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Glucocorticoid alleviates hypothalamic nerve injury via remodeling HPA axis homeostasis in stressed rats 糖皮质激素通过重塑应激大鼠的 HPA 轴平衡缓解下丘脑神经损伤
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-28 DOI: 10.1016/j.bbr.2024.115223

Excessive stress can exceed the adjustment ability of body and cause injury and dysfunction, while elucidation of the mechanism and prevention measures of stress-related injury are still insufficient. The present study was to observe the effect of glucocorticoid (GC) on stress-induced hypothalamic nerve injury and elucidate the potential mechanism. The present study intended to establish a chronic restraint stress rat model for follow-up study. Open field test and elevated plus maze test were used to observe behavioral changes of stress rats; Enzyme-linked immunosorbent assay (ELISA) was used to detect changes in the levels of hypothalamus-pituitary-adrenal (HPA) axis-related hormones and inflammatory factors in hypothalamus; toluidine blue staining was used to observe pathological changes of hypothalamus. The results showed that stress rats showed obvious anxiety-like behaviors, the levels of HPA axis-related hormones and inflammatory factors showed abnormal fluctuations, and morphological results showed significant nerve injury in hypothalamus. Low-dose GC treatment significantly improved behavioral changes, alleviated hypothalamic nerve injury, and restored hypothalamic levels of inflammatory factors, serum levels of GC, corticotropin-releasing hormone (CRH), and adrenocorticotropic hormone (ACTH) and GC level in adrenal cortex of stressed rats, while GC receptor (GR) inhibitor, CRH receptor inhibitor, and adrenalectomy reversed the ameliorative effects of low-dose GC. Our study clarified that low-dose GC can restore stress coping ability by reshaping the homeostasis of the HPA axis, thus alleviating behavioral abnormalities and hypothalamic nerve injury in stressed rats.

过度应激会超出机体的调节能力,导致机体损伤和功能障碍,而应激相关损伤的机制和预防措施的阐明尚不充分。本研究旨在观察糖皮质激素(GC)对应激诱导的下丘脑神经损伤的影响,并阐明其潜在机制。本研究旨在建立一个慢性束缚应激大鼠模型进行后续研究。采用开阔地试验和高架迷宫试验观察应激大鼠的行为变化;采用酶联免疫吸附试验(ELISA)检测下丘脑-垂体-肾上腺(HPA)轴相关激素和下丘脑炎症因子水平的变化;采用甲苯胺蓝染色观察下丘脑的病理变化。结果显示,应激大鼠表现出明显的焦虑样行为,HPA轴相关激素和炎症因子水平出现异常波动,形态学结果显示下丘脑神经损伤明显。小剂量GC治疗可明显改善应激大鼠的行为变化,减轻下丘脑神经损伤,恢复下丘脑炎症因子水平、血清GC、促肾上腺皮质激素释放激素(CRH)和促肾上腺皮质激素(ACTH)水平以及肾上腺皮质GC水平,而GC受体(GR)抑制剂、CRH受体抑制剂和肾上腺切除术逆转了小剂量GC的改善作用。我们的研究明确了小剂量GC可以通过重塑HPA轴的平衡来恢复应激应对能力,从而缓解应激大鼠的行为异常和下丘脑神经损伤。
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引用次数: 0
AQP4 is upregulated in schizophrenia and Its inhibition attenuates MK-801-induced schizophrenia-like behaviors in mice AQP4 在精神分裂症中上调,抑制 AQP4 可减轻 MK-801 诱导的小鼠精神分裂症样行为
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-28 DOI: 10.1016/j.bbr.2024.115220

Background

The pathophysiology and molecular mechanisms of schizophrenia (SCZ) remain unclear, and the effective treatment resources are still limited. The goal of this study is to identify the expression of AQP4 in SCZ patients and explore whether AQP4 inhibition could ameliorate schizophrenia-like behaviors and its mechanisms.

