脑卒中（IS）患者的神经功能缺损，但它对急性IS患者海马远端损伤的影响及其潜在机制仍难以捉摸。因此，我们进行了蛋白质组学分析，以确定 SA 治疗急性 IS 的潜在靶点。在大脑中动脉闭塞（MCAO）大鼠中，SA能明显缩小脑梗死体积，减轻缺血半影和海马的神经元损伤，并缓解神经功能缺损。此外，与假体组相比，MCAO 组发现了 74 个上调蛋白和 50 个下调蛋白，而与 MCAO 组相比，SA 组发现了 52 个上调蛋白和 50 个下调蛋白。生物信息学分析表明，SA 可通过调节急性炎症反应和小胶质细胞活化发挥神经保护作用。此外，SA 下调了 Iba-1、TNF-α、IL-1β 和 IL-6 的表达水平，同时上调了 IL-4 和 IL-10 的表达水平。同样，它还下调了通过蛋白质组学分析确定的三种关键蛋白（Kng1、Brd9 和 Magl）的表达水平，这三种蛋白可能介导了 SA 的抗炎作用。总之，这些结果表明南澳大利亚能减轻海马和缺血半影区的神经元损伤，改善神经功能缺损。蛋白质组分析表明，这种效应与急性炎症反应的调节有关。SA通过抑制小胶质细胞活化和神经炎症减轻了IS后的远端海马损伤。最后，Kng1、Brd9 和 Magl 被确定为介导 SA 抗炎作用的潜在靶点。

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引用次数: 0

Neuronal regeneration in the area postrema of adult mouse medulla oblongata following glutamate-induced neuronal elimination 谷氨酸诱导神经元消亡后成年小鼠延髓后区的神经元再生

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-07 DOI: 10.1016/j.neuroscience.2024.11.009

Rena Fujii , Yuri Nambu , Nitin Sawant Shirikant , Eriko Furube , Mitsuhiro Morita , Ryoichi Yoshimura , Seiji Miyata

Neural stem cells and/or progenitor cells (NSCs/NPCs) in the subventricular and subgranular zones of the adult mammal forebrain generate new neurons and are involved in partial repair after injury. Recently, NSCs/NPCs were identified in the area postrema (AP) of the medulla oblongata of the hindbrain. In this study, we used the properties of fenestrate capillaries to observe specific neuronal elimination in the AP of adult mice and investigated subsequent neuronal regeneration by neurogenesis. Subcutaneous administration of monosodium glutamate (MSG) induced prominent Fos expression in HuC/D⁺ neurons in the AP 2 h after administration. MSG administration caused a marked decrease in HuC/D⁺ neuronal density by neuronal death 3 to 21 days after administration, which recovered to the control level 35 days later. After MSG administration, the density of TUNEL⁺ dying neurons and phagocytic microglia surrounding or engulfing neurons increased. Within 7 days of MSG administration, the number of BrdU⁺　Sox2⁺ and BrdU⁺ Math1⁺ cells increased markedly, and at least the BrdU⁺ Math1⁺ cells similarly increased for the next following 7 days. A remarkable number of HuC/D⁺ neurons with BrdU⁺ nuclei were observed 35 days after MSG administration. This study reveals that neurogenesis occurs in the AP of adult mice, recovering and maintaining normal neuronal density after neuronal death.

成年哺乳动物前脑室下区和粒下区的神经干细胞和/或祖细胞（NSCs/NPCs）可产生新的神经元，并参与损伤后的部分修复。最近，我们在后脑延髓后区（AP）发现了 NSCs/NPCs。在这项研究中，我们利用栅栏状毛细血管的特性观察了成年小鼠 AP 中特定神经元的消除，并研究了神经元随后通过神经发生再生的情况。皮下注射谷氨酸钠（MSG）2小时后，AP中的HuC/D+神经元会出现明显的Fos表达。MSG给药后3至21天，神经元死亡导致HuC/D+神经元密度显著下降，35天后恢复到对照组水平。服用味精后，TUNEL+濒死神经元和围绕或吞噬神经元的吞噬小胶质细胞的密度增加。在服用 MSG 的 7 天内，BrdU+ Sox2+ 和 BrdU+ Math1+ 细胞的数量明显增加，至少 BrdU+ Math1+ 细胞的数量在接下来的 7 天内也同样增加。施用 MSG 35 天后，观察到大量带有 BrdU+ 核的 HuC/D+ 神经元。这项研究揭示了成年小鼠AP中发生的神经发生，可在神经元死亡后恢复并维持正常的神经元密度。

