•Throughout Chinese history, LJF was an important Chinese medicinal herb, which was widely used to treat respiratory infectious diseases, due to its antioxidant, anti-inflammatory, and antimicrobial properties.•The bioactive molecules derived from LJF and prescriptions containing LJF play antiviral roles through various ways, and influence the manifestation and pathogenesis of viral infections.•LJF could provide promising bioactive ingredients for further antiviral drug development for the prevention and treatment of emerging respiratory infectious diseases.

It has been reported that Banxia-houpo decoction (BXHPD) serves as the anti-depressant treatment for a mild and severe depressive disease with limited side effects. The present study was performed to evaluate the protective effect of BXHPD on chronic unpredicted mild stress (CUMS)-induced depression and explore its effect on TrkA/Akt-mediated microglia polarization. The CUMS procedure was carried out, and the mice were intragastrically treated with BXHPD once daily. The selective TrkA inhibitor GW441756 was applied to further investigate the role of TrkA in BXHPD-mediated microglia polarization. The behaviour test including open field test (OFT), sucrose preference test (SPT), novelty-suppressed feeding test (NSFT), tail suspension test (TST) and forced swim test (FST) was performed. The concentrations of pro-inflammatory cytokines IL-6, TNF-α, IL-1β, IL-12 and anti-inflammatory cytokines IL-4, IL-10 were determined using Enzyme-linked immunosorbent assay. The population of Iba1+ cells and the length of microglia processes were observed under the fluorescence microscope. The mRNA expressions of Arg1, Ym1 and Fizzl1 were measured by PCR. The protein expressions of TrkA, p-Tyr490-TrkA, p-Ser473-Akt, p-Ser473-Akt1, p-Ser474-Akt2, p-CREB and Jmjd3 were detected by western blot. Our results showed that BXHPD attenuated CUMS-induced depressive-like behaviour, promoted anti-inflammatory cytokines, inhibited pro-inflammatory cytokines, suppressed microglia activation, promoted M2 phenotype-specific indices and upregulated the expressions of TrkA, p-Tyr490-TrkA, p-Ser473-Akt, p-Ser473-Akt1, p-Ser474-Akt2, p-CREB and Jmjd3. The above beneficial effect of BXHPD can be blocked by TrkA inhibitor GW441756. This work demonstrated that BXHPD exerted an anti-depressant effect by promoting M2 phenotype microglia polarization via TrkA/Akt pathway.

目的:探讨脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)对有氧运动促进心肌梗死后心肌血管生成、改善心功能的协同效应及其机制.方法:细胞实验中,利用平行板流动小室建立12 dyn/cm2的层流剪切力(laminar shear stress,LSS)以模拟运动对血管壁的生理效应.Western blot分别检测非循环流体、循环流体、循环流体加人重组BDNF蛋白(50 ng/mL)处理的人脐静脉内皮细胞HUVEC中BDNF蛋白表达水平、BDNF高亲和力受体TrkB及其下游Akt通路磷酸化水平,Transwell细胞迁移实验和小管形成实验检测HUVEC的体外血管生成能力.动物实验中,60只12周龄雄性Sprague-Dawley(SD)大鼠随机分为假手术组(Sham)、心肌梗死组(MIC)、心肌梗死+BDNF组(MICB)、心肌梗死+运动组(MIE)、心肌梗死+运动+BDNF组(MIEB);造模术前及术后1周分别进行心彩超检查,随后开始为期4周的有氧运动训练,MIEB组大鼠在运动前10 min尾静脉注射人重组BDNF蛋白(0.4 μg/kg),MICB组仅注射等量BDNF;训练结束行心彩超检查后腹腔麻醉取材,免疫组化检测心肌梗死周围区血管密度.结果:循环流体产生的LSS可诱发HUVEC中BDNF蛋白表达增加,TrkB及其下游Akt通路磷酸化程度持续增强,循环流体中BDNF水平随干预时间的延长而升高.非循环流体产生的LSS可诱发HUVEC上BDNF蛋白表达增加,但TrkB及其下游Akt通路均处于未激活状态.增加循环流体中BDNF浓度可提高TrkB及其下游Akt通路活化程度,进一步提高HUVEC体外血管生成能力.心肌梗死大鼠有氧运动结合尾静脉注射BDNF较单纯注射BDNF和单纯运动组大鼠心肌血管密度显著增高、心功能改善.结论:运动通过LSS以BDNF浓度依赖性模式诱发HUVEC上TrkB持续磷酸化并激活其下游Akt信号通路,提高细胞迁移及小管形成能力;外源性补充BDNF可协同有氧训练强化运动的促心肌血管生成效应,进一步改善心功能.