Methods

Microarray datasets of PFC compared with healthy control were searched in the Gene Expression Omnibus (GEO) database, and differentially expressed genes (DEGs) were analyzed with the GEO2R online tool. The Venny online tool and metascape online software were used to identify common abnormally expressed genes and conduct cell type signature enrichment analysis. SCZ mouse models were induced with MK-801, an NMDA receptor antagonist (intraperitoneal injection, 0.1 mg/kg/day for 7 days), and C6 cell models were treated with 100 μM MK-801. RT-qPCR, Western Blotting, and immunofluorescence were employed to determine the expression of AQP4, proinflammatory cytokines, and GFAP. Open field tests and social interaction tests were performed to evaluate the schizophrenia-like behaviors.

Results

Bioinformatics analysis identified upregulation of AQP4 in the PFC of SCZ patients compared with healthy controls. Cell type signature enrichment analysis showed that all three DEGs lists were strongly enriched in the FAN EMBRYONIC CTX ASTROCYTE 2 category. Upregulation of AQP4 was also observed in MK-801-treated C6 cells and the PFC of MK-801-induced SCZ mouse model. Moreover, AQP4 inhibition with TGN-020 (an inhibitor of AQP4) improved anxiety-like behavior and social novelty preference defects in MK-801-treated mice. AQP4 inhibition also reduced the expression of IL-1β, IL-6, and TNF-α in MK-801-treated C6 cells and mouse model.

Conclusions

AQP4 is upregulated in the PFC of SCZ patients compared with healthy controls. AQP4 inhibition could alleviate the anxiety-like behavior and social novelty defects in MK-801-treated mice, this may be due to the role of AQP4 in the regulation of the expression of proinflammatory cytokines.

背景精神分裂症(SCZ)的病理生理学和分子机制尚不清楚,有效的治疗资源仍然有限。方法在基因表达总库(Gene Expression Omnibus,GEO)数据库中检索PFC与健康对照组比较的微阵列数据集,用GEO2R在线工具分析差异表达基因(DEGs)。利用 Venny 在线工具和 metascape 在线软件识别常见的异常表达基因,并进行细胞类型特征富集分析。用NMDA受体拮抗剂MK-801诱导SCZ小鼠模型(腹腔注射,0.1 mg/kg/天,连续7天),用100 μM MK-801处理C6细胞模型。采用 RT-qPCR、Western 印迹法和免疫荧光法测定 AQP4、促炎细胞因子和 GFAP 的表达。结果生物信息学分析发现,与健康对照组相比,AQP4在SCZ患者的PFC中上调。细胞类型特征富集分析表明,所有三个DEGs列表都在FAN EMBRYONIC CTX ASTROCYTE 2类别中强富集。在MK-801处理的C6细胞和MK-801诱导的SCZ小鼠模型的PFC中也观察到了AQP4的上调。此外,用TGN-020(一种AQP4抑制剂)抑制AQP4可改善MK-801处理小鼠的焦虑样行为和社会新奇偏好缺陷。结论与健康对照组相比,AQP4在SCZ患者的PFC中上调。抑制AQP4可减轻MK-801处理的小鼠的焦虑样行为和社会新奇性缺陷,这可能是由于AQP4在调节促炎细胞因子表达中的作用。
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引用次数: 0
Frontal EEG alpha asymmetry predicts foreign language anxiety while speaking a foreign language 额叶脑电图阿尔法不对称预测说外语时的外语焦虑症
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-28 DOI: 10.1016/j.bbr.2024.115216

Engaging in dialog requires interlocutors to coordinate sending and receiving linguistic signals to build a discourse based upon interpretations and perceptions interconnected with a range of emotions. Conversing in a foreign language may induce emotions such as anxiety which influence the quality communication. The neural processes underpinning these interactions are crucial to understanding foreign language anxiety (FLA). Electroencephalography (EEG) studies reveal that anxiety is often displayed via hemispheric frontal alpha asymmetry (FAA). To examine the neural mechanisms underlying FLA, we collected self-reported data on the listening and speaking sections of the Second language skill specific anxiety scale (L2AS) over behavioral, cognitive, and somatic domains and recorded EEG signals during participation in word chain turn-taking activities in first (L1, Chinese) and second (L2, English) languages. Regression analysis showed FAA for the L2 condition was a significant predictor primarily of the behavioral and somatic domains on the L2AS speaking section. The results are discussed along with implications for improving communication during L2 interactions.

