Neuroscience Research最新文献

In Vivo Two-Photon Imaging Reveals Stochastic and Synchronized Extracellular Signal-Regulated Kinase Dynamics in Neurons of Awake Mice. 体内双光子成像揭示了清醒小鼠神经元中随机和同步的细胞外信号调节激酶动力学。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2026-02-02 DOI: 10.1016/j.neures.2026.105032

Ceylin Zeybek, Yohei Kondo, Michiyuki Matsuda, Hiroko Yukinaga

The neocortex is essential for higher-order brain functions such as cognition, perception, language, and motor control. Although extracellular signal-regulated kinase (ERK) activity in neurons has been well studied for its role in memory formation, its activity patterns in the awake mice brain remain unclear. This study aimed to investigate the spatiotemporal dynamics of ERK activity in neocortical neurons of awake mice using in vivo imaging. We used Förster resonance energy transfer (FRET)-based biosensor and two-photon microscopy to examine ERK activity in vivo through a cranial window. Visual cortical neurons exhibited NMDA receptor-dependent ERK activation in response to visual stimuli. Beyond stimulus-induced activation, we discovered spontaneous and stochastic ERK activation patterns categorized as single, multi-pulsatile, and sustained activations, which were consistent across various cortical regions, including the visual and somatosensory cortices. Furthermore, synchronized ERK activation among neurons was observed, suggesting a coordinated ERK activation mechanism within neuronal networks that may contribute to sensory information processing. These findings reveal a highly dynamic ERK activation in neocortical cells and provide new insights regarding the functional role of ERK in the awake brain.

新皮层对于认知、感知、语言和运动控制等高级大脑功能至关重要。尽管细胞外信号调节激酶（ERK）在神经元中的活性在记忆形成中的作用已经得到了很好的研究，但其在清醒小鼠大脑中的活动模式仍不清楚。本研究旨在利用活体成像技术研究清醒小鼠新皮质神经元ERK活性的时空动态。我们使用Förster共振能量转移（FRET）为基础的生物传感器和双光子显微镜检查ERK活性在体内通过颅窗。视觉皮层神经元对视觉刺激表现出NMDA受体依赖性的ERK激活。除了刺激诱导的激活，我们还发现了自发和随机的ERK激活模式，分为单脉冲、多脉冲和持续激活，这些激活模式在不同的皮质区域（包括视觉和体感皮质）中是一致的。此外，观察到神经元之间ERK的同步激活，表明神经元网络中ERK的协调激活机制可能有助于感觉信息处理。这些发现揭示了新皮质细胞中ERK的高度动态激活，并为ERK在清醒大脑中的功能作用提供了新的见解。

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引用次数: 0

Triple equivalence in modelling insight and creativity: Classical and quantum perspectives. 三重等效建模洞察力和创造力：经典和量子的观点。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2026-01-24 DOI: 10.1016/j.neures.2026.105025

Takuya Isomura

Understanding the emergence of novel ideas in the brain-which is a hallmark of insight and creativity-remains a fundamental challenge in neuroscience. While traditional frameworks such as predictive coding, the Bayesian brain hypothesis, and the free-energy principle emphasise the approximation of external milieu states, internal generative processes that create new ideas rather than imitate remain underexplored. This review proposes a normative account of insight and creativity grounded in a triple equivalence between neural dynamics, Bayesian inference, and algorithmic computation. This equivalence provides a formal framework for understanding how neural circuits driven by mental actions can spontaneously generate creative ideas. Moreover, such creativity requires an efficient exploration of the algorithmic space to minimise free energy. Insight corresponds to a non-local search strategy that enables escape from local minima, thereby distinguishing it from conventional predictive processing. To this end, quasi-quantum neural networks that leverage superpositional coding can be considered to account for efficient global search. From this perspective, insight and creativity emerge through a self-organising exploratory process, offering a view of the brain as a spontaneous algorithm generator, rather than a predictor of its external milieu.

理解大脑中新想法的出现——这是洞察力和创造力的标志——仍然是神经科学的一个基本挑战。虽然预测编码、贝叶斯大脑假说和自由能原理等传统框架强调对外部环境状态的近似，但创造新想法而不是模仿的内部生成过程仍未得到充分探索。这篇综述提出了一种基于神经动力学、贝叶斯推理和算法计算之间三重等价的洞察力和创造力的规范描述。这种等价性为理解由心理活动驱动的神经回路如何自发产生创造性想法提供了一个正式框架。此外，这种创造力需要对算法空间进行有效探索，以最大限度地减少自由能。Insight对应于一种非局部搜索策略，可以避免局部最小值，从而将其与传统的预测处理区分开来。为此，利用叠加编码的准量子神经网络可以考虑考虑高效的全局搜索。从这个角度来看，洞察力和创造力是通过自我组织的探索过程产生的，提供了一种观点，即大脑是一个自发的算法生成器，而不是外部环境的预测器。

