Neuroscience Research最新文献_第4页

Fluoxetine enhances the treatment of depression linked to opioid-induced constipation in mice by influencing the metabolomic profile 氟西汀通过影响代谢组学特征来增强与阿片类药物引起的便秘相关的小鼠抑郁症的治疗。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-11-08 DOI: 10.1016/j.neures.2025.104983

Chun Wang , Shiqin Yao , Bowen Tian , Zhifeng Zhao , Yanrong Wang , Xiaoliang Li , Xuzhao Li , Qinxian Huang

This study was intended to verify the potential role of Fluoxetine (Flx) in treating depression associated with opioid-induced constipation (OIC). We established a mouse model of chronic unpredictable mild stress (CUMS) and used loperamide to induce constipation based on the CUMS mice, generating a mouse model of depression associated with OIC (CUMS+OIC). The depressive behavior was evaluated via the open field and sucrose preference tests, while constipation was evaluated using defecation frequency and fecal water content. Liquid chromatography-mass spectrometry (LC-MS)-based metabolomics and bioinformatics analyses were performed. Treatment with Flx alleviated the depressive behavior of mice and inhibited OIC. We identified 153 differential metabolites between the control and the CUMS+OIC groups, among which 51 were downregulated while the other 102 were upregulated. These metabolites were involved in metabolic pathways such as pyrimidine metabolism, purine metabolism, and beta-alanine metabolism. Moreover, 64 differential metabolites between the Flx and the CUMS+OIC groups were involved in nicotinate and nicotinamide metabolism, and prion disease metabolism metabolic pathways. Through cluster analysis, we identified metabolites deregulated by CUMS+OIC and restored by Flx. Conclusively, Flx can improve the behavior and metabolic profile changes of CUMS associated with OIC, providing a basis for treating depression-related constipation.

本研究旨在验证氟西汀（Flx）在治疗阿片类药物引起的便秘（OIC）相关抑郁症中的潜在作用。我们建立小鼠慢性不可预知轻度应激（CUMS）模型，并在CUMS小鼠的基础上应用洛哌丁胺诱导便秘，建立OIC相关抑郁小鼠模型（CUMS+OIC）。抑郁行为通过空地测试和蔗糖偏好测试来评估，便秘则通过排便次数和粪便含水量来评估。以液相色谱-质谱（LC-MS）为基础进行代谢组学和生物信息学分析。用Flx治疗可减轻小鼠抑郁行为，抑制OIC。我们在对照组和CUMS+OIC组之间鉴定了153种差异代谢物，其中51种下调，102种上调。这些代谢物参与代谢途径，如嘧啶代谢、嘌呤代谢和β -丙氨酸代谢。此外，Flx组与CUMS+OIC组之间的64种差异代谢物涉及烟酸和烟酰胺代谢以及朊病毒疾病代谢途径。通过聚类分析，我们发现了被CUMS+OIC解除调控而被Flx恢复的代谢物。综上所述，Flx可以改善与OIC相关的CUMS的行为和代谢谱变化，为治疗抑郁症相关性便秘提供依据。

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引用次数: 0

Advances in non-human primate models for Alzheimer's disease research 非人类灵长类动物阿尔茨海默病研究的进展。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-11-08 DOI: 10.1016/j.neures.2025.104984

Daisuke Joho , Kenya Sato , Wakako Kumita , Takaomi C. Saido , Erika Sasaki , Hiroki Sasaguri

Alzheimer’s disease (AD) is the most common progressive neurodegenerative disease. It is characterized by cognitive decline and brain pathology, including amyloid-β (Aβ) plaques, neurofibrillary tangles, and neuroinflammation. While rodent models have contributed to our understanding of a multiplicity of disease mechanisms, their limitations in replicating human age-related neurodegenerative diseases pose challenges for translating research findings to the clinical setting. The common marmoset (Callithrix jacchus), a small non-human primate, has emerged as a promising model for neuroscience and aging research. Age-related Aβ and tau pathologies develop naturally in the marmoset, which also possess a brain network organization, including a default mode network, that closely resembles that of humans. AD-related pathologies have also been experimentally induced in marmosets through injection of materials extracted from post-mortem brain tissue of AD patients. Recent advances in genome-editing technologies have enabled the development of marmoset models carrying familial AD mutations. These models offer new opportunities to investigate early pathological changes in the disease and to evaluate potential therapeutic agents. Taken together, these findings highlight the value of the marmoset as a translational model bridging the gap between rodent studies and human AD research.

