Depressive Like Behavior(抑郁样行为)研究综述
Depressive Like Behavior 抑郁样行为 - MATERIALS AND METHODS The present systematic review was conducted using PubMed, Embase and ScienceDirect databases, from 2000 to 2020, using the following key terms: Nandrolone AND Cognition, Nandrolone AND Learning, Nandrolone AND Memory, Nandrolone AND (Synaptic plasticity or Hippocampal synaptic plasticity), Nandrolone AND (Aggression or Aggressive-like behavior), Nandrolone AND (Anxiety or Anxiety-like behavior), Nandrolone AND (Depression or Depressive-like behavior). [1] By comparison, SAMP6 mice develop depressive-like behavior that is associated with a rise in the GABA-producing bacterial genus Parabacteroides. [2] Those weaned at 15 days of age exhibited higher depressive-like behavior, lesser reactivity time to sucrose, and higher intake of palatable food than the control group. [3] In a rescue experiment, the effects of CORT on development of depressive-like behaviors and increased NGAL and IL18 protein levels in the kidney were blocked by CRISPR-mediated knockdown of hippocampal Mkp-1 prior to CORT exposure. [4] Our results showed that ibrutinib treatment significantly reduced lipopolysaccharide (LPS)-induced depressive-like behaviors and neuroinflammation via inhibiting NF-kB activation, decreasing proinflammatory cytokine levels, and normalizing redox signaling and its downstream components, including Nrf2, HO-1, and SOD2, as well as glial cell activation markers, such as Iba-1 and GFAP. [5] Here, we tested the hypothesis that anxiogenic and depressive-like behaviors driven by consuming a HFD involve compromised duodenal barrier integrity and subsequent phenotypic changes to glia and neurons along the gut-brain axis. [6] It was found that XAN administration significantly reversed the depressive-like behaviors of CUMS-treated mice. [7] This study aimed to explore the effects and mechanisms of DS in attenuating depressive-like behaviors and cognitive deficiency induced by simulated weightlessness and isolation [hindlimb suspension and isolation (HLSI)] in rats. [8] The adult non-human primate stress-induced model of depressive-like behavior is an excellent model for the study of mechanisms; however, an adolescent nonhuman primate model is still lacking. [9] Open field exploratory behavior results showed that blast exposed rats treated with meloxicam engaged in significantly more locomotor activities and possibly a lesser degree of responses thought to reflect anxiety and depressive-like behaviors than any of the other groups. [10] We hypothesize that exposure to hypobaric hypoxia at high altitude increases endophenotypes of self-directed suicidal violence, including biological signatures of chronic inflammation and vulnerability to anxiety-like and depressive-like behavioral responses in a sex-specific manner. [11] BACKGROUND We recently reported that tumor necrosis factor (TNF) signaling via the TNFR1 and TNFR2 receptors mediates the effects of long-term exercise on locomotion, cognition and anxiety, but not depressive-like behavior. [12] The study was conducted to investigate the depressive-like behavior induced by chronic ethanol exposure in mice and to explore the mechanism in cells. [13] However, CCD failed to provoke a depressive-like behavioral response in either 5-Htt genotype. [14] Our results indicated that peripheral repeated administration of lipopolysaccharides (LPS) (1 mg/kg, intra peritoneally) induced depressive-like