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Astaxanthin protects cognitive function of vascular dementia. 虾青素保护血管性痴呆的认知功能。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-11-18 DOI: 10.1186/s12993-020-00172-8
Ningwei Zhu, Xiao Liang, Ming Zhang, Xiaolan Yin, Hui Yang, Yajun Zhi, Guizhen Ying, Jialing Zou, Lei Chen, Xiaokun Yao, Hongwei Li

Objective: The purpose of this study was to evaluate the effect of astaxanthin (AST) on cognition function, inflammatory response and oxidative stress in vascular dementia (VD) mice.

Method: VD mice model was established by left unilateral common carotid arteries occlusion (LUCCAO). Following LUCCAO, AST was intragastrically administered for 30 days. Object recognition test and morris water maze test were used to evaluate cognitive function. Hematoxylin and eosin staining was performed to observe the hippocampal neuron structure. Enzyme-linked immunosorbent assay kit and bicinchoninic acid kit were respectively adopted to measure IL-1β and IL-4 protein expression and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in hippocampus and prefrontal cortex.

Results: AST improved the discrimination ability of VD mice. The escape latency and path length of VD mice treated with AST were dramatically reduced. Besides, AST 200 mg/kg enhanced crossing platform time and the number of times crossing the platform quadrant, and alleviated the morphological impairment in VD mice. Moreover, we found that AST inhibited IL-1β expression and MDA content, whereas promoted IL-4 expression and SOD activity in a dose-dependent manner.

Conclusion: AST could improve cognitive impairment and hippocampal neurons in VD mice, which may be related to suppression of inflammatory response and oxidative stress.

目的:探讨虾青素(AST)对血管性痴呆(VD)小鼠认知功能、炎症反应和氧化应激的影响。方法:建立左单侧颈总动脉闭塞(LUCCAO)小鼠VD模型。LUCCAO后,AST灌胃30 d。采用物体识别测验和morris水迷宫测验评价认知功能。采用苏木精和伊红染色观察海马神经元结构。采用酶联免疫吸附测定试剂盒和比辛胆酸测定试剂盒分别测定海马和前额叶皮层组织中IL-1β、IL-4蛋白表达及超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果:AST提高了VD小鼠的识别能力。AST治疗后VD小鼠的逃逸潜伏期和路径长度明显缩短。此外,AST 200 mg/kg可增加VD小鼠穿越平台的时间和穿越平台象限的次数,并可减轻形态学损伤。此外,我们发现AST抑制IL-1β表达和MDA含量,而促进IL-4表达和SOD活性呈剂量依赖性。结论:AST可改善VD小鼠的认知功能障碍和海马神经元,其机制可能与抑制炎症反应和氧化应激有关。
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引用次数: 12
Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats. 在鱼藤酮治疗的大鼠中,强迫运动激活纹状体中的NrF2通路,改善帕金森病的运动和行为表现。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-11-06 DOI: 10.1186/s12993-020-00171-9
Dina M Monir, Motamed E Mahmoud, Omyma G Ahmed, Ibrahim F Rehan, Amany Abdelrahman

Background: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive loss of nigrostriatal dopaminergic neurons leading to dopamine depletion and problems of movement, emotions, and cognition. While the pathogenesis of PD is not clear, damage of dopaminergic neurons by oxygen-derived free radicals is considered an important contributing mechanism. This study aimed to evaluate the role of treadmill exercise in male Wister rats as a single treatment and as an aid-therapy with L-dopa for rotenone-induced PD. To study the role of the Nrf2- ARE pathway as a mechanism involved in exercise-associated improvement in rotenone-induced PD in rats.

Method: Animals were divided into 5 groups, (Control, rotenone, rotenoneexercise, rotenoneL-dopa, and rotenoneexerciseL-dopa (combination)groups). After the PD induction, rats in the rotenoneexercise and combination groups were daily treadmill exercised for 4 weeks.

Results: Treadmill exercise significantly improved behavioral and motor aspects of rotenone-induced PD. When treadmill exercise was introduced as a single intervention, it amended most behavioral aspects of PD, gait fully corrected, short-term memory, and motor coordination. Where L-dopa corrected locomotor activity and motor coordination but failed to improve short-term memory and only partially corrected the gait of rotenone-treated rats. When treadmill exercise was combined with L-dopa, all features of PD were corrected. It was found that exercise upregulated some of its associative genes to Nrf2 pathways such as TFAM, Nrf2 and NQO.1 mRNA expression.