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引用次数: 0

A chloro substituted organoselenium mitigates stress-associated memory impairment and hippocampal glutamatergic function in a repeated Forced Swim Stress Model 在重复强迫游泳应激模型中，一种氯代有机硒可减轻应激相关记忆损伤和海马谷氨酸能功能。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-07 DOI: 10.1016/j.neuroscience.2024.11.007

Vanessa A. Zborowski, Carolina C. Martins, Luiza S. Marques, Suélen O. Heck, Cristina W. Nogueira

Stress is triggered by a threatening event that alters the regulation of emotion, behavior, and cognition. The effects of stress on memory in animal models are well-documented. Firstly, this study aimed to determine whether the repeated forced swim stress (FSS) protocol induces memory impairment comparable to single prolonged stress (SPS) in the Y-maze test. The second objective was to evaluate whether (p-ClPhSe)₂ pretreatment mitigates stress-associated memory impairment and hippocampal glutamatergic neurotransmission in FSS-exposed mice. Mice subjected to FSS and SPS protocols reduced time spent in the novel arm of the Y-maze test compared to the control group, with no observed changes in locomotor or exploratory behavior. (p-ClPhSe)₂ was administered to mice at a dose of 5 mg/kg, 30 min before the first forced swimming session on days 1 and 2. Mice underwent a Y-maze test, after which they were euthanized, and hippocampal samples were collected. (p-ClPhSe)₂ pretreatment protected against the reduction in time spent in the novel arm by mice subjected to FSS. Repeated FSS exposure increased hippocampal protein levels of NMDAR subunits 2A, 2B, and EAAT1 compared to controls. (p-ClPhSe)₂ pretreatment prevented this increase. In conclusion, (p-ClPhSe)₂ mitigated stress-induced memory impairment in FSS-exposed mice, normalizing hippocampal NMDAR 2A, 2B, and EAAT1 protein levels.

压力是由威胁事件引发的，它会改变情绪、行为和认知的调节。在动物模型中，应激对记忆的影响已得到充分证实。首先，本研究旨在确定在Y迷宫试验中，重复强迫游泳应激（FSS）方案是否会诱发与单次延长应激（SPS）相当的记忆损伤。第二个目的是评估（p-ClPhSe）2预处理是否能减轻应激相关的记忆损伤，以及应激小鼠海马谷氨酸能神经递质的损伤。与对照组相比，接受 FSS 和 SPS 方案的小鼠在 Y 型迷宫测试的新奇臂中花费的时间减少了，但运动或探索行为没有发生变化。(在第 1 天和第 2 天第一次强迫游泳前 30 分钟给小鼠注射 5 毫克/千克剂量的（p-ClPhSe）2。小鼠接受 Y 型迷宫测试，之后安乐死，并采集海马样本。(p-ClPhSe）2预处理可防止小鼠在FSS作用下在新手臂上花费的时间减少。与对照组相比，重复暴露于FSS会增加NMDAR亚基2A、2B和EAAT1的海马蛋白水平。(p-ClPhSe)2 预处理可防止这种增加。总之，（p-ClPhSe）2 可减轻应激诱导的 FSS 暴露小鼠记忆损伤，使海马 NMDAR 2A、2B 和 EAAT1 蛋白水平恢复正常。

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引用次数: 0

Hand and foot overestimation in visually impaired human adults 视障成人的手脚高估。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-07 DOI: 10.1016/j.neuroscience.2024.10.055

Lara A. Coelho , Claudia L.R. Gonzalez , Carolina Tammurello , Claudio Campus , Monica Gori