Mutations in genes encoding amyloid precursor protein (APP) and presenilins (PSs) cause familial forms of Alzheimer’s disease (AD), a neurodegenerative disorder strongly associated with aging. It is currently unknown whether and how AD risks affect early brain development, and to what extent subtle synaptic pathology may occur prior to overt hallmark AD pathology. Transgenic mutant APP/PS1 over-expression mouse lines are key tools for studying the molecular mechanisms of AD pathogenesis. Among these lines, the 5XFAD mice rapidly develop key features of AD pathology and have proven utility in studying amyloid plaque formation and amyloid β (Aβ)-induced neurodegeneration. We reasoned that transgenic mutant APP/PS1 over-expression in 5XFAD mice may lead to neurodevelopmental defects in early cortical neurons, and performed detailed synaptic physiological characterization of layer 5 (L5) neurons from the prefrontal cortex (PFC) of 5XFAD and wild-type littermate controls. L5 PFC neurons from 5XFAD mice show early APP/Aβ immunolabeling. Whole-cell patch-clamp recording at an early post-weaning age (P22–30) revealed functional impairments; although 5XFAD PFC-L5 neurons exhibited similar membrane properties, they were intrinsically less excitable. In addition, these neurons received smaller amplitude and frequency of miniature excitatory synaptic inputs. These functional disturbances were further corroborated by decreased dendritic spine density and spine head volumes that indicated impaired synapse maturation. Slice biotinylation followed by Western blot analysis of PFC-L5 tissue revealed that 5XFAD mice showed reduced synaptic AMPA receptor subunit GluA1 and decreased synaptic NMDA receptor subunit GluN2A. Consistent with this, patch-clamp recording of the evoked L23>L5 synaptic responses revealed a reduced AMPA/NMDA receptor current ratio, and an increased level of AMPAR-lacking silent synapses. These results suggest that transgenic mutant forms of APP/PS1 overexpression in 5XFAD mice leads to early developmental defects of cortical circuits, which could contribute to the age-dependent synaptic pathology and neurodegeneration later in life.

The molecular regulation of the temporal dynamics of circuit maturation is a key contributor to the emergence of normal structure-function relations. Developmental control of cortical MET receptor tyrosine kinase, expressed early postnatally in subpopulations of excitatory neurons, has a pronounced impact on the timing of glutamatergic synapse maturation and critical period plasticity. Here, we show that using a controllable overexpression (cto-Met) transgenic mouse, extending the duration of MET signaling after endogenous Met is switched off leads to altered molecular constitution of synaptic proteins, persistent activation of small GTPases Cdc42 and Rac1, and sustained inhibitory phosphorylation of cofilin. These molecular changes are accompanied by an increase in the density of immature dendritic spines, impaired cortical circuit maturation of prefrontal cortex layer 5 projection neurons, and altered laminar excitatory connectivity. Two photon in vivo imaging of dendritic spines reveals that cto-Met enhances de novo spine formation while inhibiting spine elimination. Extending MET signaling for two weeks in developing cortical circuits leads to pronounced repetitive activity and impaired social interactions in adult mice. Collectively, our data revealed that temporally controlled MET signaling as a critical mechanism for controlling cortical circuit development and emergence of normal behavior.

数字化虚拟解剖技术,能够提供三维解剖学的立体图像和精确结构,现在被越来越多地用于解剖课程的教学.此研究采用美国VH Dissector数字化虚拟解剖技术,评估康复治疗学专业学生解剖教学的应用效果.结果发现数字化虚拟解剖技术与传统解剖教学方法相结合,能够激发康复治疗专业学生的解剖课程学习兴趣,提高学生的学习效率,具有更好的教学效果.