Conclusion: This study suggests that forced exercise improved parkinsonian like features by activating the Nrf2 pathway.

背景:帕金森病(PD)是一种常见的神经退行性疾病,其特征是黑质纹状体多巴胺能神经元的进行性丧失,导致多巴胺消耗和运动、情绪和认知问题。虽然PD的发病机制尚不清楚,但氧源性自由基对多巴胺能神经元的损伤被认为是一个重要的机制。本研究旨在评估跑步机运动在雄性Wister大鼠中作为单一治疗和左旋多巴辅助治疗鱼藤酮诱导的PD的作用。研究Nrf2- ARE通路在鱼藤酮诱导的大鼠帕金森病运动相关改善中的作用。方法:将动物分为5组,分别为对照组、鱼藤酮组、鱼藤酮运动组、鱼藤酮左旋多巴组和鱼藤酮运动左旋多巴(联合)组。PD诱导后,鱼藤酮运动组和联合组大鼠每天在跑步机上运动4周。结果:跑步机运动显著改善鱼藤酮诱导PD的行为和运动方面。当跑步机运动作为单一干预引入时,它改善了PD的大多数行为方面,步态完全纠正,短期记忆和运动协调。左旋多巴纠正了运动活动和运动协调,但未能改善短期记忆,仅部分纠正鱼藤酮治疗大鼠的步态。当跑步机运动与左旋多巴联合使用时,PD的所有特征都得到了纠正。结果发现,运动上调了部分与Nrf2通路相关的基因,如TFAM、Nrf2和nq01 mRNA的表达。结论:本研究表明,强迫运动通过激活Nrf2通路改善帕金森样特征。
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引用次数: 8
Behavioral and Brain Functions at 15. 15岁的行为和大脑功能。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-10-23 DOI: 10.1186/s12993-020-00170-w
Wim E Crusio
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引用次数: 0
Effect of Curcuma zedoaria hydro-alcoholic extract on learning, memory deficits and oxidative damage of brain tissue following seizures induced by pentylenetetrazole in rat. 莪术水酒精提取物对戊四唑致癫痫大鼠学习记忆缺损及脑组织氧化损伤的影响。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-10-06 DOI: 10.1186/s12993-020-00169-3
Touran Mahmoudi, Zahra Lorigooini, Mahmoud Rafieian-Kopaei, Mehran Arabi, Zahra Rabiei, Elham Bijad, Sedigheh Kazemi

Background: Previous studies have shown that seizures can cause cognitive disorders. On the other hand, the Curcuma zedoaria (CZ) has beneficial effects on the nervous system. However, there is little information on the possible effects of the CZ extract on seizures. The aim of this study was to investigate the possible effects of CZ extract on cognitive impairment and oxidative stress induced by epilepsy in rats.

Methods: Rats were randomly divided into different groups. In all rats (except the sham group), kindling was performed by intraperitoneal injection of pentylenetetrazol (PTZ) at a dose of 35 mg/kg every 48 h for 14 days. Positive group received 2 mg/kg diazepam + PTZ; treatment groups received 100, 200 or 400 mg/kg CZ extract + PTZ; and one group received 0.5 mg/kg flumazenil and CZ extract + PTZ. Shuttle box and Morris Water Maze tests were used to measure memory and learning. On the last day of treatments PTZ injection was at dose of 60 mg/kg, tonic seizure threshold and mortality rate were recorded in each group. After deep anesthesia, blood was drawn from the rats' hearts and the hippocampus of all rats was removed.

Results: Statistical analysis of the data showed that the CZ extract significantly increased the tonic seizure threshold and reduced the pentylenetetrazol-induced mortality and the extract dose of 400 mg/kg was selected as the most effective dose compared to the other doses. It was also found that flumazenil (a GABAA receptor antagonist) reduced the tonic seizure threshold compared to the effective dose of the extract. The results of shuttle box and Morris water maze behavioral tests showed that memory and learning decreased in the negative control group and the CZ extract treatment improved memory and learning in rats. The CZ extract also increased antioxidant capacity, decreased MDA and NO in the brain and serum of pre-treated groups in compared to the negative control group.

