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Effects of non-invasive prefrontal neuromodulation on acute cortisol response to stress: A systematic review and meta-analysis 非侵入性前额叶神经调节对应激急性皮质醇反应的影响:系统回顾和荟萃分析
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-07 DOI: 10.1016/j.bbr.2025.115930
Qiyi Wang , Yang Wang , Hanshuo Bao , Jiale Zhong
Dysregulated stress response, involving altered connectivity between the hypothalamic-pituitary-adrenal (HPA) axis and prefrontal cortex (PFC), is linked to psychiatric disorders. Non-invasive brain stimulation (NIBS) may modulate cortisol release by influencing PFC activity; however, quantitative evidence remains limited. This systematic review and meta-analysis included 16 randomized controlled trials examining NIBS effects on stress-induced cortisol release in healthy individuals. Studies were identified from five databases and analyzed following PRISMA guidelines using random-effects models. Results showed that NIBS significantly reduced acute cortisol response to stress (SMD = −0.72, 95 % CI [-1.16, −0.28], p < 0.01). Subgroup analyses indicated greater efficacy for transcranial magnetic stimulation (TMS) compared to transcranial direct current stimulation (tDCS). Stimulation applied before or after the stressor was more effective than during-task application. Female participants showed more pronounced cortisol modulation than males. Sensitivity analyses confirmed result robustness, and no publication bias was detected. When developing NIBS-based neuromodulation protocols for stress modulation, factors such as stimulation type, timing, and participant characteristics may warrant careful consideration. Overall, the evidence suggests that NIBS may modulate acute stress responses in healthy individuals.
应激反应失调,包括下丘脑-垂体-肾上腺(HPA)轴和前额皮质(PFC)之间连接的改变,与精神疾病有关。无创脑刺激(NIBS)可能通过影响PFC活动调节皮质醇释放;然而,定量证据仍然有限。本系统综述和荟萃分析包括16项随机对照试验,研究NIBS对健康个体应激诱导的皮质醇释放的影响。从五个数据库中确定研究,并按照PRISMA指南使用随机效应模型进行分析。结果显示,NIBS显著降低应激急性皮质醇反应(SMD = - 0.72, 95 % CI [-1.16, - 0.28], p <; 0.01)。亚组分析显示经颅磁刺激(TMS)比经颅直流电刺激(tDCS)更有效。在压力源之前或之后施加刺激比在任务施加时更有效。女性参与者表现出比男性更明显的皮质醇调节。敏感性分析证实了结果的稳健性,未发现发表偏倚。在制定基于nibs的压力调节神经调节方案时,刺激类型、时间和参与者特征等因素可能需要仔细考虑。总的来说,证据表明NIBS可能调节健康个体的急性应激反应。
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引用次数: 0
Immediate modulatory effects of transcutaneous auricular vagus nerve stimulation in healthy males: A multi-bands resting-state fMRI study 经皮耳迷走神经刺激对健康男性的即时调节作用:一项多波段静息状态fMRI研究。
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-06 DOI: 10.1016/j.bbr.2025.115922
Hang Zhang , Xiaomeng Xue , Zihao Mu , Chun Wang , Junze Zheng , ZhaoShun Wang , Yu Han , Shanshan Gao , Wenxuan Zhang , Anning Ren , Lanfen Chen , Xize Jia , Xizhen Wang
Transcutaneous auricular vagus nerve stimulation (taVNS) is a noninvasive neuromodulation technique that shows promise in treating disorders such as depression and insomnia. Previous studies have mainly focused on disease-specific populations, making it difficult to distinguish taVNS-induced neural changes from disease-related confounding factors. To investigate its immediate effects, we recruited 24 healthy males and randomly assigned them to a taVNS group (n = 12) or a sham group (n = 12). The taVNS group received 30 min of stimulation, while the sham group received a brief initial stimulation (<15 s) followed by device placement without power. Resting-state functional magnetic resonance imaging (rs-fMRI) scans were acquired pre-taVNS and post-taVNS. The paired sample t-test in the taVNS group showed reduced regional homogeneity (ReHo) in the left precentral gyrus (Precentral_L) (conventional frequency band) and left postcentral gyrus (Postcentral_L) (slow 4 frequency band). Functional connectivity (FC) analysis based on peak ReHo coordinates showed that the FC between Precentral_L and the right fusiform gyrus (Fusiform_R) (conventional band and slow band 4) and the right calcarine cortex (Calcarine_R) (slow band 5) was weakened, and the FC between the Postcentral_L and the Postcentral_L (conventional band), the Fusiform_R and the left cuneus (Cuneus_L) (slow band 4), and the Postcentral_L (slow band 5) was weakened. No significant differences were observed between the groups. These findings suggest that taVNS modulates neural activity in different frequency bands in healthy males, providing insights into its regulatory mechanisms and facilitating future applications in cognitive enhancement and targeted brain stimulation.