参与对话需要对话者协调语言信号的发送和接收,以建立基于与一系列情感相互关联的解释和感知的话语。用外语对话可能会诱发焦虑等情绪,从而影响交流质量。这些相互作用的神经过程对于理解外语焦虑(FLA)至关重要。脑电图(EEG)研究显示,焦虑通常通过大脑半球额叶α不对称(FAA)表现出来。为了研究 FLA 的神经机制,我们收集了第二语言技能焦虑量表(L2AS)听力和口语部分的行为、认知和躯体领域的自我报告数据,并记录了第一语言(第一语言,中文)和第二语言(第二语言,英语)参与单词链轮流活动时的脑电信号。回归分析表明,第二语言条件下的 FAA 主要对第二语言口语部分的行为和躯体领域有显著的预测作用。本文讨论了这一结果以及对改善 L2 互动中的交流的影响。
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引用次数: 0
Enhancing spatial memory and pattern separation: Long-term effects of stimulant treatment in individuals with ADHD 增强空间记忆和模式分离:多动症患者接受兴奋剂治疗的长期效果。
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-26 DOI: 10.1016/j.bbr.2024.115211

This study explores the under-researched domain of long-term stimulant treatment in children and adolescents diagnosed with attention deficit hyperactivity disorder (ADHD). The necessity for extended treatment duration, often accompanied by safety concerns and side effects leading to treatment discontinuation, underscores the significance of this investigation. Concurrently, comparative studies have revealed adverse impacts on vulnerable regions within the hippocampal formation, accompanied by behavioral perturbations. We employed computerized tests and virtual reality to assess spatial memory, pattern separation, and object recognition memory in a cohort of children diagnosed with ADHD receiving stimulant treatment. We compared their performance to a group of neurotypical peers. Our findings indicate that the ADHD group exhibited a lower performance in spatial memory, pattern separation, and object recognition memory than ND group. Intriguingly, a positive relationship emerged between the duration of stimulant treatment and performance in these variables. Notably, this improvement was not immediate to MPH treatment but becomes significant after 24 months of treatment. In contrast to previous comparative investigations, our study did not reveal a detrimental impact on spatial navigation, object recognition memory, or pattern separation, despite the known interplay of these cognitive processes with the hippocampal formation. These results shed new light on the nuanced effects of stimulant treatment in ADHD, underscoring the need for a more comprehensive understanding of long-term treatment outcomes.

本研究探讨了被诊断患有注意力缺陷多动障碍(ADHD)的儿童和青少年长期接受兴奋剂治疗这一研究不足的领域。由于必须延长治疗时间,而延长治疗时间往往伴随着安全问题和副作用,导致治疗中断,因此这项研究意义重大。与此同时,比较研究显示,药物对海马形成内的脆弱区域产生了不利影响,并伴有行为干扰。我们采用计算机化测试和虚拟现实技术,对一组接受兴奋剂治疗的多动症患儿的空间记忆、模式分离和物体识别记忆进行了评估。我们将他们的表现与一组神经正常的同龄人进行了比较。我们的研究结果表明,ADHD 组在空间记忆、模式分离和物体识别记忆方面的表现低于 ND 组。耐人寻味的是,兴奋剂治疗的持续时间与这些变量的表现之间出现了正相关。值得注意的是,这种改善并不是 MPH 治疗后立即出现的,而是在治疗 24 个月后变得显著。与以往的比较研究不同,我们的研究没有发现对空间导航、物体识别记忆或模式分离的不利影响,尽管这些认知过程与海马形成之间存在已知的相互作用。这些结果为了解兴奋剂治疗对多动症的细微影响提供了新的视角,强调了对长期治疗结果进行更全面了解的必要性。
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引用次数: 0
Inflammatory injury induces pain sensitization that is expressed beyond the site of injury in male (and not in female) mice 炎症损伤会诱导雄性小鼠(而非雌性小鼠)对损伤部位以外的疼痛敏感。
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-25 DOI: 10.1016/j.bbr.2024.115215