Previous research has shown that visual impairment results in reduced audio, tactile and proprioceptive ability. One hypothesis is that these issues arise from inaccurate body representations. Few studies have investigated metric body representations in a visually impaired population. We designed an ecologically valid behavioural task in which visually impaired adults haptically explored various sized gloves or shoes. They were asked to indicate if they perceived each clothing item as bigger than the size of their hand or foot. In the post-hoc analyses we fit psychometric curves to the data to extract the point of subjective equality. We then compared the results to age/sex matched controls. We hypothesized the blind participants body representations should be more distorted. Because previous research has shown that females are more likely to overestimate body size, we predicted sex differences in the sighted participants. However, because blind adults have no exposure to visual ideals of body size, we predicted that there would be no sex differences. Our results showed that blind participants overestimated their hands and feet to a similar degree. Sighted controls overestimated their hands significantly more than their feet. Taken together, our results partially support our hypothesis and suggest that visual deprivation, even for short periods result in hand size overestimation.

以往的研究表明，视觉障碍会导致听觉、触觉和本体感觉能力下降。一个假设是，这些问题是由不准确的身体表征引起的。很少有研究对视障人群的度量身体表征进行调查。我们设计了一项生态学上有效的行为任务，让视障成年人触觉探索各种尺寸的手套或鞋子。我们要求他们指出是否认为每件衣服都比他们的手或脚的尺寸大。在事后分析中，我们对数据进行了心理测量曲线拟合，以提取主观相等点。然后，我们将结果与年龄/性别匹配的对照组进行比较。我们假设盲人参与者的身体表征应该更加扭曲。由于之前的研究表明女性更容易高估身体尺寸，因此我们预测视力正常的参与者会出现性别差异。然而，由于成年盲人没有接触过身体尺寸的视觉理想，我们预测不会出现性别差异。我们的结果显示，盲人参与者高估自己手脚的程度相似。视力正常的对照组高估手的程度明显高于高估脚的程度。综上所述，我们的结果部分支持了我们的假设，并表明视觉剥夺，即使是短时间的视觉剥夺，也会导致手的尺寸被高估。

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引用次数: 0

Perinatal anoxia associated with sensorimotor restriction causes muscle atrophy and microglial activation: Meta-analysis of preclinical studies with implications for cerebral palsy 与感觉运动限制相关的围产期缺氧会导致肌肉萎缩和小胶质细胞活化：临床前研究的元分析及其对脑瘫的影响。

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-06 DOI: 10.1016/j.neuroscience.2024.10.056

Glayciele Leandro de Albuquerque , Vanessa da Silva Souza , Caio Matheus Santos da Silva Calado , Marcos Antônio da Silva Araújo , Lucas Rafael da Silva Fraga , Diego Bulcão Visco , Raul Manhães-de-Castro , Ana Elisa Toscano

Several experimental cerebral palsy models have been created to investigate cellular and molecular mechanisms involved in this condition and develop new therapeutic strategies. The model that has come closest to a motor phenotype similar to cerebral palsy is the one that combines perinatal anoxia with hindlimb sensorimotor restriction, as it induces visible changes at the peripheral and central levels. This systematic review with meta-analysis presents the impact of the cerebral palsy model that associates perinatal anoxia with hindlimb sensorimotor restriction on the nervous, muscular and skeletal systems. Studies with perinatal anoxia associated with sensorimotor restriction and which evaluated outcomes related to skeletal, muscle, or nervous tissue were recovered from the databases: Embase, PubMed, Scopus, and Web of Science. The methodological and quantitative assessment was performed after eligibility screening (PROSPERO - ID: CRD42023477770). After screening of 4,641 articles, 21 studies with a moderate quality of evidence were chosen to be included in this review and 11 articles were included in the meta-analysis. The results of the meta-analysis reported a significant reduction in the media area of the soleus muscle fibers, increased number of glia cells and glia/neuron index in the somatosensory cortex, increased microglial activation in the hippocampus, and no changes in the corpus callosum thickness or neuron cells. The combination of perinatal anoxia and sensorimotor restriction entails muscle deficits and excessive activation of glial cells in brain areas. These results contribute to a methodological refinement of cerebral palsy models and favor new studies proposed for methodological elucidation in animal experimentation.