经皮耳迷走神经刺激(taVNS)是一种无创神经调节技术,在治疗抑郁症和失眠等疾病方面显示出前景。以往的研究主要集中在疾病特异性人群,因此很难将tavns诱导的神经变化与疾病相关的混杂因素区分开来。为了研究其即时效果,我们招募了24名健康男性,并将他们随机分为taVNS组(n=12)和假手术组(n=12)。taVNS组给予30分钟的刺激,假手术组给予短暂的初始刺激(
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引用次数: 0
Dysregulated immune system in chronic stress male rats is an outcome of altered mRNA expression, cytokines, and Th1/Th2 balance 慢性应激雄性大鼠免疫系统失调是mRNA表达、细胞因子和Th1/Th2平衡改变的结果。
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-06 DOI: 10.1016/j.bbr.2025.115921
Zeju Luo , Yiheng Huang , Luhan Tang , Qikang Gao , Gonglin Hou , Jianzhong Shao , Yunyun Shen
Chronic stress is known to cause immune system dysfunction, which can contribute to the development of various highly prevalent diseases. Nevertheless, the mechanisms underlying immune dysregulation during chronic stress remain poorly understood. In this study, we examined the effects of 35-day chronic unpredictable mild stress (CUMS) on behavioral patterns, lymphocyte subpopulation ratios, serum cytokine levels, and the peripheral blood leukocyte transcriptome in 20 male Sprague–Dawley rats. After 35 days of CUMS exposure, the rats exhibited established features of chronic unpredictable mild stress, including increased anxiety-like behavior and depression-like behavior. We found a significant increase in the proportion of Th2 cells among lymphocytes, leading to a Th1/Th2 imbalance. Additionally, serum levels of the pro-inflammatory cytokines IL-1α, IL-1β, IFN-γ, and GM-CSF were significantly decreased, whereas the concentration of IL-2 was markedly elevated. Transcriptomic profiling revealed broad alterations in gene expression after CUMS, particularly in pathways related to immune system function. Our findings indicate that chronic stress induces immune dysregulation through a Th1/Th2 imbalance and associated changes in key immune-related genes (including Maf, Irf4, Gfi1, and Bcl6b), suggesting a potential mechanism for stress-induced immune dysfunction.