Pain is a crucial protective mechanism for the body. It alerts us to potential tissue damage or injury and promotes the avoidance of harmful stimuli. Injury-induced inflammation and tissue damage lead to pain sensitization, which amplifies responses to subsequent noxious stimuli even after an initial primary injury has recovered. This phenomenon, commonly referred to as hyperalgesic priming, was investigated in male and female mice to determine whether it is specific to the site of previous injury. We used 10μl of 50 % Freund's complete adjuvant (CFA) administered to the left hind paw as a model of peripheral injury. Both male and female mice exhibited robust site-specific mechanical hypersensitivity after CFA, which resolved within one-week post-injection. After injury resolution, only male CFA-primed mice showed enhanced and prolonged mechanical sensitivity in response to a chemical challenge or a single 0.5 mA electric footshock. Among CFA-primed male mice, shock-induced mechanical hypersensitivity was expressed in both the left (previously injured) and the right (uninjured) hind paws, suggesting a pivotal role for altered centralized processes in the expression of pain sensitization. These findings indicate that pain history regulates sensory responses to subsequent mechanical and chemical pain stimuli in a sex-specific manner—foot-shock-induced hyperalgesic priming expression among male mice generalized beyond the initial injury site.

疼痛是人体的一种重要保护机制。它提醒我们注意潜在的组织损伤或伤害,并促进避免有害刺激。损伤引起的炎症和组织损伤会导致痛觉过敏,即使在最初的原发性损伤恢复后,也会放大对后续有害刺激的反应。我们在雄性和雌性小鼠身上研究了这种通常被称为超痛引物的现象,以确定这种现象是否与之前受伤的部位有关。我们使用 10μl 50%弗氏完全佐剂(CFA)给左后爪作为外周损伤模型。注射CFA后,雄性和雌性小鼠都表现出强烈的部位特异性机械过敏反应,并在注射后一周内缓解。损伤缓解后,只有雄性CFA引物小鼠对化学挑战或单次0.5mA电击脚表现出更强和更持久的机械敏感性。在CFA诱导的雄性小鼠中,左后爪(之前受伤)和右后爪(未受伤)均表现出电击诱导的机械过敏性,这表明中枢过程的改变在痛觉过敏的表达中起着关键作用。这些研究结果表明,疼痛历史以性别特异性的方式调节对后续机械和化学疼痛刺激的感觉反应--雄性小鼠足部冲击诱导的痛觉过敏表达已超越了最初的受伤部位。
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引用次数: 0
Heavy metals exposure and Alzheimer’s disease: Underlying mechanisms and advancing therapeutic approaches 重金属暴露与阿尔茨海默病:基本机制和先进的治疗方法。
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-24 DOI: 10.1016/j.bbr.2024.115212

Heavy metals such as lead, cadmium, mercury, and arsenic are prevalent in the environment due to both natural and anthropogenic sources, leading to significant public health concerns. These heavy metals are known to cause damage to the nervous system, potentially leading to a range of neurological conditions including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and attention-deficit hyperactivity disorder (ADHD). The present study examines the complex relationship between heavy metal exposure and AD, focusing on the underlying mechanisms of toxicity and potential therapeutic approaches. This review article highlights how these metals can impair brain function through mechanisms such as oxidative stress, inflammation, and neurotransmitter disruption, ultimately contributing to neurodegenerative diseases like AD. It also addresses the challenges in diagnosing heavy metal-induced cognitive impairments and emphasizes the need for further research to explore effective treatment strategies and preventive measures against heavy metal exposure.