功能解剖学是我国康复治疗学本科专业的重要基础学科课程之一，是研究正常人体解剖结构与机体功能关系的一门 学科，具有重要的学科地位和指导作用。随着现代社会需求的不断增加以及我国康复治疗学专业的飞速发展，如何 对康复治疗学专业的功能解剖学课程进行教学标准、教学模式、教学质量考核的整体改革，从而有效提升教学效 果，激发学生的主观能动性，值得思考和探讨。

随着内科康复及围手术期康复迅速发展、残疾人群体日渐庞大、人口老龄化日趋明显,我国康复医疗需求骤增,而现有康复治疗师数量与服务质量均难以满足社会需求,提高康复治疗师的医疗服务质量迫在眉睫.胜任力导向的医学教育作为第三次医学教育改革的核心特征,为康复治疗师培养方法改革开辟了新思路.此文结合康复治疗师岗位胜任力要求,以规范化培训作为教育模式改革的突破口,探索以岗位胜任力为导向的康复治疗师人才培养模式改革.

目的:研究上肢机器人训练对脑卒中偏瘫患者上肢运动功能的影响.方法:选取40例脑卒中偏瘫患者,随机分为对照组和研究组,对照组予以常规的康复训练,研究组在常规康复训练基础上结合上肢机器人训练.两组均连续训练4周.治疗前、后分别采用Fugl-Meyer运动功能量表上肢部分(FMA-UE)以及Barthel指数(BI)评定患者上肢运动功能及日常生活能力.结果:两组病例康复训练后的Barthel指数评分均有显著提高,差异具有统计学意义(P<0.05).与对照组相比,研究组患者的Fugl-Meyer运动功能量表上肢部分评分显著增高(P<0.05).结论:上肢机器人训练可有效提高脑卒中偏瘫患者的上肢运动功能和运动质量.

目的 研究脑源性神经营养因子(BDNF)对内皮细胞Sestrin2表达的影响及机制,并探讨其在血管新生中的作用.方法 用100 μg/L的BDNF分别处理人脐静脉内皮细胞(HUVEC)1 h、2h、4h、6h、8h,实时荧光定量PCR检测Sestrin2 mRNA水平,免疫荧光和Western blot检测Sestrin2蛋白表达.将HUVEC分为6组:对照组(Control组)、BDNF组(加BDNF 100 μg/L)、BDNF+TrkB-Fc(1 mg/L)组、BDNF+KT-5823 (500 nmol/L)组、BDNF+L-NAME(10-4 mol/L)组、BDNF+DMSO组,共干预4h,Western blot检测Sestrin2蛋白表达.将HUVEC分为4组:对照组(Control组)、BDNF组(加BDNF 100μg/L)、BDNF+ Sestrin2 siRNA组和BDNF+Control siRNA组,共干预6h,细胞迁移实验和小管成形实验分别检测HUVEC迁移能力和血管生成能力.结果 与0h和1h组比较,100 μg/L BDNF分别干预HUVEC2、4及6h时段,Sestrin2 mRNA水平显著增高(P＜0.001),在2、4及8h时段Sestrin2蛋白表达显著增高(P＜0.05);阻断NO/PKG通路可抑制BDNF诱导的Sestrin2表达上调(P＜O.001);抑制Sestrin2表达后,HUVEC迁移及小管形成能力较BDNF干预组显著降低(P＜0.01).结论 BDNF通过NO/PKG通路促进内皮细胞表达Sestrin2,从而提高内皮细胞血管生成能力.

Traditional Chinese medicine (TCM) is a systematic medicine. It provides alternative strategies for the treatment of depression with its clinical experience, comprehensive diagnosis, and treatment theory. Chinese herbal medicine (CHM) is the major form of TCM prescription, and numerous CHMs have been demonstrated to possess remarkable antidepressant-like properties. A diversity of mechanisms have been implicated in CHM-associated antidepressant property. This paper reviewed the neuroplastic mechanisms underlying the antidepressant actions of CHM, finding that CHM repairs neuroplasticity by improving neurogenesis, neurotrophic factors, synaptic spine morphology, cell signaling, glutamatergic system, monoamine neurotransmitters, and neural apoptosis. CHM thereby exerts an antidepressant effect, attempting to offer a better understanding of the mechanisms implicated in TCM-related antidepressant-like efficacy and laying a foundation for the scientific evaluation and development of TCM in treating depression.