众所周知,慢性压力会导致免疫系统功能障碍,从而导致各种高度流行疾病的发展。然而,慢性应激期间免疫失调的机制仍然知之甚少。在这项研究中,我们研究了35天的慢性不可预测轻度应激(CUMS)对20只雄性Sprague-Dawley大鼠的行为模式、淋巴细胞亚群比率、血清细胞因子水平和外周血白细胞转录组的影响。暴露于CUMS 35天后,大鼠表现出慢性不可预测的轻度应激的既定特征,包括增加的焦虑样行为和抑郁样行为。我们发现淋巴细胞中Th2细胞的比例显著增加,导致Th1/Th2失衡。此外,血清促炎因子IL-1α、IL-1β、IFN-γ和GM-CSF水平显著降低,而IL-2浓度显著升高。转录组学分析揭示了CUMS后基因表达的广泛改变,特别是在与免疫系统功能相关的途径中。我们的研究结果表明,慢性应激通过Th1/Th2失衡和关键免疫相关基因(包括Maf、Irf4、Gfi1和Bcl6b)的相关变化诱导免疫失调,提示应激诱导免疫功能障碍的潜在机制。
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引用次数: 0
Alpha-pinene attenuates neuroinflammatory responses in the rat hippocampus and improves spatial working memory deficits associated with morphine dependence and withdrawal α -蒎烯减轻大鼠海马神经炎症反应,改善与吗啡依赖和戒断相关的空间工作记忆缺陷。
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-05 DOI: 10.1016/j.bbr.2025.115920
Shamseddin Ahmadi , Bestan Yousif Abdullah , Shnya Dlshad Taeeb , Hawsar Rashid Ahmed , Mohammad Majidi
Chronic morphine exposure leads to changes in neural function, with neuroinflammation playing a key role in these disruptions. The monoterpene compound α-pinene has been shown to possess properties that counteract inflammation. This study focused on assessing how α-pinene reduces inflammation and improves spatial working memory deficits resulting from frequent morphine exposure and following the drug washout. First, spatial working memory was assessed by using the Y-maze test in male Wistar rats. Then, levels of proinflammatory cytokines and expression of their receptors in the rat hippocampus were analyzed using ELISA and western blot methods. The findings demonstrated that 10 days of morphine administration weakened spatial memory, an effect that was partially alleviated by concurrent α-pinene treatment during morphine exposure. Although 30 days washout period modestly improved the memory deficit, α-pinene administration during withdrawal further augmented the recovery of memory function. Molecular analyses revealed substantial rises in hippocampal levels of TNFα, IL-1β, and IL-6, alongside expression of their associated receptors (TNFR, IL1R, and IL6R) as well as NF-κB following the morphine exposure and 30 days of the washout period. Conversely, the hippocampal concentrations of IL-10 as an inhibitory factor in inflammation were reduced. Notably, α-pinene treatment, whether administered during dependence induction or throughout withdrawal, markedly normalized proinflammatory cytokine levels and receptor expression in the hippocampus by affecting total NF-κB levels, but not its phosphorylation. It can be concluded that α-pinene may serve as a potential natural therapy for the management of neuroinflammation and recovering spatial memory following chronic morphine exposure and withdrawal.
慢性吗啡暴露会导致神经功能的改变,而神经炎症在这些破坏中起着关键作用。单萜化合物α-蒎烯已被证明具有抵抗炎症的特性。本研究的重点是评估α-蒎烯如何减轻炎症和改善频繁吗啡暴露和药物洗脱后的空间工作记忆缺陷。首先,采用y型迷宫测试方法评估雄性Wistar大鼠的空间工作记忆。然后用ELISA和western blot方法分析大鼠海马中促炎细胞因子的水平及其受体的表达。结果表明,吗啡给药10天后,大鼠的空间记忆减弱,而在吗啡暴露期间同时给予α-蒎烯可部分缓解这一影响。虽然30天的洗脱期适度改善了记忆缺陷,但在停药期间给予α-蒎烯进一步增强了记忆功能的恢复。分子分析显示,在吗啡暴露和30天的洗脱期后,海马组织中TNFα、IL-1β和IL-6水平以及相关受体(TNFR、IL1R和IL6R)和NF-κB的表达显著升高。相反,作为炎症抑制因子的IL-10的海马浓度降低。值得注意的是,α-蒎烯治疗,无论是在依赖性诱导期间还是在戒断期间给予,通过影响NF-κB总水平,但不影响其磷酸化,显着正常化了海马中促炎细胞因子水平和受体表达。由此可见,α-蒎烯可能作为一种潜在的自然疗法,用于治疗慢性吗啡暴露和戒断后的神经炎症和恢复空间记忆。
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引用次数: 0
Mechanistic study of platelet-derived exosome-mediated miR-320a on attenuation of schizophrenia-like behavior in rat models via ITGβ modulation 血小板源性外泌体介导的miR-320a通过ITGβ调节大鼠模型中精神分裂症样行为衰减的机制研究
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-05 DOI: 10.1016/j.bbr.2025.115917
Shan Hu , Luxin Deng , Zhi Cai , Qiong Yuan , Ling Jiang , Chengcen Luo , Yuhan Wang , Yuanshuai Huang

Background

MiRNA-320a is aberrantly expressed in individuals with schizophrenia, and integrin β1 (ITGβ1) has been identified as a direct target of miRNA-320a. ITGβ1 may play a role in neurotransmitter-related signaling pathways that contribute to the pathophysiology of schizophrenia. Objective: This study aimed to investigate the potential of platelet-derived exosomes as a drug delivery vehicle for miR-320a to alleviate schizophrenia-like behavioral manifestations.