由于自然和人为原因,铅、镉、汞和砷等重金属在环境中普遍存在,引发了重大的公共健康问题。众所周知,这些重金属会对神经系统造成损害,可能导致一系列神经系统疾病,包括阿尔茨海默病(AD)、帕金森病(PD)、肌萎缩性脊髓侧索硬化症(ALS)、多发性硬化症(MS)和注意力缺陷多动障碍(ADHD)。本研究探讨了重金属暴露与注意力缺失多动症之间的复杂关系,重点是毒性的潜在机制和潜在的治疗方法。这篇综述文章重点介绍了这些金属如何通过氧化应激、炎症和神经递质干扰等机制损害大脑功能,最终导致神经退行性疾病(如注意力缺失症)。文章还探讨了诊断重金属引起的认知障碍所面临的挑战,并强调了进一步研究探索有效治疗策略和预防重金属暴露措施的必要性。
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引用次数: 0
Effects of combined postweaning social isolation and ketamine administration on schizophrenia-like behaviour in male Sprague Dawley rats 断奶后社会隔离和氯胺酮联合用药对雄性 Sprague Dawley 大鼠精神分裂症样行为的影响
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-23 DOI: 10.1016/j.bbr.2024.115214

The pathophysiology behind negative and cognitive symptoms of schizophrenia is not well understood, thus limiting the effectiveness of treatment on these symptoms. Developing reliable animal model of schizophrenia is vital to advance our understanding on the neurobiological basis of the disorder. Double hit is used to refer to the use of two schizophrenia inducing interventions viz ketamine exposure and social isolation. In this study we aim to investigate the robustness of double hit model of schizophrenia in inducing negative and cognitive symptoms of schizophrenia. On postnatal day (PND) 23, thirty-two male Sprague Dawley rats were randomly grouped into four equal groups as follows: group housed + saline (GH), group housed + ketamine (GHK), isolated + saline (SI), and isolated + ketamine (SIK). A single ketamine dose (16 mg/kg) was administered 3 times a week for four weeks. Isolated animals were housed singly throughout the study. The following behavioural tests were carried out: elevated plus maze, three chamber social interaction, resident intruder tests, and novel object recognition (NOR). The SIK group exhibited high anxiety levels, with increased ACTH, corticosterone and norepinephrine concentration when compared to the other groups. The SIK animals also presented with reduced social interaction and decreased oxytocin concentration. SIK rats were more aggressive towards a juvenile intruder but had low testosterone concentration. The SIK group or double hit model showed impaired visual learning and memory and increased expression of proinflammatory cytokines. This suggest that the double hit model is more robust in inducing negative and cognitive symptoms of schizophrenia than each treatment alone.