Conclusion: It is concluded that the CZ extract has beneficial effects on learning and memory impairment in PTZ-induced epilepsy model, which has been associated with antioxidant effects in the brain or possibly exerts its effects through the GABAergic system.

背景:以往的研究表明癫痫发作可引起认知障碍。另一方面,莪术(Curcuma zedoaria)对神经系统有益。然而,关于CZ提取物对癫痫发作的可能影响的信息很少。本研究旨在探讨CZ提取物对癫痫大鼠认知功能障碍和氧化应激的影响。方法:将大鼠随机分为不同组。除假手术组外,所有大鼠均通过腹腔注射戊四唑(PTZ)进行点火,剂量为35 mg/kg / 48 h,连续14天。阳性组患者给予地西泮2 mg/kg + PTZ;治疗组分别给予100、200、400 mg/kg CZ提取物+ PTZ;1组给予氟马西尼加CZ提取物+ PTZ 0.5 mg/kg。穿梭箱和莫里斯水迷宫测试用于测量记忆和学习。在治疗的最后一天,PTZ注射剂量为60 mg/kg,记录各组强直性癫痫发作阈值和死亡率。深度麻醉后,从大鼠心脏抽血,并去除所有大鼠的海马体。结果:数据统计分析显示,CZ提取物显著提高强直性癫痫发作阈值,降低戊四唑致病死率,与其他剂量相比,选择400mg /kg提取物为最有效剂量。与有效剂量的提取物相比,氟马西尼(一种GABAA受体拮抗剂)降低了强直性癫痫发作阈值。穿梭箱和Morris水迷宫行为测试结果显示,阴性对照组大鼠的记忆和学习能力下降,CZ提取物处理大鼠的记忆和学习能力提高。与阴性对照组相比,CZ提取物提高了预处理组大鼠脑和血清的抗氧化能力,降低了MDA和NO。结论:CZ提取物对ptz诱导的癫痫模型的学习记忆障碍有一定的改善作用,其作用机制可能与脑内抗氧化作用有关,或可能通过gaba能系统发挥作用。
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引用次数: 11
Excitability, synaptic balance, and addiction: The homeostatic dynamics of ionotropic glutamatergic receptors in VTA after cocaine exposure. 兴奋性、突触平衡和成瘾:暴露于可卡因后 VTA 中离子型谷氨酸能受体的平衡动态。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-06-11 DOI: 10.1186/s12993-020-00168-4
Thiago C Moulin, Helgi B Schiöth

Glutamatergic AMPA and NMDA receptors in the ventral tegmental area (VTA) are central for cocaine first exposure and posterior craving maintenance. However, the exact rules that coordinate the synaptic dynamics of these receptors in dopaminergic VTA neurons and behavioral outcomes are poorly understood. Additionally, synaptic homeostatic plasticity is present in response to chronic excitability changes in neuronal circuits, adjusting the strength of synapses to stabilize the firing rate. Despite having correspondent mechanisms, little is known about the relationship between continuous cocaine exposure and homeostatic synaptic changes in the VTA neurons. Here, we assess the role of homeostatic mechanisms in the neurobiology of cocaine addiction by providing a brief overview of the parallels between cocaine-induced synaptic potentiation and long-term synaptic adaptations, focusing on the regulation of GluA1- and GluN1- containing receptors.

腹侧被盖区(VTA)中的谷氨酸能 AMPA 和 NMDA 受体是首次接触可卡因和之后维持渴求的核心。然而,协调多巴胺能 VTA 神经元中这些受体的突触动态和行为结果的确切规则却鲜为人知。此外,神经元回路中还存在突触同态可塑性,以应对长期的兴奋性变化,调整突触强度以稳定发射率。尽管存在相应的机制,但人们对持续暴露于可卡因与 VTA 神经元中的突触稳态变化之间的关系知之甚少。在这里,我们通过简要概述可卡因诱导的突触电位和长期突触适应之间的相似之处,评估了稳态机制在可卡因成瘾的神经生物学中的作用,重点是含GluA1-和GluN1-受体的调节。
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引用次数: 0
Maternal depression is associated with altered functional connectivity between neural circuits related to visual, auditory, and cognitive processing during stories listening in preschoolers. 母亲抑郁与学龄前儿童听故事时视觉、听觉和认知处理相关神经回路之间功能连接的改变有关。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-04-27 DOI: 10.1186/s12993-020-00167-5
Rola Farah, Paige Greenwood, Johnathan Dudley, John Hutton, Robert T Ammerman, Kieran Phelan, Scott Holland, Tzipi Horowitz-Kraus