Human genetic studies established MET gene as a risk factor for autism spectrum disorders. We have previously shown that signaling mediated by MET receptor tyrosine kinase, expressed in early postnatal developing forebrain circuits, controls glutamatergic neuron morphological development, synapse maturation, and cortical critical period plasticity. Here we investigated how MET signaling affects synaptic plasticity, learning and memory behavior, and whether these effects are age-dependent. We found that in young adult (postnatal 2-3 months) Met conditional knockout (Metfx/fx:emx1cre, cKO) mice, the hippocampus exhibits elevated plasticity, measured by increased magnitude of long-term potentiation (LTP) and depression (LTD) in hippocampal slices. Surprisingly, in older adult cKO mice (10-12 months), LTP and LTD magnitudes were diminished. We further conducted a battery of behavioral tests to assess learning and memory function in cKO mice and littermate controls. Consistent with age-dependent LTP/LTD findings, we observed enhanced spatial memory learning in 2-3 months old young adult mice, assessed by hippocampus-dependent Morris water maze test, but impaired spatial learning in 10-12 months mice. Contextual and cued learning were further assessed using a Pavlovian fear conditioning test, which also revealed enhanced associative fear acquisition and extinction in young adult mice, but impaired fear learning in older adult mice. Lastly, young cKO mice also exhibited enhanced motor learning. Our results suggest that a shift in the window of synaptic plasticity and an age-dependent early cognitive decline may be novel circuit pathophysiology for a well-established autism genetic risk factor.

This study aimed to explore the protective effects of Wenshen-Yanggan decoction on dopaminergic (DA) neuron injury in a rotenone-induced mouse model with chronic Parkinson's disease (PD) and explore its mechanism of action. Ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was used to measure the content of six main components in the Wenshen-Yanggan decoction. The chronic PD mouse model was established by treating 10-month-old healthy wild C57BL/6 male mice with rotenone 30 mg/kg/day for 28 days in succession. The pole test and rotarod test were applied to detect the rescue effect of Wenshen-Yanggan decoction in high, medium, and low dosages, respectively, on PD-like behaviors in mice with chronic PD. The protective effect of Wenshen-Yanggan decoction on the mesencephalic nigrostriatal DA neuron injury was determined employing tyrosine hydroxylase (TH) immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was adopted to measure the inflammatory cytokines in serum, including TNF-α (tumor necrosis factor-alpha), IFN-γ (interferon gamma), NF-κB (nuclear factor kappa-B), and IL-1β (interleukin-1 beta). Western blotting was performed to quantify the expression of phosphorylated c-Jun N-terminal kinase (p-JNK), cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), and NF-κB in the brain. Our results showed that the Wenshen-Yanggan decoction in high, medium, and low dosages reduced the turning time of mice (P < 0.01, P < 0.01,  and P < 0.05). The high and medium dosages shortened the total climbing time of PD mice in the pole test (P < 0.01 and P < 0.05). Meanwhile, the high, medium, and low dosages increased the rod-standing time of PD mice in the rotarod test (P < 0.01, P < 0.05,  and P < 0.05). Besides, the decoction reversed the decrease in TH-positive neurons induced by rotenone, upregulated TH protein expression, and downregulated the α-syn expression in the PD model. Moreover, the decoction in high dosage significantly inhibited the expression of p-JNK, cleaved caspase-3, and NF-κB in the midbrain of PD mice (P < 0.05, P < 0.05,  and P < 0.01), upregulated the expression of Bcl-2 (P < 0.05), and decreased the content of TNF-α, IFN-γ, NF-κB, and IL-1β in the serum (P < 0.001, P < 0.001, P < 0.001,  and P < 0.001). Taken together, the Wenshen-Yanggan decoction could protect mice from rotenone-induced chronic PD, which might be related to the reduction of the DA neuron apoptosis via suppressing the inflammatory reaction and the neuronal apoptosis pathway.

目的 探讨越鞠甘麦大枣汤(越甘汤)对产后抑郁症(Postpartum depression,PPD)小鼠的快速抗抑郁作用,并从脑源性神经营养因子(BDNF)-酪氨酸蛋白激酶B(TrkB)通路探讨PPD的发病机制及中药起效的作用机制.方法 将40只Balb/c雌性小鼠随机分为2组,空白组不给予任何刺激,孕前应激组给予慢性束缚刺激.3周后将孕前应激组小鼠进行雌雄合笼交配怀孕,分娩后3周检测小鼠的糖水偏好率和强迫游泳不动时间.将孕前应激组诱导建立的PPD小鼠随机分为3组:模型组、越甘汤组和氯胺酮组,检测药物对小鼠的干预作用,并取小鼠前额叶检测BDNF、TrkB、糖原合酶激酶3β (GSK3β)和p-GSK3β蛋白的表达.结果 产后3周,与空白组比较,模型组的糖水偏好率显著降低(P＜0.01),强迫游泳不动时间显著延长(P＜0.01),前额叶BDNF、TrkB及p-GSK3β/GSK3β的表达均显著下调(P＜0.05).单次给予越甘汤或氯胺酮24 h之后,小鼠的糖水偏好率显著升高(P＜0.01),强迫游泳不动时间显著减少(P＜0.01),前额叶BDNF、TrkB及p-GSK3β/GSK3β的蛋白表达显著上调(P＜0.05).结论 慢性孕前应激诱导Balb/c小鼠表现出产后抑郁样症状,其发病机制可能与激活其前额叶BDNF-TrkB通路有关.越甘汤对PPD模型小鼠的快速抗抑郁作用可能与改善前额叶BDNF-TrkB信号通路有关.