阿尔茨海默病（AD）是最常见的进行性神经退行性疾病。其特征是认知能力下降和脑病理，包括淀粉样蛋白-β (Aβ)斑块，神经原纤维缠结和神经炎症。虽然啮齿动物模型有助于我们对多种疾病机制的理解，但它们在复制人类与年龄相关的神经退行性疾病方面的局限性为将研究结果转化为临床环境带来了挑战。普通狨猴（Callithrix jacchus）是一种小型的非人类灵长类动物，已经成为神经科学和衰老研究的一个有希望的模型。与年龄相关的a β和tau病理在狨猴中自然发展，它们也拥有与人类非常相似的大脑网络组织，包括默认模式网络。通过注射从AD患者死后脑组织中提取的材料，也在实验中诱导了狨猴AD相关病理。基因组编辑技术的最新进展使携带家族性阿尔茨海默病突变的狨猴模型得以发展。这些模型为研究疾病的早期病理变化和评估潜在的治疗药物提供了新的机会。综上所述，这些发现突出了狨猴作为一种翻译模型的价值，弥合了啮齿动物研究和人类阿尔茨海默病研究之间的差距。

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引用次数: 0

iPSC-derived neural organoids in dementia research: Recent advances and future directions ipsc衍生的类神经器官在痴呆症研究中的最新进展和未来方向。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-11-03 DOI: 10.1016/j.neures.2025.104980

Shogo Shima , Takayuki Kondo , Haruhisa Inoue

Neural organoids are self-assembled three-dimensionally shaped aggregates generated from pluripotent stem cells for the purpose of generating brain-like structures. The features of the disease, from molecular to functional levels, can be recapitulated by neural organoids derived from patient induced pluripotent stem cells (iPSCs). These features are not fully reproduced by other culture systems or in vivo models. Neural organoids have been applied to model dementia including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis/frontotemporal dementia, and they have recapitulated aspects of their complex pathophysiology, including neuronal network dysfunction and accumulation of pathogenic proteins. Although research using neural organoids still faces challenges such as heterogeneity and the absence of non-neural lineage cells, these limitations are being progressively addressed. Recent advances, including the integration of gene-editing technologies and the co-assembly of organoids with specific cell types, have demonstrated the remarkable potential of this approach. This article reviews current research on iPSC-derived neural organoids for dementia, discussing both the technical hurdles and the potential for translational applications.

神经类器官是由多能干细胞产生的自组装的三维形状聚集体，目的是产生类脑结构。来自患者诱导多能干细胞（iPSCs）的类器官可以从分子到功能水平概括疾病的特征，这是其他培养系统或体内模型无法完全复制的。神经类器官已被应用于痴呆模型，包括阿尔茨海默病、帕金森病和肌萎缩侧索硬化症/额颞叶痴呆，它们概括了其复杂病理生理学的各个方面，包括神经网络功能障碍和致病性蛋白的积累。尽管使用神经类器官进行研究存在一些挑战，包括它们的异质性和缺乏非神经谱系的细胞，但研究人员已经尝试克服这些限制，并证明了它们在与基因编辑技术和类器官组装系统以及特定类型细胞结合方面的实用性。本文综述了目前关于ipsc衍生类器官治疗痴呆症的研究，讨论了技术障碍和转化应用的潜力。

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引用次数: 0

Traumatic brain injury and Alzheimer’s disease related neurodegenerative diseases: Insights from animal models 创伤性脑损伤和阿尔茨海默病相关的神经退行性疾病：来自动物模型的见解。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-11-01 DOI: 10.1016/j.neures.2025.104979