behavior, neuroinflammation and O&NS in mice. [15] GB-S (10 and 20 mg/kg) significantly restores neurobehavioral impairments based on improved locomotion, reduced anxiety- and depressive-like behavior. [16] To elucidate if such dipoles influence depressive-like behavior, without external stimulation, the comparative effect of conducting and insulated electrodes along with the glial response is studied in unstressed rats. [17] We found that this deletion caused anxiety-like but not depressive-like behaviors in adult male mice. [18] While CGRP has been rigorously studied for its role in migraines owing to its vasodilation and inflammation activities, the effects of CGRP overexpression on depressive-like behaviors remain insufficiently understood. [19] BACKGROUND Anxious-depressive-like behavior has been recognized as an early endophenotype in Alzheimer's disease (AD). [20] This study aimed to determine resveratrol’s effect on physical and psychological stress-induced depressive-like behavior. [21] This study firstly compared the gene expression profiles between neuropathic pain animals with and without depressive-like behavior, and we suggested the early changes in the activities of MAPK signaling pathway, c-Fos and Gadd45β might be related to late-onset depressive behavior induced by peripheral nerve injury. [22] Depressive-like behavior is a highly prevalent worldwide neuropsychiatric disorder that owns a complex pathophysiologic mechanism. [23] Here, we investigated the impact of dHi, iHi or vHi lesions on anxiety- and depressive-like behaviors under baseline or antidepressant treatment conditions in male C57BL/6 mice (n = 8–10). [24] In a genetically modified mouse line with depressive-like behavior, Smpd1 mRNA expression in dorsal hippocampal tissue was significantly decreased after treatment with a common antidepressant. [25] On the FST, there was a dose-response effect of intranasal NPY, with 1,200 μg, but not 600 μg, preventing the development of the SPS-elicited depressive-like behavior. [26] Since recent GWAS data and experimental studies associated RXR-mediated signaling with depression, we explored here the relevance of RXR and vitamin A5/X-mediated signaling in the control of stress adaptation and depressive-like behaviors in mice. [27] Lipopolysaccharide decreased the bodyweight, sucrose preference in SPT (depressive-like behavior), spontaneous activity in OFT (anxiety-like behavior) and increased the immobility time in FST (depressive-like behavior). [28] Furthermore, our new approach reveals the transmembrane proteome remodeling landscape in the brain of a mouse depression model, which led to the identification of two previously unknown GPCR regulators of depressive-like behaviors. [29] However, promoting ANH could not deal with the cognitive dysfunction and depressive-like behaviors in CCH rats. [30] Rats with hippocampal insulin resistance exhibited anxiety-like behaviors and behavioral despair without differences in anhedonia, suggesting that some but not all components of depressive-like behaviors were affected. [31] MO protected mice from PTZ– and MES–induced seizures and mortality, and ameliorated seizure severity, fear-avoidance, depressive-like behavior, cognitive deficits, oxidative stress and neuronal cell loss in PTZ–kindled rats. [32] We tested the hypothesis that BDNF deficient mice are vulnerable to the induction of depressive-like behavior following peripheral immune challenge. [33] Systemic injection