Methods

Platelet-derived exosomes were loaded with miR-320a via electroporation. Schizophrenia model rats were established using MK-801. The behavioral changes in the rats were assessed using the Morris water maze test and the open field test. Additionally, quantitative polymerase chain reaction (qPCR) was employed to measure the expression levels of miR-320a and ITGβ in the rat brain tissue. Furthermore, ultra-high-pressure liquid chromatography-tandem mass spectrometry (LC-MS) was used to analyze the levels of various neurotransmitters in the rat brain.

Results

Our findings indicated that treatment with platelet exosomes delivering miR-320 significantly improved the anxiety behavior and cognitive function of the rats with the schizophrenia model. The results showed that platelet exosomes loaded with miR-320a could significantly downregulate the expression of ITGβ, and LC-MS analysis indicated a decreasing trend in serotonin (5-HT).

Conclusion

The findings of this study offer a novel perspective on the treatment of schizophrenia and suggest that P-exos-miR-320a may represent a promising therapeutic strategy, though further validation is needed.
背景:MiRNA-320a在精神分裂症患者中异常表达,整合素β1 (itg - β1)已被确定为MiRNA-320a的直接靶点。ITGβ1可能在神经递质相关信号通路中发挥作用,有助于精神分裂症的病理生理。目的:本研究旨在探讨血小板来源的外泌体作为miR-320a的药物递送载体,缓解精神分裂症样行为表现的潜力。方法:通过电穿孔将血小板来源的外泌体装载miR-320a。用MK-801建立精神分裂症模型大鼠。采用Morris水迷宫试验和空地试验评估大鼠的行为变化。此外,采用定量聚合酶链反应(qPCR)检测miR-320a和ITGβ在大鼠脑组织中的表达水平。采用超高压液相色谱-串联质谱法(LC-MS)分析大鼠脑内各种神经递质水平。结果:我们的研究结果表明,使用血小板外泌体递送miR-320治疗可显著改善精神分裂症模型大鼠的焦虑行为和认知功能。结果显示,负载miR-320a的血小板外泌体可以显著下调ITGβ的表达,LC-MS分析显示血清素(5-HT)呈下降趋势。结论:本研究的发现为精神分裂症的治疗提供了一个新的视角,并表明P-exos-miR-320a可能是一种有希望的治疗策略,尽管需要进一步验证。
{"title":"Mechanistic study of platelet-derived exosome-mediated miR-320a on attenuation of schizophrenia-like behavior in rat models via ITGβ modulation","authors":"Shan Hu ,&nbsp;Luxin Deng ,&nbsp;Zhi Cai ,&nbsp;Qiong Yuan ,&nbsp;Ling Jiang ,&nbsp;Chengcen Luo ,&nbsp;Yuhan Wang ,&nbsp;Yuanshuai Huang","doi":"10.1016/j.bbr.2025.115917","DOIUrl":"10.1016/j.bbr.2025.115917","url":null,"abstract":"<div><h3>Background</h3><div>MiRNA-320a is aberrantly expressed in individuals with schizophrenia, and integrin β1 (ITGβ1) has been identified as a direct target of miRNA-320a. ITGβ1 may play a role in neurotransmitter-related signaling pathways that contribute to the pathophysiology of schizophrenia. Objective: This study aimed to investigate the potential of platelet-derived exosomes as a drug delivery vehicle for miR-320a to alleviate schizophrenia-like behavioral manifestations.</div></div><div><h3>Methods</h3><div>Platelet-derived exosomes were loaded with miR-320a via electroporation. Schizophrenia model rats were established using MK-801. The behavioral changes in the rats were assessed using the Morris water maze test and the open field test. Additionally, quantitative polymerase chain reaction (qPCR) was employed to measure the expression levels of miR-320a and ITGβ in the rat brain tissue. Furthermore, ultra-high-pressure liquid chromatography-tandem mass spectrometry (LC-MS) was used to analyze the levels of various neurotransmitters in the rat brain.</div></div><div><h3>Results</h3><div>Our findings indicated that treatment with platelet exosomes delivering miR-320 significantly improved the anxiety behavior and cognitive function of the rats with the schizophrenia model. The results showed that platelet exosomes loaded with miR-320a could significantly downregulate the expression of ITGβ, and LC-MS analysis indicated a decreasing trend in serotonin (5-HT).