Xinyi Zhao , Zhuohao He

Alzheimer’s disease and related neurodegenerative diseases (ADRD) represent a major global public health challenge, with their disease mechanisms remain largely unknown, and few treatments are available. Increasing epidemiological evidence underscores the critical role of traumatic brain injury (TBI) in the initiation and progression of ADRD, suggesting shared pathogenic mechanisms between these conditions. While there are still lack of perfect AD models in the field, TBI models may serve as useful and alternative platforms for investigating ADRD. In this review we delineate the definition and epidemiological characteristics of TBI. We further briefly compare the major experimental TBI animal models, outlining their respective strengths and limitations in replicating human neuropathology. Finally, we provide our perspective on potential mechanistic links between TBI and ND, including axonal injury, calcium homeostasis dysregulation, mitochondrial dysfunction, chronic neuroinflammation, blood-brain barrier disruption, and genetic susceptibility. We believe advancing preclinical and translational research on TBI not only enhances our understanding of the pathogenesis in ADRD but also holds promise for developing interventions to mitigate long-term consequences and improving clinical outcomes for many neurodegenerative diseases.

阿尔茨海默病和相关神经退行性疾病（ADRD）是一项重大的全球公共卫生挑战，其发病机制在很大程度上仍然未知，而且很少有治疗方法。越来越多的流行病学证据强调了创伤性脑损伤（TBI）在ADRD的发生和发展中的关键作用，表明这些疾病之间有共同的致病机制。虽然该领域仍缺乏完善的AD模型，但TBI模型可以作为研究ADRD的有用和替代平台。在这篇综述中，我们描述了TBI的定义和流行病学特征。我们进一步简要地比较了主要的实验性脑外伤动物模型，概述了它们各自在复制人类神经病理学方面的优势和局限性。最后，我们提供了关于创伤性脑损伤和ND之间潜在机制联系的观点，包括轴突损伤、钙稳态失调、线粒体功能障碍、慢性神经炎症、血脑屏障破坏和遗传易感性。我们相信，推进TBI的临床前和转化研究不仅可以增强我们对ADRD发病机制的理解，而且还有望开发干预措施，以减轻长期后果，改善许多神经退行性疾病的临床结果。

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引用次数: 0

Diurnal modulation of optogenetically evoked neural signals 光遗传诱发的神经信号的昼夜调节。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-10-31 DOI: 10.1016/j.neures.2025.104981

Yuki Donen , Yoko Ikoma , Ko Matsui

Neural signal processing in the cerebral cortex is often regarded as robust and stereotyped; however, the brain’s internal environment undergoes dynamic fluctuations across the day. Whether these diurnal rhythms modulate cortical responsiveness and plasticity remains unclear. Here, we examined diurnal modulation of neural responsiveness and plasticity in the primary visual cortex (V1). Using transgenic rats expressing channelrhodopsin-2 (ChR2), we optically stimulated V1 neurons with brief light pulses and recorded local field potentials (LFPs) over several days. V1 responses to single-pulse stimulation showed clear diurnal variation, with delta- and gamma-band activity modulated in a time-of-day–dependent manner. Administration of the adenosine A1 receptor antagonist DPCPX enhanced neural responses at Zeitgeber time (ZT) 0 (Sunrise) but not at ZT 12 (Sunset). LTP-like potentiation was observed only when train stimulation was applied at Sunrise, indicating that plasticity is also gated by diurnal phase. These findings demonstrate that both excitability and plasticity of V1 circuits are regulated by diurnal factors. Although it remains unclear whether these effects are driven by intrinsic circadian rhythms or light/dark-triggered mechanisms, our results highlight that cortical processing is dynamically modulated across the day, with implications for sensory function, learning, and neuromodulatory regulation.

大脑皮层的神经信号处理通常被认为是稳健和刻板的；然而，大脑的内部环境在一天中会经历动态波动。这些昼夜节律是否调节皮层的反应性和可塑性尚不清楚。在这里，我们研究了初级视觉皮层（V1）的神经反应性和可塑性的昼夜调节。利用表达通道视紫红质-2 （ChR2）的转基因大鼠，我们用短光脉冲光刺激V1神经元，并在数天内记录局部场电位（LFPs）。V1对单脉冲刺激的反应显示出明显的日变化，δ和γ波段的活动以一天中的时间依赖的方式调制。腺苷A1受体拮抗剂DPCPX在Zeitgeber时间（ZT） 0（日出）增强神经反应，但在ZT 12（日落）没有增强。只有在日出时施加训练刺激时才观察到ltp样增强，这表明可塑性也受昼夜相位的控制。这些发现表明V1回路的兴奋性和可塑性都受昼夜因素的调节。尽管目前尚不清楚这些影响是由内在的昼夜节律还是由光/暗触发机制驱动的，但我们的研究结果强调，皮层处理在一天中是动态调节的，对感觉功能、学习和神经调节有影响。