with lipopolysaccharide can lead to depressive-like behavior in experimental animals by inducing neuroinflammation and is considered to be a classic model of depression. [34] Results: Cessation of nicotine, tobacco smoke, nicotine vapor, and e-cigarette aerosol exposure leads to nicotine withdrawal symptoms such as somatic withdrawal signs, changes in locomotor activity, anxiety- and depressive-like behavior, learning and memory deficits, attention deficits, hyperalgesia, and dysphoria. [35] In contrast, overexpression of miR-204-5p within the DG region of CUS rats alleviated oxidative stress and neuroinflammation by directly targeting the regulator of G protein signaling 12 (RGS12), effects which were accompanied with amelioration of depressive-like behaviors in these CUS rats. [36] Lastly, DAGL inhibition during either chronic alcohol consumption or protracted withdrawal was devoid of anxiogenic and depressive-like behavioral effects. [37] We demonstrate that the ADAR1 inducer (IFN-γ) alleviates the depressive-like behaviors of BALB/c mice treated with chronic unpredictable stress (CUS) exposure. [38] Although, this environmental intervention did not produce significant changes in the neurogenic process affected by chronic mild stress, fluoxetine plus environmental enrichment showed similar effects to those caused by environmental enrichment to reverse depressive-like behaviors. [39] RESULT The results showed that severe depressive-like behavior was induced by four weeks of CUS. [40] A series of behavioral tests and intrahippocampal pilocarpine (H-PILO) microinjection at sub-convulsive and convulsive doses in a rat model demonstrated that exposure to crack cocaine during the embryonic period leads to anxiogenic-like behavior and long-term memory impairment in both genders and promotes depressive-like behavior in the female. [41] Here we aim to study the specific role of each melatonin receptor (MT1 and MT2) subtype in melatonin regulation of circadian CBT and its possible relationship with depressive-like behaviors. [42] Lipopolysaccharide decreased the bodyweight, sucrose preference in SPT (depressive-like behavior), spontaneous activity in OFT (anxiety-like behavior) and increased the immobility time in FST (depressive-like behavior). [43] Pain, anxiety and depressive like behaviors were assessed in animals. [44] Depressive like behaviors, anxiety like behavior and memory impairment were tested using open field test, forced swimming test, elevated plus maze and Morris water maze. [45] Besides, 4-week administration of CoQ10 could reverse the depressive like behavior and bioenergetic effects of STZ in the treated groups. [46] Overexpressing ISG15 in the prefrontal cortex of neonatal cubs (P0) could mimic dendritic pathology and depressive like behaviors, while downregulating ISG15 rescued these abnormalities in the offsprings. [47]材料和方法 本系统评价是使用 PubMed、Embase 和 ScienceDirect 数据库进行的，从 2000 年到 2020 年，使用以下关键术语：诺龙与认知、诺龙与学习、诺龙与记忆、诺龙与（突触可塑性或海马突触可塑性）、诺龙与（攻击性或攻击性行为）、Nandrolone AND（焦虑或焦虑样行为）、Nandrolone AND（抑郁或抑郁样行为）。 [1] 相比之下，SAMP6 小鼠出现抑郁样行为，这与产生 GABA 的细菌副杆菌属的增加有关。 [2] 与对照组相比，在 15 日龄断奶的人表现出更高的抑郁样行为、更少的蔗糖反应时间和更高的可口食物摄入量。 [3] 在一项救援实验中，CORT 对抑郁样行为发展和肾脏中 NGAL 和 IL18 蛋白水平增加的影响被 CRISPR 介导的海马 Mkp-1 敲低在 CORT 暴露之前阻断。 [4] 我们的研究结果表明，依鲁替尼治疗通过抑制 NF-kB 活化、降低促炎细胞因子水平和使氧化还原信号及其下游成分（包括 Nrf2、HO-1 和 SOD2）正常化，显着降低脂多糖 (LPS) 诱导的抑郁样行为和神经炎症。 ，以及胶质细胞激活标志物，如 Iba-1 和 GFAP。 [5] 在这里，我们测试了一个假设，即由食用 HFD 驱动的焦虑和抑郁样行为涉及十二指肠屏障完整性受损以及随后沿肠-脑轴的神经胶质和神经元的表型变化。 [6] 发现 XAN 给药显着逆转了 CUMS 治疗小鼠的抑郁样行为。 [7] 本研究旨在探讨 DS 在减轻大鼠模拟失重和隔离 [后肢悬吊和隔离 (HLSI)] 引起的抑郁样行为和认知缺陷方面的作用和机制。 [8] 成年非人类灵长类动物应激诱导的抑郁样行为模型是研究机制的绝佳模型；然而，仍然缺乏青少年非人类灵长类动物模型。 [9] 开放场探索行为结果表明，与其他任何组相比，用美洛昔康治疗的暴露于爆炸的大鼠的运动活动明显更多，并且可能反映焦虑和抑郁样行为的反应程度较低。 [10] 我们假设在高海拔地区暴露于低压缺氧会增加自我导向的自杀暴力的内表型，包括慢性炎症的生物学特征以及以性别特异性方式对焦虑样和抑郁样行为反应的脆弱性。 [11] 背景 我们最近报道了通过 TNFR1 和 TNFR2 受体的肿瘤坏死因子 (TNF) 信号传导介导长期运动对运动、认知和焦虑的影响，但对抑郁样行为没有影响。 [12] 该研究旨在调查小鼠慢性乙醇暴露引起的抑郁样行为，并探索细胞中的机制。 [13] 然而，CCD 未能在任一 5-Htt 基因型中引发抑郁样行为反应。 [14] 我们的结果表明，外周反复给予脂多糖 (LPS)（1 mg/kg，腹膜内）可诱导小鼠出现抑郁样行为、神经炎症和 O&NS。 [15] GB-S（10 和 20 mg/kg）通过改善运动、减少焦虑和抑郁样行为显着恢复神经行为障碍。 [16] 为了阐明这种偶极子是否会在没有外部刺激的情况下影响抑郁样行为，在无压力的大鼠中研究了导电电极和绝缘电极的比较效应以及神经胶质反应。 [17] 我们发现这种缺失会导致成年雄性小鼠出现焦虑样行为，但不会导致抑郁样行为。 [18] 虽然 CGRP 因其血管舒张和炎症活动而在偏头痛中的作用已被严格研究，但 CGRP 过表达对抑郁样行为的影响仍知之甚少。 [19] 背景 焦虑抑郁样行为已被认为是阿尔茨海默病 (AD) 的早期内表型。 [20] 本研究旨在确定白藜芦醇对生理和心理压力引起的抑郁样行为的影响。 [21] 本研究首先比较了有和没有抑郁样行为的神经性疼痛动物的基因表达谱，我们认为 MAPK 信号通路、c-Fos 和 Gadd45β 活性的早期变化可能与迟发性抑郁行为有关。周围神经损伤。 [22] 抑郁样行为是一种在世界范围内高度流行的神经精神疾病，具有复杂的病理生理机制。 [23] 在这里，我们研究了 dHi、iHi 或 vHi 损伤对雄性 C57BL/6 小鼠（n = 8-10）在基线或抗抑郁治疗条件下的焦虑和抑郁样行为的影响。 [24] 在具有抑郁样行为的转基因小鼠品系中，用普通抗抑郁药治疗后，背侧海马组织中 Smpd1 mRNA 的表达显着降低。 [25] 在 FST 上，鼻内 NPY 存在剂量反应效应，1,200 μg，但不是 600 μg，阻止了 SPS 引发的抑郁样行为的发展。 [26] 由于最近的 GWAS 数据和实验研究将 RXR 介导的信号传导与抑郁症联系起来，我们在这里探讨了 RXR 和维生素 A5/X 介导的信号传导在控制小鼠压力适应和抑郁样行为中的相关性。 [27] 脂多糖降低了体重、SPT 中的蔗糖偏好（抑郁样行为）、OFT 中的自发活动（焦虑样行为）并增加了 FST 中的不动时间（抑郁样行为）。 [28] 此外，我们的新方法揭示了小鼠抑郁模型大脑中的跨膜蛋白质组重塑景观，这导致了两种以前未知的抑郁样行为的 GPCR 调节因子的鉴定。 [29] 然而，促进ANH并不能处理CCH大鼠的认知功能障碍和抑郁样行为。 [30] 具有海马胰岛素抵抗的大鼠表现出焦虑样行为和行为绝望，而在快感缺乏方面没有差异，这表明抑郁样行为的一些但不是所有成分都受到了影响。 [31] MO 保护小鼠免受 PTZ 和 MES 诱导的癫痫发作和死亡，并改善 PTZ 点燃的大鼠的癫痫发作严重程度、恐惧回避、抑郁样行为、认知缺陷、氧化应激和神经元细胞丢失。 [32] 我们测试了 BDNF 缺陷小鼠在外周免疫攻击后易受抑郁样行为诱导的假设。 [33] 全身注射脂多糖可通过诱导神经炎症导致实验动物出现抑郁样行为，被认为是抑郁症的经典模型。 [34] 结果：停止尼古丁、烟草烟雾、尼古丁蒸汽和电子烟气溶胶暴露会导致尼古丁戒断症状，例如躯体戒断症状、运动活动变化、焦虑和抑郁样行为、学习和记忆缺陷、注意力缺陷、痛觉过敏和烦躁不安。 [35] 相比之下，在 CUS 大鼠 DG 区内过表达 miR-204-5p 通过直接靶向 G 蛋白信号 12 (RGS12) 的调节因子来减轻氧化应激和神经炎症，这些作用伴随着这些 CUS 中抑郁样行为的改善老鼠。 [36] 最后，在慢性饮酒或长期戒断期间的 DAGL 抑制没有焦虑和抑郁样行为影响。 [37] 我们证明 ADAR1 诱导剂 (IFN-γ) 减轻了接受慢性不可预测压力 (CUS) 暴露治疗的 BALB/c 小鼠的抑郁样行为。 [38] 尽管这种环境干预并未对受慢性轻度压力影响的神经源性过程产生显着变化，但氟西汀加环境富集显示出与环境富集引起的逆转抑郁样行为相似的效果。 [39] 结果 结果表明，4周的CUS诱发了严重的抑郁样行为。 [40] 在大鼠模型中以亚惊厥和惊厥剂量进行的一系列行为测试和海马内毛果芸香碱 (H-PILO) 显微注射表明，在胚胎期暴露于可卡因可导致两性的焦虑样行为和长期记忆障碍并促进女性的抑郁行为。 [41] 在这里，我们旨在研究每个褪黑激素受体（MT1 和 MT2）亚型在昼夜 CBT 的褪黑激素调节中的具体作用及其与抑郁样行为的可能关系。 [42] 脂多糖降低了体重、SPT 中的蔗糖偏好（抑郁样行为）、OFT 中的自发活动（焦虑样行为）并增加了 FST 中的不动时间（抑郁样行为）。 [43] 在动物中评估疼痛、焦虑和抑郁样行为。 [44] 使用旷场测试、强迫游泳测试、高架十字迷宫和莫里斯水迷宫测试抑郁样行为、焦虑样行为和记忆障碍。 [45] 此外，服用 4 周的辅酶 Q10 可以逆转 STZ 在治疗组中的抑郁样行为和生物能量效应。 [46] 在新生幼崽 (P0) 的前额叶皮层中过度表达 ISG15 可以模仿树突病理和抑郁样行为，而下调 ISG15 可以挽救后代的这些异常。 [47]
open field test 野外试验
While SAS decreased the total distance travelled in the open-field test the first time the mice encountered the test, it did not influence this parameter on the long-term and it did not induce other behavioral changes such as anxiety- or depressive-like behavior. [1] In addition, their depressive-like behaviors, anxiety-like behaviors, and sociability were recorded using sucrose preference, a forced swim, social interaction, tail suspension, and open field tests. [2] Results: Our results show that rifaximin ameliorated depressive-like behavior induced by CUMS, as reflected by sucrose preference, the open field test and the Morris water maze. [3] Depressive-like behaviors were investigated by body weight alteration, open field test (OFT), and sucrose preference test (SPT). [4] Mechanical and thermal hyperalgesia as well as depressive-like behaviors