精神分裂症阴性症状和认知症状背后的病理生理学尚不十分清楚,因此限制了对这些症状的治疗效果。开发可靠的精神分裂症动物模型对于促进我们了解精神分裂症的神经生物学基础至关重要。双击是指使用两种精神分裂症诱导干预措施,即氯胺酮暴露和社会隔离。在这项研究中,我们旨在研究双击精神分裂症模型在诱导精神分裂症阴性和认知症状方面的稳健性。在出生后第23天(PND),32只雄性Sprague Dawley大鼠被随机分为以下四组:饲养组+生理盐水组(GH)、饲养组+氯胺酮组(GHK)、隔离组+生理盐水组(SI)和隔离组+氯胺酮组(SIK)。每周注射 3 次氯胺酮(16 毫克/千克),连续注射 4 周。隔离动物在整个研究过程中单独饲养。进行了以下行为测试:高架加迷宫、三室社交互动、常住入侵者测试和新物体识别(NOR)。与其他组相比,SIK 组表现出较高的焦虑水平,其促肾上腺皮质激素、皮质酮和去甲肾上腺素浓度均有所升高。SIK 动物还表现出社交互动减少和催产素浓度降低。SIK 大鼠对幼年入侵者更具攻击性,但睾酮浓度较低。SIK 组或双击模型显示视觉学习和记忆受损,促炎细胞因子表达增加。这表明双击模型在诱导精神分裂症的阴性和认知症状方面比单独使用每种治疗方法更有效。
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引用次数: 0
Correlation between compulsive behaviors and plastic changes in the dendritic spines of the prefrontal cortex and dorsolateral striatum of male rats 强迫行为与雄性大鼠前额叶皮层和背外侧纹状体树突棘的可塑性变化之间的相关性
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-23 DOI: 10.1016/j.bbr.2024.115199

Obsessive-compulsive disorder (OCD) is a mental affliction characterized by compulsive behaviors often manifested in intrusive thoughts and repetitive actions. The quinpirole model has been used with rats to replicate compulsive behaviors and study the neurophysiological processes associated with this pathology. Several changes in the dendritic spines of the medial prefrontal cortex (mPFC) and dorsolateral striatum (DLS) have been related to the occurrence of compulsive behaviors. Dendritic spines regulate excitatory synaptic contacts, and their morphology is associated with various brain pathologies. The present study was designed to correlate the occurrence of compulsive behaviors (generated by administering the drug quinpirole) with the morphology of the different types of dendritic spines in the mPFC and DLS. A total of 18 male rats were used. Half were assigned to the experimental group, the other half to the control group. The former received injections of quinpirole, while the latter rats were injected with physiological saline solution, for 10 days in both cases. After the experimental treatment, the quinpirole rats exhibited all the parameters indicative of compulsive behavior and a significant correlation with the density of stubby and wide neckless spines in both the mPFC and DLS. Dendritic spines from both mPFC and DLS neurons showed plastic changes correlatively with the expression of compulsive behavior induced by quinpirole. Further studies are suggested to evaluate the involvement of glutamatergic neurotransmission in the neurobiology of OCD.

强迫症(OCD)是一种以强迫行为为特征的精神疾病,通常表现为侵入性思维和重复性动作。喹吡酮模型被用于复制强迫行为和研究与这种病症相关的神经生理过程。内侧前额叶皮层(mPFC)和背外侧纹状体(DLS)树突棘的一些变化与强迫行为的发生有关。树突棘调节兴奋性突触接触,其形态与各种脑部病变有关。本研究旨在将强迫行为(通过服用药物喹吡罗产生)的发生与 mPFC 和 DLS 中不同类型树突棘的形态相关联。实验共使用了 18 只雄性大鼠。一半被分配到实验组,另一半被分配到对照组。前者接受喹吡罗注射,后者接受生理盐水注射,均持续 10 天。经过实验治疗后,喹吡罗大鼠表现出了强迫行为的所有指标,并且与 mPFC 和 DLS 中粗壮和宽大无颈棘突的密度显著相关。mPFC和DLS神经元的树突棘与喹吡罗诱导的强迫行为表现呈可塑性变化。建议进一步研究以评估谷氨酸能神经递质在强迫症神经生物学中的参与。
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引用次数: 0
Dopaminergic manipulations affect the modulation and meta-modulation of movement speed: Evidence from two pharmacological interventions 多巴胺能操作影响运动速度的调节和元调节:来自两种药物干预的证据。
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-23 DOI: 10.1016/j.bbr.2024.115213