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引用次数: 0

Predictive coding in the primate brain: From visual to fronto-limbic systems 灵长类动物大脑中的预测编码：从视觉到额边缘系统

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-10-25 DOI: 10.1016/j.neures.2025.104972

Ryo Ito , Satoko Amemori , Ken-ichi Amemori

Predictive coding theory has emerged as a powerful framework for understanding neural information processing, offering a unified account of perception, cognition, and behavior through hierarchical minimization of prediction error. Notably, recent studies emphasize that the anatomical hierarchy and neurophysiological dynamics of the primate visual cortex are closely aligned with this framework. In this review, we examine the neural implementation of hierarchical information processing in the primate cerebral cortex from multiple perspectives, focusing on predictive coding theory. We aim to integrate findings from mathematical modeling, cortical microcircuits, laminar structure, neural oscillations, and clinical research. One of the central themes emerging from this integrative perspective is that interareal communication in the cortex is characterized by frequency-specific neural dynamics. Beta-band oscillations support top-down signals, whereas gamma-band oscillations convey bottom-up signals. These patterns closely reflect the directionality of anatomically defined projections. We also highlight that neural networks trained to predict upcoming visual input can develop functional properties observed in the primate visual system without these properties being explicitly supervised. Finally, we argue that hierarchical interaction provides a valuable perspective for understanding large-scale network dysfunctions associated with disorders such as depression and anxiety. These abnormalities may reflect disruptions in predictive signaling across functional domains rather than isolated regional deficits.

预测编码理论已经成为理解神经信息处理的一个强大框架，通过预测误差的分层最小化，提供了对感知、认知和行为的统一描述。值得注意的是，最近的研究强调，灵长类动物视觉皮层的解剖层次和神经生理动力学与这一框架密切相关。在这篇综述中，我们从多个角度研究了灵长类动物大脑皮层分层信息处理的神经实现，重点是预测编码理论。我们的目标是整合数学模型、皮质微电路、层流结构、神经振荡和临床研究的发现。从这一综合观点中出现的一个中心主题是，皮层的区域间交流以频率特异性神经动力学为特征。β波段振荡支持自上而下的信号，而伽马波段振荡传递自下而上的信号。这些模式紧密地反映了解剖上确定的突起的方向性。我们还强调，经过训练以预测即将到来的视觉输入的神经网络可以在没有明确监督的情况下发展在灵长类视觉系统中观察到的功能特性。最后，我们认为层次互动为理解与抑郁和焦虑等疾病相关的大规模网络功能障碍提供了一个有价值的视角。这些异常可能反映了跨功能域的预测信号的中断，而不是孤立的区域缺陷。

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引用次数: 0

Axonal sprouting from adjacent dorsal root ganglia following cervical dorsal root avulsion in mice 小鼠颈背根撕脱后邻近背根神经节轴突萌发。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-10-16 DOI: 10.1016/j.neures.2025.104971

Gaku Kanemoto , Takahide Itokazu , Toru Nakanishi , Takeru Furumiya , Seiji Okada , Toshihide Yamashita

Brachial plexus injury is a neurological injury caused by trauma, and effective treatments remain limited. Understanding its pathology is necessary to develop new therapeutic strategies. In this study, we used a dorsal root avulsion mouse model to determine whether injury-induced alterations in feedback circuitry from the dorsal root ganglion (DRG) to motor neurons contribute to functional recovery. We visualized axons originating from DRG neurons by directly injecting adeno-associated virus encoding green fluorescent protein (AAV-GFP) into the DRG adjacent to the injury site and analyzed the total length of axons on the lateral side of the ventral horn in the spinal cord. Following injury, the fine motor function of the affected forepaw was immediately impaired and then gradually recovered. In parallel, axons originating from an adjacent, uninjured DRG extended into the deafferented spinal segments, possibly contributing to the reinnervation of motor neurons that had lost their original sensory input. Indeed, after spontaneous motor recovery, when we performed an additional dorsal root avulsion originating from the adjacent DRG, functional impairment of the forepaw re-emerged. Our results demonstrate that the plasticity of the adjacent DRG may facilitate the recovery of fine motor function after dorsal root injury.