were induced using the open field test and forced swimming test. [5] Open field test, elevated plus maze test, and tail suspension test were used to assess anxiety- and depressive-like behaviors. [6] We found that the rats exhibited the depressive-like behavior by the sucrose preference, forced swimming, and open-field tests. [7] We found no effect of age dynamics on the locomotor activity and anxiety in the open-field test as well as on depressive-like behavior in the tail-suspension test. [8] The following day, mice were subjected to an open field test (anxiety-like behavior), followed by forced swim testing (depressive-like behavior). [9] Interestingly, chronic, but not acute, CDN1163 administration induced anxiogenic and depressive-like behavioral effects in mice, as assessed in the open field test (OFT) and the forced swim test (FST), respectively. [10]虽然 SAS 减少了小鼠第一次遇到测试时在旷场测试中行进的总距离，但它不会长期影响该参数，也不会引起其他行为变化，例如焦虑或抑郁样行为. [1] 此外，使用蔗糖偏好、强迫游泳、社交互动、悬尾和野外测试记录了他们的抑郁样行为、焦虑样行为和社交能力。 [2] 结果：我们的结果表明，利福昔明改善了由 CUMS 引起的抑郁样行为，这反映在蔗糖偏好、旷场试验和莫里斯水迷宫中。 [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9] nan [10]
forced swimming test 强迫游泳试验
Forced Swimming Test (FST) was used to evaluate depressive-like behaviors. [1] The treatments with curcumin prevented the depressive-like behavior in the Forced Swimming Test and they had anxiolytic effects on the non-stressed animals. [2] (m-CF3-PhSe)2 treatment reverted the reserpine-increased thermal hyperalgesia and depressive-like behavior observed in the hot-plate test and forced swimming test, respectively. [3] Additionally, MFB lesions induced depressive-like behaviors in the sucrose preference and forced swimming tests. [4] Animals were submitted to forced swimming test, to evaluate depressive-like behavior, and to open field test, to evaluate locomotory activity. [5] We showed that MS caused depressive-like behaviors determined as an increase in the immobility time in the forced swimming test (FST) and decreased grooming time in the splash test. [6] Results: Animals with PCOS developed depressive-like behaviors compared with control in forced swimming test (P < 0. [7] After earth-based simulation for 21 days, the rats exhibited the depressive-like behavior according to the sucrose preference and forced swimming test. [8] Our findings show that AGO can attenuate the depressive-like behavior that significantly appeared in both sucrose preference and forced swimming tests. [9]强迫游泳测试（FST）用于评估抑郁样行为。 [1] 姜黄素治疗可防止强迫游泳试验中的抑郁样行为，并且它们对非应激动物具有抗焦虑作用。 [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9]
chronic unpredictable mild 慢性不可预知的轻度
Chronic unpredictable mild stress (CUMS) was applied for 6 weeks to induced a depressive-like behavior, characterized by decreased locomotor activity, sucrose preference and the NE, DA and 5-HT levels in cortex. [1] In this study, we focused on the role and mechanisms of miR-129-5p in depression by successfully constructing mice models of depressive-like behavior via chronic unpredictable mild stress (CUMS) exposure. [2] The aim of this study was to explore the effects of HT on chronic unpredictable mild stress (CUMS) induced depressive-like behaviors. [3] In our study, depressive-like behavior was induced in mice by chronic unpredictable mild stress (CUMS) model. [4] This study was to investigate whether and how miR-144 involves in depressive-like behaviors in a chronic unpredictable mild stress (CUMS) animal model. [5] The present study aimed to assess Cur’s