SophoraflavanoneG (SG), an important prenylated flavonoid isolated from Sophoraalopecuroides.L, is effective for many illnesses. The present study was designed to investigate whether the compound could reverse depressive-like symptoms and investigate its possible mechanisms. Chronic Unpredictable Mild Stress (CUMS) mice were treated with fluoxetine and SG. The immobility time in forced swimming test (FST) and tail suspension test (TST) were recorded. The levels of pro-inflammatory cytokines and neurotransmitters in the hippocampus were evaluated. Furthermore, the protein expressions of PI3K, AKT, mTOR, p70S6K, BDNF, and Trkb in hippocampus were detected. Rapamycin, the selective mTOR inhibitor, was used to estimate the potential mechanism. As a result, after 7 days of SG treatment, the immobility time in FST and TST was declined obviously. The levels of IL-6, IL-1 beta, and TNF-alpha in the hippocampus were significantly reduced, and the quantity of 5-HT and NE was raised considerably in SG-treated group compared with the CUMS-exposed group. Additionally, SG could up-regulate the expressions of PI3K, AKT, mTOR, 70S6K, BDNF, and Trkb. The blockade of mammalian target of rapamycin signaling blunted the antidepressant effect and reversed the up-regulation of BDNF expression caused by SG. These findings suggested that SG treatment alleviated depressive-like symptoms via mTOR-mediated BDNF/Trkb signaling.

目的 探讨越鞠甘麦大枣汤对产后抑郁症(PPD)小鼠的抗抑郁作用及其对小鼠海马SIRT1-ERK1/2信号通路的影响.方法 40只雌性Balb/c小鼠随机分为对照组、模型组、艾司西酞普兰组和越鞠甘麦大枣汤组,每组10只.除对照组外,各组小鼠均接受束缚刺激6周.对照组和应激小鼠均与正常雄性Balb/C小鼠合笼交配,小鼠分娩3周后,给药2周观察药效,蛋白免疫印迹检测小鼠海马SIRT1、ERK1/2、P-ERK1/2、P90RSK及CREB的表达.结果 与对照组相比,模型组小鼠糖水偏好下降(P<0.05),强迫游泳不动时间增加(P<0.01),体质量降低(P<0.05).越鞠甘麦大枣汤和艾司西酞普兰均增加小鼠糖水偏好(均P<0.05),降低小鼠强迫游泳不动时间(均P<0.05).分子水平上,与对照组相比,模型组小鼠海马SIRT1、P-ERK/ERK、P90RSK、CREB等蛋白的表达降低(均P<0.05);越鞠甘麦大枣汤和艾司西酞普兰均增加小鼠海马SIRT1、P-ERK/ERK、P90RSK、CERB等蛋白的表达(均P<0.05).结论 越鞠甘麦大枣汤能改善PPD小鼠的抑郁样行为,可能与其上调小鼠海马SIRT1-ERK1/2信号通路有关.

α-Cyperone (Cy) is a major active compound of Cyperus rotundus that has various pharmacological activities. But whether Cy possesses antidepressant effect is unknown. In this study, we exposed mice to chronic unpredictable mild stress (CUMS) with or without intervention with Cy. Our results showed that Cy significantly improved the depressive phenotypes in sucrose preference test, tail suspension test and forced swimming test. Meanwhile, increased SIRT3 expression, reduced ROS production and activated NF-κB signal were detected in the hippocampus of mice. NLRP3 inflammasome related proteins including NLRP3, ASC, Caspase-1, IL-1β, IL-18 and GSDMD-N were downregulated after Cy administration. Synaptic proteins including Synapsin-1 and PSD-95 and dendritic spine density were improved after Cy treatment. Moreover, the protective effects of Cy in CUMS mice were compromised when co-administrated with SIRT3 inhibitor 3-TYP. Taken together, these findings suggested that Cy has therapeutic potential for treating depression and that this antidepressant effect may be attributed to SIRT3 stimulated neuroplasticity enhancement by suppressing NLRP3 inflammasome.