</div></div><div><h3>Conclusion</h3><div>The findings of this study offer a novel perspective on the treatment of schizophrenia and suggest that P-exos-miR-320a may represent a promising therapeutic strategy, though further validation is needed.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"498 ","pages":"Article 115917"},"PeriodicalIF":2.3,"publicationDate":"2025-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145470420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Electroacupuncture ameliorates mitochondrial dysfunction and alleviates traumatic brain injury via the PANX1/ATP/Ca2+ pathway 电针通过PANX1/ATP/Ca2+通路改善线粒体功能障碍,减轻创伤性脑损伤。
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-04 DOI: 10.1016/j.bbr.2025.115918
Quanxiu Liu , Fang Tan , Jinpeng Wen , Chi Ma , Zitong Wang , Xu Fan
Traumatic brain injury (TBI) involves complex pathophysiological processes. This study investigates the therapeutic effects of electroacupuncture (EA) on mitochondrial dysfunction and TBI in rats through the PANX1/ATP/Ca2+ pathway, thereby providing effective intervention targets for TBI. A TBI rat model was established using the cortical controlled impact method, followed by behavioral tests (modified neurological severity score, rotarod test, grip strength test, and balance beam test) to assess the neurological function. Brain edema, neuronal apoptosis, and oxidative stress were evaluated using histological staining, Enzyme-linked immunosorbent assay, and Western blotting. The results showed that EA treatment significantly improved the motor coordination, reduced the brain water content, and preserved neuronal integrity. Moreover, EA reduced levels of oxidative stress, inflammation, and apoptosis markers. EA also inhibited the PANX1/ATP/Ca2+ pathway, Ca2+ levels, caspase-3 activation, and mitochondrial Cyt C, while enhancing ATP, NAD+ /NADPH levels, and mitochondrial respiratory chain complex activity. These findings suggest that EA mitigates mitochondrial dysfunction and oxidative stress, thereby improving neurological outcomes and reducing brain edema in TBI rats. Inhibition of PANX1 expression further confirmed its role in modulating TBI-related pathology via the PANX1/ATP/Ca2+ axis.
创伤性脑损伤(TBI)是一个复杂的病理生理过程。本研究探讨电针(EA)通过PANX1/ATP/Ca2+通路对大鼠线粒体功能障碍和TBI的治疗作用,从而为TBI提供有效的干预靶点。采用皮质控制冲击法建立脑损伤大鼠模型,并进行行为学测试(改良神经严重程度评分、旋转杆测试、握力测试、平衡木测试)评估神经功能。采用组织学染色、酶联免疫吸附试验和Western blotting评估脑水肿、神经元凋亡和氧化应激。结果表明,EA治疗显著改善了大鼠的运动协调性,降低了脑含水量,并保持了神经元的完整性。此外,EA还能降低氧化应激、炎症和细胞凋亡标志物的水平。EA还抑制PANX1/ATP/Ca2+通路、Ca2+水平、caspase-3激活和线粒体Cyt C,同时增强ATP、NAD+/NADPH水平和线粒体呼吸链复合物活性。这些发现表明,EA减轻了线粒体功能障碍和氧化应激,从而改善了脑损伤大鼠的神经预后,减少了脑水肿。PANX1表达的抑制进一步证实了其通过PANX1/ATP/Ca2+轴调节tbi相关病理的作用。
{"title":"Electroacupuncture ameliorates mitochondrial dysfunction and alleviates traumatic brain injury via the PANX1/ATP/Ca2+ pathway","authors":"Quanxiu Liu ,&nbsp;Fang Tan ,&nbsp;Jinpeng Wen ,&nbsp;Chi Ma ,&nbsp;Zitong Wang ,&nbsp;Xu Fan","doi":"10.1016/j.bbr.2025.115918","DOIUrl":"10.1016/j.bbr.2025.115918","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) involves complex pathophysiological processes. This study investigates the therapeutic effects of electroacupuncture (EA) on mitochondrial dysfunction and TBI in rats through the PANX1/ATP/Ca<sup>2+</sup> pathway, thereby providing effective intervention targets for TBI. A TBI rat model was established using the cortical controlled impact method, followed