臂丛神经损伤是一种由外伤引起的神经系统损伤，有效的治疗方法仍然有限。了解其病理是开发新的治疗策略的必要条件。在这项研究中，我们使用背根撕脱小鼠模型来确定损伤引起的从背根神经节（DRG）到运动神经元的反馈回路的改变是否有助于功能恢复。我们通过将编码绿色荧光蛋白（AAV-GFP）的腺相关病毒直接注射到临近损伤部位的DRG，观察了源自DRG神经元的轴突，并分析了脊髓腹角外侧轴突的总长度。损伤后，前爪精细运动功能立即受损，然后逐渐恢复。与此同时，来自相邻未损伤的DRG的轴突延伸到失传入脊髓节段，可能有助于失去原始感觉输入的运动神经元的再神经支配。事实上，在自发运动恢复后，当我们从邻近的DRG进行额外的背根撕脱术时，前爪的功能损伤再次出现。我们的研究结果表明，邻近DRG的可塑性可能有助于背根损伤后精细运动功能的恢复。

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引用次数: 0

Causal role of persistent neural activity in the mouse medial prefrontal cortex in promotion of wakefulness 小鼠内侧前额叶皮层持续神经活动在促进清醒中的因果作用。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-10-16 DOI: 10.1016/j.neures.2025.104969

Sakiko Honjoh , Ayako Imamura , Saiko Akahira , Yoan Cherasse , Akiko Ihara , Takeshi Sakurai , Koichi Miyatake

During wakefulness, cortical neurons fire tonically and asynchronously to constantly support ongoing cognitive functions, whereas they show synchronized cessation of firing, so called ‘OFF periods’, during NREM sleep. Previous studies reported that cortical neurons start showing local OFF periods even in awake animals as sleep pressure builds up during the course of sleep deprivation. However, spatio-temporal dynamics of OFF periods across the cerebral cortex during prolonged wakefulness remained unknown. In this study, our extracellular recording in free-behaving mice showed that prolonged wakefulness causes neuronal firing lapses in the medial prefrontal cortex (mPFC) but not in motor cortex, suggesting the importance of mPFC in maintaining cognition during wakefulness. We next examined cortical area-specific effects of sustained neural activation on vigilance states. Chemogenetic activation of excitatory neurons in mPFC, but not in motor or sensory cortex, promoted wakefulness. Additionally, chemogenetic inhibition of mPFC reduced time spent in wakefulness, further supporting the causal role of mPFC in wakefulness.

在清醒状态下，皮质神经元以紧张性和异步方式放电，以持续支持正在进行的认知功能，而在非快速眼动睡眠期间，它们表现出同步的放电停止，即所谓的“关闭期”。先前的研究报告说，即使在清醒的动物中，当睡眠压力在睡眠剥夺的过程中增加时，皮质神经元也会出现局部关闭期。然而，在长时间清醒期间，大脑皮层的OFF期时空动态仍然未知。在这项研究中，我们对自由行为小鼠的细胞外记录显示，长时间的清醒会导致内侧前额叶皮层（mPFC）的神经元放电失效，但不会导致运动皮层的神经元放电失效，这表明mPFC在清醒状态下维持认知的重要性。接下来，我们研究了持续神经激活对警觉性状态的皮质区域特异性影响。兴奋性神经元在mPFC的化学发生激活，而不是在运动或感觉皮层，促进觉醒。此外，mPFC的化学发生抑制减少了清醒状态的时间，进一步支持了mPFC在清醒状态中的因果作用。

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引用次数: 0

Hindering tau fibrillization by disrupting transient precursor clusters 干扰瞬态前体簇阻碍Tau纤化。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-10-01 DOI: 10.1016/j.neures.2025.104968

Tomomi Takahashi , Takashi Nonaka , Reiko Ohtani , Masato Hasegawa , Yukiko Hori , Taisuke Tomita , Rei Kurita