beneficial effects on depressive-like behaviors using a chronic unpredictable mild stress (CUMS) model and its possible molecular mechanisms. [6] The male SD rats with depressive-like behaviors were stimulated with chronic unpredictable mild stress (CUMS) including ice-water swimming for 5 min, food deprivation for 24 h, water deprivation for 24 h, stimulating tail for 1 min, turning night into day, shaking for 15 min (once/s), and wrap restraint (5 min/time) every day for 21 days. [7] The Chronic unpredictable mild stress (CUMS) method were selected to induce depressive-like behaviors of rats. [8] In our study, depressive-like behavior was induced in mice by chronic unpredictable mild stress (CUMS) model. [9]应用慢性不可预测的轻度压力 (CUMS) 6 周以诱导抑郁样行为，其特征是运动活动减少、蔗糖偏好以及皮质中的 NE、DA 和 5-HT 水平。 [1] 在这项研究中，我们通过慢性不可预测的轻度压力 (CUMS) 暴露成功构建了抑郁样行为的小鼠模型，重点关注 miR-129-5p 在抑郁症中的作用和机制。 [2] nan [3] nan [4] nan [5] nan [6] nan [7] nan [8] nan [9]
tail suspension test 尾悬挂试验
chinense could decrease depressive-like behaviors of mice, increase sucrose preference, and shorten the time of immobility in tail suspension test. [1] Behavioral analysis revealed increased immobility time in the forced swim and tail suspension tests, and decreased sucrose intake in SD mice, all indicative of depressive-like behavior. [2] In animal models of depression (forced swimming and tail suspension test), EAFMEWF and NHFMEWF demonstrated a dose-dependent antidepressant-like effect; explicitly, the depressive-like behaviors significantly declined in EAFMEWF-treated dosing groups in contrast to the control group. [3] Our results indicated that CUS induced a depressive-like behavior, as demonstrated by an increase in the immobility time and latency to first grooming in the tail suspension test and splash test, respectively. [4] Analysis of depressive-like behaviors with the forced swim and tail suspension tests were not observed. [5] To address this question, we observed depressive-like behavior of OBX mice in the tail-suspension test, and determined the quantity of myelin proteins in the prefrontal cortex (PFC), striatum and hippocampus on day 14 or 21 after surgery. [6] We evaluated the depressive-like behavior by using the tail suspension test (TST) and the splash test (ST). [7]chinense可以减少小鼠的抑郁样行为，增加对蔗糖的偏好，缩短悬尾试验的不动时间。 [1] 行为分析显示，在强迫游泳和悬尾测试中，静止时间增加，SD 小鼠的蔗糖摄入量减少，所有这些都表明存在抑郁样行为。 [2] nan [3] nan [4] nan [5] nan [6] nan [7]
sucrose preference test 蔗糖偏好测试
Young plasma significantly improved CUMS-induced depressive-like behaviors, evidenced by the increased sucrose consumption ratio in the sucrose preference test and the reduced immobility time in the forced swimming test. [1] Our results showed that long-term exposure to aversive stimuli significantly enhanced depressive-like behavior evaluated by the sucrose preference test and the forced swimming test and increased anxiety-like behaviors evaluated using the open field test. [2] A reduction in sucrose preference is a key characteristic of depressive-like behaviors after spinal cord injury as judged by the sucrose preference test, the hypothalamic-pituitary-adrenal axis and adult hippocampal neurogenesis. [3] The depressive-like behaviors of mice were evaluated by sucrose preference test, forced swimming test (FST), and tail suspension test (TST). [4] This study showed that dietary CAP improved depressive-like behavior (sucrose preference test, forced swimming test, tail suspension test) and levels of 5-HT and TNF-α in serum of LPS-induced mice with depression-like behaviors. [5] 5, 135, or 270 mg/kg) significantly reverses the depressive-like behaviors in rats with a 5-week CUMS exposure, as demonstrated by increased sucrose consumption in the sucrose preference test, and decreased immobility time in the tail suspension and forced swim test. [6]年轻血浆显着改善了 CUMS 诱导的抑郁样行为，这可以通过蔗糖偏好测试中增加的蔗糖消耗率和强迫游泳测试中减少的不动时间来证明。 [1] 我们的研究结果表明，长期暴露于厌恶刺激显着增强了通过蔗糖偏好测试和强迫游泳测试评估的抑郁样行为，并增加了使用旷场测试评估的焦虑样行为。 [2] nan [3] nan [4] nan [5] nan [6]