by behavioral tests (modified neurological severity score, rotarod test, grip strength test, and balance beam test) to assess the neurological function. Brain edema, neuronal apoptosis, and oxidative stress were evaluated using histological staining, Enzyme-linked immunosorbent assay, and Western blotting. The results showed that EA treatment significantly improved the motor coordination, reduced the brain water content, and preserved neuronal integrity. Moreover, EA reduced levels of oxidative stress, inflammation, and apoptosis markers. EA also inhibited the PANX1/ATP/Ca<sup>2+</sup> pathway, Ca<sup>2+</sup> levels, caspase-3 activation, and mitochondrial Cyt C, while enhancing ATP, NAD+ /NADPH levels, and mitochondrial respiratory chain complex activity. These findings suggest that EA mitigates mitochondrial dysfunction and oxidative stress, thereby improving neurological outcomes and reducing brain edema in TBI rats. Inhibition of PANX1 expression further confirmed its role in modulating TBI-related pathology via the PANX1/ATP/Ca<sup>2+</sup> axis.</div></div>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"498 ","pages":"Article 115918"},"PeriodicalIF":2.3,"publicationDate":"2025-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Salicin ameliorates Alzheimer’s-like pathology by modulation of NTSP/CSP/GLM pathways: An integrated in silico and in vivo approach 水杨苷通过调节NTSP/CSP/GLM通路改善阿尔茨海默病样病理:一种集成在硅和体内的方法
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-03 DOI: 10.1016/j.bbr.2025.115907
Padmaja Kore , Utkarsha Patil , Shrinath Bodkhe , Deepti Bandawane , Aishwarya Pandit , Anuradha More
Alzheimer’s disease (AD) is marked by modifiable and non-modifiable risk factors. Despite existing treatments, effective therapies to halt or reverse AD progression remain limited, highlighting the urgent need for new multitarget strategies. Phytotherapy as an anti-AD approach has emerged as an increasingly promising strategy in combating neurodegeneration, triggered by suppression of neuronal oxidation and inflammation. Salicin is a natural substance found in willow bark with anti-inflammatory and antioxidant effects. The present study investigates the protective effects of Salicin on neurodegeneration triggered by Scopolamine (Scop). Network pharmacology identified target pathways and genes involved in AD pathogenesis and suggested Salicin as a potential therapeutic agent. Molecular docking elucidated interactions within these target pathways. Scop (1 mg/kg, i.p.) induced memory dysfunction, and Salicin was administered at 12.5, 25, and 50 mg/kg (i.p.). Behavioral parameters were assessed for recognition and spatial memory using Novel Object Recognition (NOR) and Radial Arm Maze (RAM), respectively. AChE, BDNF, and PSEN-1 levels were studied as per in silico predictions, and microscopic changes in hippocampus and cortex were observed via histopathology. Top three pathways of Salicin were identified. The results of in silico and in vivo analyses demonstrate that the protective effects of Salicin are mediated through the Neurotrophin Signaling Pathway (NTSP), Cholinergic Synapse Pathway (CSP), and Glycerolipid Metabolism Pathway (GLM), which are critically implicated in AD progression. Relevant behavioral and histopathological improvements were observed. This study provides preliminary evidence supporting the potential of Salicin as a therapeutic candidate for AD, offering valuable direction for future research.