Background: Maternal depression can influence the early activity of a mother reading stories to a young child, as depressed mothers are less likely to read to their children. Here, maternal depression association to neurobiological circuitry of narrative comprehension, visualization, and executive functions during stories listening was examined in 21 4-year-old girls and their mothers. Maternal depression scores were collected from the mothers, and functional MRI during stories listening was collected from the children.

Results: Increased maternal depression was related to decreased functional connectivity between visualization and auditory regions and increased connectivity between the right visual cortex and dorsolateral prefrontal cortex in the children.

Conclusions: This study highlights the need to monitor maternal depression and provide interventions to ensure positive linguistic outcomes in children.

背景:母亲抑郁会影响母亲给幼儿读故事的早期活动,因为抑郁的母亲不太可能给孩子读故事。在此,我们研究了 21 名 4 岁女孩及其母亲在听故事时母亲抑郁与叙事理解、可视化和执行功能神经生物学回路的关系。研究收集了母亲的抑郁评分,并收集了孩子听故事时的功能磁共振成像:结果:母亲抑郁程度的增加与儿童视觉和听觉区域之间功能连接的减少以及右侧视觉皮层和背外侧前额叶皮层之间连接的增加有关:本研究强调了监测母亲抑郁情况并提供干预措施以确保儿童获得积极语言成果的必要性。
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引用次数: 0
Naringin provides neuroprotection in CCL2-induced cognition impairment by attenuating neuronal apoptosis in the hippocampus. 柚皮苷对ccl2诱导的认知障碍具有神经保护作用,其机制是减轻海马神经元凋亡。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-02-27 DOI: 10.1186/s12993-020-00166-6
Jiang-Yi Long, Jian-Min Chen, Yuan-Jun Liao, Yi-Jun Zhou, Bing-Yu Liang, Yan Zhou

Background: Chemokine C-C motif ligand 2 (CCL2) is one of the most widely recognised proinflammatory chemokines in cognitive disorders. Currently, CCL2-targeting drugs are extremely limited. Thus, this study aimed to explore the neuroprotection afforded by naringin in CCL2-induced cognitive impairment in rats.

Methods: Before the CCL2 intra-hippocampal injection, rats were treated with naringin for 3 consecutive days via intraperitoneal injection. Two days post-surgery, the Morris water maze (MWM) and novel object recognition (NORT) tests were performed to detect spatial learning and memory and object cognition, respectively. Nissl staining and dUTP nick-end labelling (TUNEL) staining were performed to assess histopathological changes in the hippocampus. Commercial kits were used to measure the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA). Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine the relative mRNA expression of interleukin 1β, (IL-1β), interleukin 6 (IL-6), glutamate/aspartate transporter (GLAST), glutamate transporter-1 (GLT-1), phosphate-activated glutaminase (PAG), cysteine aspartic acid-specific protease 8 (caspase-8), cysteine aspartic acid-specific protease 3 (caspase-3), cell lymphoma/leukaemia-2 (Bcl-2), and Bcl-2 associated X protein (Bax).

Results: In the MWM, the average escape latency and average swimming distance were significantly reduced and the crossing times were increased in the naringin-treated groups, compared with the CCL2 group. The NORT results revealed that, compared with the CCL2 rats, the discrimination index in the naringin-treated rats increased significantly. Nissl and TUNEL staining revealed that naringin protected the structure and survival of the neurons in the CA1 zone of the hippocampus. In the naringin-treated groups, the SOD and GSH-Px activities were increased, whereas the MDA levels were decreased. Furthermore, in the naringin-treated groups, the relative mRNA expression of IL-1β and IL-6 was significantly decreased; GLAST and GLT-1 mRNA expression levels were increased, whereas PAG was decreased. In the naringin-treated groups, the relative mRNA expression levels of caspase-8, caspase-3, and Bax were decreased, whereas that of Bcl-2 was increased.