forced swim test 强迫游泳试验
Inhibiting the microRNA significantly restores the hippocampal SERPINF1 mRNA and protein expression, and ameliorates the depressive-like behaviors including sucrose preference and extended immobility time in the forced swim test. [1] Here we reported that specific stimulation of astrocytic Sig-1R using adeno-associated virus (AAV) significantly attenuated lipopolysaccharide (LPS)- induced depressive-like behavior in the forced swim test (FST), tail suspension test (TST), sucrose preference test, and improved the memory function in novel object recognition test. [2] Saffron extract reduced depressive-like behavior in the forced swim test. [3] To explain the consequences of depressive-like behavior and anxiety, animals were exposed to the forced swim test (FST), open field test (OFT), and elevated plus maze (EPM). [4] Mice were tested for depressive-like behaviors (forced swim test (FST)), acoustic startle response (ASR), and pre-pulse inhibition (PPI). [5] Prevention of weaning from maternal milk was previously shown to result in stress-induced immobility during the forced swim test (FST), indicative of depressive-like behavior, accompanied by neurochemical, gut microbial and metabolic alterations in rats. [6]抑制 microRNA 可显着恢复海马 SERPINF1 mRNA 和蛋白质表达，并改善强迫游泳测试中的抑郁样行为，包括蔗糖偏好和延长不动时间。 [1] 在这里，我们报道了使用腺相关病毒 (AAV) 对星形细胞 Sig-1R 的特异性刺激显着减弱了脂多糖 (LPS) 在强迫游泳试验 (FST)、悬尾试验 (TST)、蔗糖偏好试验中诱导的抑郁样行为，并改进了新物体识别测试中的记忆功能。 [2] nan [3] nan [4] nan [5] nan [6]
chronic social defeat 长期的社会失败
AIMS C57BL/6J mice are well-known to exhibit resilience to chronic social defeat stress (CSDS) for induction of depressive-like behavior. [1] First, we subjected male mice to either physical or vicarious chronic social defeat stress (CSDS), paradigms known to induce long-term depressive-like behavior and changes in VTA signaling. [2] METHODS Depressive-like behaviors in C57BL/6J mice were developed by chronic social defeat stress. [3] The objective of the study is to elucidate the impact of Rb1 treatment on chronic social defeat stress (CSDS)–induced depressive-like behaviors and its related mechanism. [4] The chronic social defeat stress (CSDS) model is a mouse model of psychosocial stress that exhibits depressive-like behavior and chronic pain. [5]目标 众所周知，C57BL/6J 小鼠表现出对慢性社交失败压力 (CSDS) 的恢复能力，可诱导抑郁样行为。 [1] 首先，我们对雄性小鼠进行身体或替代性慢性社会挫败压力 (CSDS)，已知这些范例会诱发长期抑郁样行为和 VTA 信号变化。 [2] nan [3] nan [4] nan [5]
via morphological functional 通过形态泛函
Experimental evidence suggests that prolonged stress in mice induces depressive-like behaviors via morphological, functional and molecular changes affecting the mesolimbic and mesocortical dopaminergic pathways. [1] Experimental evidences suggest that prolonged stress in mice induces depressive-like behaviors via morphological, functional and molecular changes affecting the mesolimbic and mesocortical dopaminergic pathways. [2] Experimental evidences suggest that prolonged stress in mice induces depressive-like behaviors via morphological, functional and molecular changes affecting the mesolimbic and mesocortical dopaminergic pathways. [3]实验证据表明，小鼠长期压力通过影响中脑边缘和中皮质多巴胺能通路的形态、功能和分子变化诱导抑郁样行为。 [1] 实验证据表明，小鼠长期压力通过影响中脑边缘和中脑皮质多巴胺能通路的形态、功能和分子变化诱导抑郁样行为。 [2] nan [3]