Tau protein, a central player in Alzheimer’s disease (AD), exhibits cytotoxicity upon ﬁbril formation. Understanding the early stages of tau ﬁbrillization is therefore critical for the development of eﬀective therapeutics. Previous work [Rasmussen. et. al, J. Mol. Biol., 2023] reported the rapid formation of Thioﬂavin T (ThT)-inactive clusters upon mixing tau with anionic polymers, yet the functional role of these clusters remained unclear. Here, we demonstrate that these transient clusters act as obligatory precursors in the ﬁbrillization pathway. Using small-angle X-ray scattering (SAXS) and ThT ﬂuorescence, we show that disrupting the clusters via NaCl addition hinders ﬁbril formation, highlighting their reversible and targetable nature. This behavior is analogous to polymer crystallization, in which disordered chains undergo structural ordering through intermediate precursor states. We propose that similar physical principles underlie the aggregation of other intrinsically disordered proteins such as α-synuclein.

Tau蛋白是阿尔茨海默病（AD）的核心参与者，在纤维形成时表现出细胞毒性。因此，了解tau纤维化的早期阶段对于开发有效的治疗方法至关重要。以前的工作[Rasmussen]。等。J. Mol.生物学。[j]， 2023]报道了在将tau与阴离子聚合物混合后快速形成ThT -非活性簇，但这些簇的功能作用尚不清楚。在这里，我们证明了这些瞬态簇在成纤化途径中充当强制性前体。利用小角x射线散射（SAXS）和ThT荧光，我们发现通过NaCl加入破坏簇阻碍了原纤维的形成，突出了它们的可逆性和靶向性。这种行为类似于聚合物结晶，其中无序链通过中间前驱体状态进行结构排序。我们提出类似的物理原理是其他内在无序蛋白（如α-突触核蛋白）聚集的基础。

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引用次数: 0

Modeling natural neural networks of decision making with artificial neural networks 用人工神经网络建模自然神经网络的决策。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-09-26 DOI: 10.1016/j.neures.2025.104961

Akihiro Funamizu , Ryo Karakida

One main focus in neuroscience is to understand the relationship between decision making and various brain regions. Researchers use machine learning approaches to model the neural circuits of cerebral cortices, cerebellum, and basal ganglia. This review focuses on artificial neural networks (ANNs), particularly recurrent neural networks (RNNs), to model cortical functions for decision making. We first introduce the basic architecture of RNNs and explain how researchers compare the activity and circuits between artificial and biological networks. We also summarize how RNNs model the prefrontal and posterior parietal cortical in tasks involving short-term memory, perceptual decision making, and value-based decision making. We then show our recent challenges to develop a real-cyber hybrid network, that integrates neuronal activity in mice with RNN-based artificial units to better generate continuous-time body movements, compared to conventional RNNs that only use artificial units. The hybrid network tries to develop RNNs which have similar activity to the brain by using real neurons, rather than developing artificial RNNs and comparing their functions with biological brain. We propose that such integrative approaches in neuroscience and AI will further our understanding of both natural and artificial intelligence in the field of neuro-AI.

神经科学的一个主要焦点是了解决策与大脑各区域之间的关系。研究人员使用机器学习方法来模拟大脑皮层、小脑和基底神经节的神经回路。本文综述了人工神经网络（ANNs），特别是递归神经网络（RNNs），以模拟皮层功能的决策。我们首先介绍rnn的基本结构，并解释研究人员如何比较人工网络和生物网络之间的活动和电路。我们还总结了rnn如何在涉及短期记忆、感知决策和基于价值的决策的任务中对前额叶和后顶叶皮层进行建模。然后，我们展示了我们最近的挑战，即开发一个真实的网络混合网络，与仅使用人工单元的传统rnn相比，该网络将小鼠的神经元活动与基于rnn的人工单元相结合，以更好地产生连续时间的身体运动。混合网络试图通过使用真实的神经元来开发具有与大脑相似活动的rnn，而不是开发人工rnn并将其功能与生物大脑进行比较。我们认为，这种神经科学和人工智能的整合方法将进一步加深我们对神经人工智能领域的自然智能和人工智能的理解。

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引用次数: 0