Conclusion: Collectively, these data indicated that naringin alleviated the CCL2-induced cognitive impairment. The underlying mechanisms could be associated with the inhibition of neuroinflammation, oxidative stress, apoptosis, and the regulation of glutamate metabolism.

背景:趋化因子C-C基序配体2 (CCL2)是认知障碍中最广泛认识的促炎趋化因子之一。目前,针对ccl2的药物非常有限。因此,本研究旨在探讨柚皮苷对ccl2诱导的大鼠认知功能障碍的神经保护作用。方法:大鼠在CCL2海马内注射前,连续3 d腹腔注射柚皮苷。术后2 d进行Morris水迷宫(MWM)和新物体识别(NORT)测试,分别检测空间学习记忆和物体认知。采用尼氏染色和dUTP镍端标记(TUNEL)染色评估海马组织病理变化。采用商品化试剂盒检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量。采用实时定量聚合酶链反应(qRT-PCR)检测白细胞介素1β (IL-1β)、白细胞介素6 (IL-6)、谷氨酸/天冬氨酸转运蛋白(GLAST)、谷氨酸转运蛋白-1 (GLT-1)、磷酸活化谷氨酰胺酶(PAG)、半胱氨酸天冬氨酸特异性蛋白酶8 (caspase-8)、半胱氨酸天冬氨酸特异性蛋白酶3 (caspase-3)、细胞淋巴瘤/白血病-2 (Bcl-2)和Bcl-2相关X蛋白(Bax) mRNA的相对表达。结果:在MWM中,与CCL2组相比,柚皮苷处理组的平均逃避潜伏期和平均游泳距离明显缩短,穿越次数明显增加。NORT结果显示,与CCL2大鼠相比,柚皮素处理大鼠的识别指数明显升高。Nissl和TUNEL染色显示柚皮苷对海马CA1区神经元的结构和存活有保护作用。柚皮素处理组SOD和GSH-Px活性升高,MDA水平降低。柚皮素处理组IL-1β、IL-6 mRNA相对表达量显著降低;GLAST和GLT-1 mRNA表达水平升高,PAG表达水平降低。柚皮素处理组caspase-8、caspase-3、Bax mRNA相对表达量降低,Bcl-2 mRNA相对表达量升高。结论:综上所述,这些数据表明柚皮苷减轻了ccl2诱导的认知功能障碍。其潜在机制可能与抑制神经炎症、氧化应激、细胞凋亡和调节谷氨酸代谢有关。
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引用次数: 16
Commercial video games and cognitive functions: video game genres and modulating factors of cognitive enhancement. 商业电子游戏和认知功能:电子游戏类型和认知增强的调节因素。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-02-03 DOI: 10.1186/s12993-020-0165-z
Eunhye Choi, Suk-Ho Shin, Jeh-Kwang Ryu, Kyu-In Jung, Shin-Young Kim, Min-Hyeon Park

Background: Unlike the emphasis on negative results of video games such as the impulsive engagement in video games, cognitive training studies in individuals with cognitive deficits showed that characteristics of video game elements were helpful to train cognitive functions. Thus, this study aimed to have a more balanced view toward the video game playing by reviewing genres of commercial video games and the association of video games with cognitive functions and modulating factors. Literatures were searched with search terms (e.g. genres of video games, cognitive training) on database and Google scholar.

Results: video games, of which purpose is players' entertainment, were found to be positively associated with cognitive functions (e.g. attention, problem solving skills) despite some discrepancy between studies. However, the enhancement of cognitive functions through video gaming was limited to the task or performance requiring the same cognitive functions. Moreover, as several factors (e.g. age, gender) were identified to modulate cognitive enhancement, the individual difference in the association between video game playing and cognitive function was found.

Conclusion: Commercial video games are suggested to have the potential for cognitive function enhancement. As understanding the association between video gaming and cognitive function in a more balanced view is essential to evaluate the potential outcomes of commercial video games that more people reported to engage, this review contributes to provide more objective evidence for commercial video gaming.