A body of research implicates dopamine in the average speed of simple movements. However, naturalistic movements span a range of different shaped trajectories and rarely proceed at a single constant speed. Instead, speed is reduced when drawing “corners” compared to “straights” (i.e., speed modulation), and the extent of this slowing down is dependent upon the global shape of the movement trajectory (i.e., speed meta-modulation) – for example whether the shape is an ellipse or a rounded square. At present, it is not known how (or whether) dopaminergic function controls continuous changes in speed during movement execution. The current paper reports effects on these kinematic features of movement following two forms of dopamine manipulation: Study One highlights movement differences in individuals with PD both ON and OFF their dopaminergic medication (N = 32); Study Two highlights movement differences in individuals from the general population on haloperidol (a dopamine receptor blocker, or “antagonist”) and placebo (N = 43). Evidence is presented implicating dopamine in speed, speed modulation and speed meta-modulation, whereby low dopamine conditions are associated with reductions in these variables. These findings move beyond vigour models implicating dopamine in average movement speed, and towards a conceptualisation that involves the modulation of speed as a function of contextual information.

大量研究表明,多巴胺与简单动作的平均速度有关。然而,自然运动的轨迹形状多种多样,很少以单一的恒定速度进行。相反,与 "直线 "相比,在画 "弯道 "时速度会降低(即速度调制),而这种速度降低的程度取决于运动轨迹的整体形状(即速度元调制)--例如,形状是椭圆还是圆角方形。目前,多巴胺能功能如何(或是否)控制运动执行过程中速度的连续变化尚不清楚。本论文报告了两种形式的多巴胺操作对这些运动学特征的影响:研究一 "强调了服用和停用多巴胺能药物的帕金森病患者(32 人)的运动差异;"研究二 "强调了服用氟哌啶醇(一种多巴胺受体阻滞剂,或称 "拮抗剂")和安慰剂的普通人群(43 人)的运动差异。有证据表明,多巴胺与速度、速度调节和速度元调节有关,低多巴胺状态与这些变量的减少有关。这些研究结果超越了将多巴胺与平均运动速度联系起来的活力模型,而转向了将速度调节作为环境信息功能的概念。
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引用次数: 0
Empirical examination of working memory performance and its neural correlates in relation to delay discounting in two large samples 在两个大样本中对工作记忆能力及其与延迟折现相关的神经相关性进行实证研究。
IF 2.6 3区 心理学 Q2 BEHAVIORAL SCIENCES Pub Date : 2024-08-22 DOI: 10.1016/j.bbr.2024.115217

The neurobiological basis of working memory and delay discounting are theorized to overlap, but few studies have empirically examined these relations in large samples. To address this, we investigated the association of neural activation during an fMRI N-Back working memory task with delay discounting area, as well as in- and out-of-scanner working memory measures. These analyses were conducted in two large task fMRI datasets, the Human Connectome Project and the Adolescent Brain Cognitive Development Study. Although in- and out-of-scanner working memory performance were significantly associated with N-back task brain activation regions, contrary to our hypotheses, there were no significant associations between working memory task activation and delay discounting scores. These findings call into question the extent of the neural overlap in delay discounting and working memory and highlight the need for more investigations directly interrogating overlapping and distinct brain regions across cognitive neuroscience tasks.

工作记忆和延迟折现的神经生物学基础被认为是重叠的,但很少有研究在大样本中对这两者的关系进行实证研究。为了解决这个问题,我们研究了 fMRI N-Back 工作记忆任务中神经激活与延迟折现区域的关联,以及扫描内和扫描外工作记忆测量的关联。这些分析是在两个大型任务 fMRI 数据集(人类连接组计划和青少年大脑认知发展研究)中进行的。虽然扫描内和扫描外的工作记忆表现与N-back任务的大脑激活区域有显著关联,但与我们的假设相反,工作记忆任务激活与延迟折现得分之间没有显著关联。这些发现使我们对延迟折现和工作记忆的神经重叠程度产生了疑问,并强调了在认知神经科学任务中直接询问重叠和不同脑区的更多研究的必要性。
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Behavioural Brain Research
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