为了研究与脑瘫有关的细胞和分子机制并开发新的治疗策略，人们创建了多种实验性脑瘫模型。最接近与脑瘫相似的运动表型的模型是将围产期缺氧与后肢感觉运动受限相结合的模型，因为它能诱导外周和中枢水平的明显变化。本系统综述和荟萃分析介绍了脑瘫模型对神经、肌肉和骨骼系统的影响，该模型将围产期缺氧与后肢感觉运动受限联系在一起。从数据库中检索了围产期缺氧与感觉运动受限相关的研究，这些研究评估了与骨骼、肌肉或神经组织相关的结果：Embase、PubMed、Scopus 和 Web of Science。经过资格筛选（PROSPERO - ID：CRD42023477770）后，进行了方法学和定量评估。在对 4,641 篇文章进行筛选后，21 篇证据质量中等的研究被纳入本综述，11 篇文章被纳入荟萃分析。荟萃分析的结果表明，比目鱼肌纤维的介质面积显著减少，躯体感觉皮层的胶质细胞数量和胶质细胞/神经元指数增加，海马的小胶质细胞激活增加，而胼胝体厚度和神经元细胞没有变化。围产期缺氧和感觉运动限制的结合会导致肌肉缺陷和脑区神经胶质细胞的过度激活。这些结果有助于完善脑瘫模型的研究方法，并有利于在动物实验中提出新的研究方法。

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引用次数: 0

Dietary regulation of silent synapses in the dorsolateral striatum 背外侧纹状体无声突触的饮食调节

IF 2.9 3区医学 Q2 NEUROSCIENCES

Neuroscience

Pub Date : 2024-11-05 DOI: 10.1016/j.neuroscience.2024.11.005

Allison M. Meyers , Federico G. Gnazzo , Eddy D. Barrera , Tikva Nabatian , Larry Chan , Jeff A. Beeler

Obesity and drugs of abuse share overlapping neural circuits and behaviors. Silent synapses are transient synapses that are important for remodeling brain circuits. They are prevalent during early development but largely disappear by adulthood. Drugs of abuse increase silent synapses during adulthood and may facilitate reorganizing brain circuits around drug-related experience, facilitating addiction and contributing to relapse during treatment and abstinence. Whether obesity causes alterations in the expression of silent synapses in a manner similar to drugs of abuse has not been examined. Using a dietary-induced obesity paradigm, mice that chronically consumed high fat diet (HFD) exhibited increased silent synapses in both direct and indirect pathway medium spiny neurons in the dorsolateral striatum. Both the time of onset of increased silent synapses and their normalization upon discontinuation of HFD occurs on an extended time scale compared to drugs of abuse. These data demonstrate that chronic consumption of HFD, like drugs of abuse, can alter mechanisms of circuit plasticity likely facilitating neural reorganization analogous to drugs of abuse.

肥胖症和滥用药物有着重叠的神经回路和行为。沉默突触是瞬时突触，对重塑大脑回路非常重要。它们在早期发育过程中普遍存在，但在成年后基本消失。滥用药物会增加成年期的沉默突触，并可能促进围绕药物相关经验的大脑回路重组，从而促进成瘾，并导致治疗和戒毒期间的复发。肥胖是否会以类似于滥用药物的方式导致无声突触表达的改变，目前尚未进行研究。通过饮食诱导肥胖范例，长期摄入高脂肪饮食（HFD）的小鼠表现出背侧纹状体中直接和间接通路中刺神经元的沉默突触增加。与滥用药物相比，无声突触增加的发生时间和停用高脂饮食后其恢复正常的时间都较长。这些数据表明，与滥用药物一样，长期服用高频分解膳食纤维也会改变回路可塑性机制，从而促进类似于滥用药物的神经重组。

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引用次数: 0