目的 探讨好忘方(HWF)对阿尔茨海默病(AD)模型小鼠认知障碍改善作用及其与PKA介导的磷酸化TAU的清除和突触可塑性的增强的关系.方法 选用东莨菪碱小鼠模型和SAMP8小鼠模型,分别给予1周和3周的药物治疗,分为空白对照组(CTL)、模型对照组(Veh)、好忘方组和多奈哌齐组(Donepezil).给药结束后通过Morris水迷宫(MWM)和新物体识别(NOR)检测小鼠的认知水平.Western blot检测SAMP8小鼠各组海马中PKA-GSK3β-TAU通路与PKA-CREB及其下游SYNAPSIN1、GLUR1、PSD95、BDNF的蛋白水平变化.结果 东莨菪碱模型下给药1周后,Morris水迷宫测试中,好忘方组和多奈哌齐组站台穿越次数与模型对照组相比明显增多(P<0.01).SAMP8模型下给药3周后,好忘方和多奈哌齐逆转了SAMP8小鼠MWM逃避潜伏期的增加,站台穿越次数及NOR指数的减少(P<0.01),激活PKA-GSK3β-TAU通路降低了TAU-Ser404蛋白水平(P<0.01),并逆转了SAMP8小鼠海马中PKA-CREB及其下游BDNF和突触蛋白SYNAPSIN1、GLUR1、PSD95蛋白水平的下降(P<0.05～0.01).且好忘方能够逆转SAMP8小鼠MWM目标象限路程比的下降(P<0.05),并在改善MWM逃避潜伏期方面优于多奈哌齐(P<0.05).结论 好忘方可改善AD模型小鼠认知障碍,这与PKA介导的磷酸化TAU的清除和突触可塑性的增强密切相关.

ETHNOPHARMACOLOGICAL RELEVANCE:Gardeniae fructus is a traditional Chinese herb which exerts antidepressant effect. However, its effective constituent and potential mechanism are still unknown.AIM OF THE STUDY:To examine whether iridoids, a type of monoterpenoids from Gardeniae fructus (IGF), exerts antidepressant effect by enhancing synaptic plasticity via AMPA receptor-mTOR signaling.MATERIALS AND METHODS:The antidepressant effect of IGF (15 mg/kg; 30 mg/kg; 45 mg/kg) was investigated in spatial restraint stress (SRS)-induced mice. The expression levels of AMPA receptor-mTOR signaling and synaptic proteins were measured by Western blot, dendritic spine density was observed in Golgi staining. AMPA receptor (AMPAR) inhibitor NBQX and mTOR inhibitor Rapamycin were employed to determine the roles of AMPAR and mTOR signaling in IGF-induced antidepressant effects.RESULTS:After IGF administration, the expression of the AMPA glutamate receptor Glutamate Receptor 1 (GluA1) was inhibited in SRS mice. We also observed a trend toward the up-regulation of the mammalian target of Rapamycin (mTOR) protein kinase, p70 ribosomal protein S6K (P70S6K) and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1). The protein levels of Synapsin-1 and PSD-95 were decreased after SRS challenge, along with declined dendritic spine density, which were all reversed with IGF treatment. Furthermore, the treatment efficacy of IGF were blocked with AMPA receptor inhibitor NBQX or mTOR inhibitor Rapamycin.CONCLUSION:IGF exerted antidepressive-like effects by stimulating AMPAR-mTOR signaling regulated synaptic plasticity enhancement. This work provided an important basis for developing IGF and Gardeniae fructus as potential anti-depressants.

在融合教育背景下,越来越多的视障学生进入普通高等学校学习,本研究通过自编问卷从视障人群和普通人群的角度开展调查,研究我国高校视障大学生帮扶服务现状,发现目前帮扶支持服务领域存在的问题,提出相应对策,并进行视障大学生帮扶服务支持体系的构建实践,力图解决当下我国视障大学生的困难和问题,促进高校融合教育的顺利实行.