背景:与强调电子游戏的负面结果(如电子游戏中的冲动性参与)不同,对认知缺陷个体的认知训练研究表明,电子游戏元素的特征有助于训练认知功能。因此,本研究旨在通过回顾商业电子游戏的类型以及电子游戏与认知功能和调节因素之间的联系,对电子游戏玩法有一个更平衡的看法。通过检索词(如电子游戏类型、认知训练)在数据库和Google scholar上检索文献。结果:尽管研究结果存在差异,但以玩家娱乐为目的的电子游戏与认知功能(如注意力、解决问题的能力)呈正相关。然而,通过电子游戏增强认知功能仅限于需要相同认知功能的任务或表现。此外,随着一些因素(如年龄,性别)被确定为调节认知增强,电子游戏玩和认知功能之间的关联的个体差异也被发现。结论:商业电子游戏被认为具有增强认知功能的潜力。从更平衡的角度理解电子游戏和认知功能之间的关系对于评估更多人参与的商业电子游戏的潜在结果至关重要,这篇综述有助于为商业电子游戏提供更客观的证据。
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引用次数: 41
Sexual dimorphism in cognitive disorders in a murine model of neuropathic pain. 神经性疼痛小鼠模型认知障碍中的两性二态性。
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2020-01-04 DOI: 10.1186/s12993-019-0164-0
Soonmi Won, Keebum Park, Hyoungsub Lim, Sung Joong Lee

Background: A sex-difference in susceptibility to chronic pain is well-known. Although recent studies have begun to reveal the sex-dependent mechanisms of nerve injury-induced pain sensitization, sex differences in the affective and cognitive brain dysfunctions associated with chronic pain have not been investigated. Therefore, we tested whether chronic pain leads to affective and cognitive disorders in a mouse neuropathic pain model and whether those disorders are sexually dimorphic.

Methods: Chronic neuropathic pain was induced in male and female mice by L5 spinal nerve transection (SNT) injury. Pain sensitivity was measured with the von Frey test. Affective behaviors such as depression and anxiety were assessed by the forced swim, tail suspension, and open field tests. Cognitive brain function was assessed with the Morris water maze and the novel object location and novel object recognition tests.

Results: Mechanical allodynia was induced and maintained for up to 8 weeks after SNT in both male and female mice. Depressive- and anxiety-like behaviors were observed 8 weeks post-SNT injury regardless of sex. Chronic pain-induced cognitive deficits measured with the Morris water maze and novel object location test were seen only in male mice, not in female mice.

Conclusions: Chronic neuropathic pain is accompanied by anxiety- and depressive-like behaviors in a mouse model regardless of sex, and male mice are more vulnerable than female mice to chronic pain-associated cognitive deficits.

背景:慢性疼痛易感性的性别差异是众所周知的。尽管最近的研究已经开始揭示神经损伤诱导的疼痛敏感化的性别依赖机制,但与慢性疼痛相关的情感和认知脑功能障碍的性别差异尚未得到研究。因此,我们在小鼠神经性疼痛模型中测试了慢性疼痛是否会导致情感和认知障碍,以及这些障碍是否具有两性二态性。方法:采用L5脊髓神经横断(SNT)损伤诱导雌雄小鼠慢性神经性疼痛。用von Frey试验测量疼痛敏感性。通过强迫游泳、悬尾和野外测试来评估抑郁和焦虑等情感行为。采用Morris水迷宫、新目标定位和新目标识别测试评估脑认知功能。结果:雄性和雌性小鼠在SNT后均能诱导并维持机械异常性疼痛长达8周。不论性别,在snt损伤后8周观察到抑郁和焦虑样行为。用Morris水迷宫和新物体定位测试测量的慢性疼痛引起的认知缺陷只在雄性小鼠中发现,而在雌性小鼠中没有发现。结论:在小鼠模型中,慢性神经性疼痛伴焦虑和抑郁样行为,雄性小鼠比雌性小鼠更容易出现慢性疼痛相关的认知缺陷。
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引用次数: 7
Traumatic injury in female Drosophila melanogaster affects the development and induces behavioral abnormalities in the offspring 雌性黑腹果蝇的创伤性损伤会影响其后代的发育并诱发其行为异常
IF 5.1 2区 心理学 Q1 Neuroscience Pub Date : 2019-10-25 DOI: 10.1186/s12993-019-0163-1
V. Chauhan, A. Chauhan
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引用次数: 6
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Behavioral and Brain Functions
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