阿尔茨海默病(AD)的特点是可改变和不可改变的危险因素。尽管已有治疗方法,但阻止或逆转AD进展的有效疗法仍然有限,因此迫切需要新的多靶点策略。植物疗法作为一种抗阿尔茨海默病的方法已经成为一种越来越有前途的治疗神经退行性疾病的策略,这种疾病是由抑制神经元氧化和炎症引起的。水杨苷是柳树皮中发现的一种天然物质,具有抗炎和抗氧化作用。本研究探讨水杨苷对东莨菪碱引起的神经退行性变的保护作用。网络药理学鉴定了AD发病机制的靶通路和基因,认为水杨苷是潜在的治疗药物。分子对接阐明了这些靶通路内的相互作用。scopp (1mg/kg, i.p.)诱导记忆功能障碍,水杨苷12.5、25和50mg/kg (i.p.)给药。采用新目标识别(NOR)和径向臂迷宫(RAM)分别评估识别和空间记忆的行为参数。根据计算机预测研究AChE、BDNF和PSEN-1水平,并通过组织病理学观察海马和皮层的微观变化。确定了水杨苷的前3条途径。体外和体内分析结果表明,水杨苷的保护作用是通过神经营养因子信号通路(NTSP)、胆碱能突触通路(CSP)和甘油脂代谢途径(GLM)介导的,这些途径与AD的进展有重要关系。观察到相关的行为和组织病理学改善。本研究为水杨苷作为阿尔茨海默病候选药物的潜力提供了初步证据,为今后的研究提供了有价值的方向。
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引用次数: 0
Female mice in established social groups use different ultrasonic vocalizations during peaceful and aggressive interactions 在已建立的社会群体中,雌性老鼠在和平和攻击性的互动中使用不同的超声波发声。
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-11-01 DOI: 10.1016/j.bbr.2025.115904
Anna V. Klenova , Benjamin Lang , Anne Jaap , Christa Thöne-Reineke , Lars Lewejohann , Paul Mieske
The ultrasonic vocalizations (USVs) of house mice (Mus musculus) have a surprisingly complex structure and have been actively studied as a model for applied questions in biomedical science. Despite this, the functional significance of different USV types and their use during natural social behaviour in diverse groups remains unclear. In this pilot long-term study, we examined the ultrasound activity of female mice housed in stable groups within an enriched environment, focusing on how behavioural context influences USV time-frequency characteristics, call type occurrence, and nonlinear phenomena. Our findings show that USVs are mainly produced in bouts, and bouts containing ten or more variable calls always accompanying direct social interactions. USV variables and types varied markedly depending on the interaction context. During aggressive encounters, USVs and entire bouts became longer, vocalization time and frequency modulation increased, while peak and minimum fundamental frequencies decreased. Additionally, aggressive context was characterized by a higher prevalence of multi-component and complex-low USVs (with peak frequency < 50 kHz), and increased nonlinear phenomena. These results suggest that USV features closely reflect emotional arousal (intensity) and probably also valence (positive/negative) in female mice during social hierarchy formation and maintenance. Notably, the relationship between arousal and nonlinear vocal phenomena in mice USVs follows patterns observed in audible vocalizations of other mammals (increase with arousal). In the future, complex-low USVs could potentially serve as non-invasive indicators of negative emotional expression in groups of female mice. This opens new possibilities for acoustic home-cage monitoring aimed at welfare assessment and other applied uses.