elevated plus maze 高架十字迷宫
The anxiety and depressive-like behavior observed in ORX animals in the open field (OF) and elevated plus-maze experiments were effectively overturned in the ORX + T group. [1] Furthermore, msP rats of both sexes exhibit higher anxiety- and depressive-like behaviors in the elevated plus maze and forced swim test, respectively, compared with unselected Wistar controls. [2] DNLA attenuated body weight loss and CUS-induced anxiety/depressive-like behaviors, as evidenced by the elevated-plus-maze test, open-field test and sucrose preference. [3]在开放场 (OF) 和高架十字迷宫实验中观察到的 ORX 动物的焦虑和抑郁样行为在 ORX + T 组中被有效地推翻。 [1] 此外，与未选择的 Wistar 对照组相比，两种性别的 msP 大鼠分别在高架十字迷宫和强迫游泳测试中表现出更高的焦虑和抑郁样行为。 [2] nan [3]
novel object recognition 新的物体识别
Additionally, L-DE-71 exposure also altered short-term novel object recognition memory but not anxiety or depressive-like behavior. [1] Relative to wild-type (WT) littermates, loss of CTRP4 does not alter exploratory, anxiety-, or depressive-like behaviors, motor function and balance, sensorimotor gating, novel object recognition, and spatial memory. [2] Additionally, L-DE-71 exposure also altered short-term novel object recognition memory but not anxiety or depressive-like behavior. [3]此外，L-DE-71 暴露也改变了短期的新物体识别记忆，但不会改变焦虑或抑郁样行为。 [1] 相对于野生型 (WT) 同窝仔猪，CTRP4 的缺失不会改变探索性、焦虑或抑郁样行为、运动功能和平衡、感觉运动门控、新物体识别和空间记忆。 [2] nan [3]
open field elevated 露天高架
Behavioral tests (open field, elevated plus maze, tail suspension and forced swim test) were conducted to evaluate the effect of JTW on depressive-like behaviors. [1] , for 21 days injected from postnatal day 60) attenuated the high anxiety level tested in the open field, elevated plus-maze and light-dark test, and depressive-like behavior in the sucrose preference and the forced swimming tests in a sex-specific manner. [2]进行了行为测试（旷场、高架十字迷宫、悬尾和强迫游泳测试）以评估 JTW 对抑郁样行为的影响。 [1] ，从出生后第 60 天开始注射 21 天）减弱了在旷野中测试的高焦虑水平、升高的十字迷宫和明暗测试以及蔗糖偏好中的抑郁样行为和性别特异性中的强迫游泳测试方式。 [2]
high fat diet 高脂肪饮食
Here, we aim to evaluate the effects of high-fat diet (HFD) consumption on depressive-like behaviors. [1] We evaluated the neuroprotection of SPJ on high fat diet (HFD) induced impaired behaviors such as memory deficit and depressive-like behaviors, and explored the underlying mechanisms. [2]在这里，我们旨在评估高脂肪饮食 (HFD) 消费对抑郁样行为的影响。 [1] 我们评估了 SPJ 对高脂饮食 (HFD) 引起的记忆缺陷和抑郁样行为等受损行为的神经保护作用，并探讨了其潜在机制。 [2]
novelty suppressed feeding 新奇抑制喂养
We found that 5-HT4R KO and WT mice displayed anxiety- and depressive-like behavior following chronic administration of corticosterone, as evidenced in the open-field and novelty suppressed feeding tests. [1] By postnatal day 60, the male Wistar rat offspring were tested for depressive-like behavior using operational conditioning, novelty suppressed feeding, sucrose preference, and open-field test. [2]我们发现 5-HT4R KO 和 WT 小鼠在长期服用皮质酮后表现出焦虑和抑郁样行为，这在开放场和新奇抑制喂养试验中得到了证明。 [1] 到出生后第 60 天，使用操作调节、新奇抑制喂养、蔗糖偏好和旷场测试对雄性 Wistar 大鼠后代的抑郁样行为进行了测试。 [2]
test open field 测试开放领域
Bilateral mechanical pain hypersensitivity, anxiety-like and depressive-like behaviors were evaluated by using von Frey test, open field, elevated plus-maze testing, and forced swimming test in mice, respectively. [1]分别采用冯弗雷试验、旷场试验、高架十字迷宫试验和小鼠强迫游泳试验评估双侧机械疼痛超敏反应、焦虑样和抑郁样行为。 [1]