家鼠(Mus musculus)的超声发声(USVs)具有令人惊讶的复杂结构,并作为生物医学应用问题的模型被积极研究。尽管如此,不同USV类型的功能意义及其在不同群体自然社会行为中的使用仍不清楚。在这项初步的长期研究中,我们研究了在丰富的环境中饲养的稳定组的雌性小鼠的超声活动,重点关注行为背景如何影响USV时频特性,呼叫类型发生和非线性现象。我们的研究结果表明,usv主要是在回合中产生的,回合包含十个或更多的变量呼叫,总是伴随着直接的社会互动。USV变量和类型因交互环境的不同而有显著差异。在激烈的战斗中,usv和整个回合变得更长,发声时间和频率调制增加,而峰值和最低基频降低。此外,侵略性环境的特点是多分量和复杂低usv(峰值频率< 50kHz)的发生率更高,非线性现象增加。这些结果表明,USV特征密切反映了雌性小鼠在社会等级形成和维持过程中的情绪唤醒(强度),可能也反映了效价(正/负)。值得注意的是,在小鼠usv中,唤醒和非线性发声现象之间的关系遵循了在其他哺乳动物的可听发声中观察到的模式(随着唤醒而增加)。在未来,复合物-低usv有可能作为雌性小鼠群体负性情绪表达的非侵入性指标。这为旨在进行福利评估和其他应用的家庭笼声监测开辟了新的可能性。
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引用次数: 0
The serotonergic 5-HT7 receptor: A therapeutic target for mitigating acute stress-induced cognitive, neuroinflammatory, and oxidative damage in the hippocampus 5-羟色胺能5-HT7受体:减轻海马急性应激诱导的认知、神经炎症和氧化损伤的治疗靶点
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-10-31 DOI: 10.1016/j.bbr.2025.115901
Nasrin Abdolmaleki , Siamak Shahidi , Ali Haeri Rohani , Parisa Habibi
This study investigates the role of 5-HT7 receptors in mediating repeated acute stress-induced impairments on memory, hippocampal neuronal health, neuroinflammation, and oxidative stress in mice. By elucidating these mechanisms, we aim to identify novel therapeutic targets to mitigate cognitive deficits resulting from acute stress. Mice were randomly assigned to four groups: control, stress, 5-HT7 receptor agonist (AS19, 5 mg/kg, i.p.) + stress, and 5-HT7 receptor antagonist (SB-269970, 2.5 mg/kg, i.p.) + stress. Cognitive and avoidance memory were assessed using the novel object recognition (NOR) and passive avoidance (PA) tests, respectively. Hippocampus tissue was analyzed for BDNF levels via ELISA, neuronal density through hematoxylin staining, and TNFα inflammatory marker via immunofluorescence. Additionally, oxidative stress markers including total oxidant status (TOS), malondialdehyde (MDA), total antioxidant capacity (TAC), superoxide dismutase (SOD), total thiol groups (TTG), and glutathione (GSH) were measured. Our findings demonstrate that repeated acute stress significantly impairs memory, reduces hippocampal BDNF levels and neuronal density, and increases neuroinflammation and oxidative stress. Crucially, administration of the 5-HT7 receptor agonist, AS19, effectively ameliorated these stress-induced deficits, while the antagonist, SB-269970, had no protective effect. These results highlight the 5-HT7 receptor as a promising therapeutic target for combating the detrimental effects of acute stress on brain health and cognitive function.
本研究探讨了5-HT7受体在小鼠记忆、海马神经元健康、神经炎症和氧化应激中介导急性应激性损伤的作用。通过阐明这些机制,我们旨在确定新的治疗靶点,以减轻急性应激引起的认知缺陷。小鼠随机分为4组:对照组、应激组、5-HT7受体激动剂(AS19, 5mg/kg, i.p)。+应激,5-HT7受体拮抗剂(SB-269970, 2.5mg/kg, i.p)+压力。认知记忆和回避记忆分别采用新目标识别(NOR)和被动回避(PA)测试进行评估。ELISA法检测海马组织BDNF水平,苏木精染色法检测神经元密度,免疫荧光法检测TNFα炎症标志物。此外,测定氧化应激标志物,包括总氧化状态(TOS)、丙二醛(MDA)、总抗氧化能力(TAC)、超氧化物歧化酶(SOD)、总硫醇群(TTG)和谷胱甘肽(GSH)。我们的研究结果表明,反复的急性应激显著损害记忆,降低海马BDNF水平和神经元密度,增加神经炎症和氧化应激。关键是,施用5-HT7受体激动剂AS19可以有效改善这些应激诱导的缺陷,而拮抗剂SB-269970则没有保护作用。这些结果突出了5-HT7受体作为对抗急性应激对大脑健康和认知功能的有害影响的有希望的治疗靶点。
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引用次数: 0
Corrigendum to “The mechanism of electroacupuncture treatment for post-stroke spasticity: A systematic review and meta-analysis” [Behav. Brain Res. 497 (2026) 115873] 《电针治疗脑卒中后痉挛的机制:一项系统综述和荟萃分析》的更正。中国生物医学工程学报,2015(5):357 - 357。
IF 2.3 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2025-10-30 DOI: 10.1016/j.bbr.2025.115897
Lei You , Mengwan Hu , Jingang Li , Jiahui Tan , Fengmin Guo , Ying Kong
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引用次数: 0
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Behavioural Brain Research
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