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引用次数: 0

Real-time classification of cortical slow-wave states by a machine learning model 基于机器学习模型的皮层慢波状态实时分类。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2026-01-22 DOI: 10.1016/j.neures.2026.105024

Minato Uemura , Hiroyuki Mizuno , Yuji Ikegaya , Tetsuhiko Kashima

During slow-wave sleep, cortical slow oscillations—composed of alternating Up/Down states (UDS)—are crucial for memory consolidation. We classified UDS from local field potentials using machine learning models, specifically a hybrid CNN + RNN and a Transformer architecture, trained on labels derived from membrane potential recordings. Both models outperformed conventional methods, achieving superior classification accuracy and markedly reducing classification errors. Notably, the Transformer model also enabled real-time inference while maintaining robust performance. This real-time classification capability facilitates closed-loop feedback experiments to manipulate neuronal activity contingent on UDS phase, providing a powerful tool for investigating the causal mechanisms underlying sleep-dependent memory consolidation.

在慢波睡眠期间，由上下交替状态（UDS）组成的皮层慢振荡对记忆巩固至关重要。我们使用机器学习模型，特别是混合CNN + RNN和Transformer架构，对来自膜电位记录的标签进行训练，从局部场电位中分类UDS。两种模型均优于传统方法，实现了较高的分类精度，并显著降低了分类误差。值得注意的是，Transformer模型还支持实时推理，同时保持健壮的性能。这种实时分类能力有助于闭环反馈实验来操纵随UDS相变化的神经元活动，为研究睡眠依赖性记忆巩固的因果机制提供了有力的工具。

引用次数: 0

Hippocampal myelin damage contributes to cognitive impairment in a rat model of trigeminal neuropathic pain: Neuroprotective and anti-inflammatory effects of atorvastatin 三叉神经性疼痛大鼠模型海马髓鞘损伤导致认知障碍：阿托伐他汀的神经保护和抗炎作用

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2026-01-16 DOI: 10.1016/j.neures.2026.105022

Yongkui Yang , Youzhi Ning , Shuangchun Peng , Changli Liao , Jia Fu , Jiaomei Zhao , Cehua Ou , Yue Zhang

Chronic neuropathic pain is increasingly recognized to impair cognitive function, yet its underlying mechanisms remain unclear. This study tested whether trigeminal neuropathic pain (TNP) modeled by distal infraorbital nerve chronic constriction injury (dION-CCI) provokes hippocampal myelin damage associated with cognitive dysfunction, and whether atorvastatin attenuates mechanical hypersensitivity and cognitive deficits. We also explored whether these effects relate to attenuation of the CD95/CD95L (Fas/Fas ligand)–NF-κB–interleukin-1β (IL-1β) axis and preservation of myelin integrity. Behavioral assessments included facial mechanical withdrawal threshold testing and Morris water maze analysis of spatial learning and memory. Hippocampal myelin integrity was examined using Western blotting of myelin basic protein (MBP), immunofluorescence, transmission electron microscopy, and Luxol Fast Blue staining. TNP rats exhibited significant facial mechanical hypersensitivity and impaired spatial learning, accompanied by decreased MBP expression and myelin disruption. Atorvastatin (10 mg/kg/day) attenuated mechanical hypersensitivity, improved learning ability, preserved myelin structure, and restored MBP levels. Inflammatory markers including CD95, CD95L, NF-κB, and IL-1β were elevated in TNP rats and downregulated by atorvastatin. These findings suggest that hippocampal myelin damage may underlie TNP-related cognitive deficits, and atorvastatin may exert neuroprotective effects by mitigating neuroinflammation and myelin injury.

慢性神经性疼痛越来越被认为会损害认知功能，但其潜在机制尚不清楚。本研究测试了由远端眶下神经慢性收缩损伤（dION-CCI）模拟的三叉神经痛（TNP）是否会引起与认知功能障碍相关的海马髓鞘损伤，以及阿托伐他汀是否会减轻机械超敏反应和认知缺陷。我们还探讨了这些效应是否与CD95/CD95L （Fas/Fas配体）-NF -κ b -白细胞介素-1β (IL-1β)轴的衰减和髓磷脂完整性的保存有关。行为评估包括面部机械戒断阈值测试和Morris水迷宫分析。采用髓鞘碱性蛋白（MBP） Western blotting、免疫荧光、透射电镜和Luxol Fast Blue染色检测海马髓鞘完整性。TNP大鼠表现出明显的面部机械过敏和空间学习障碍，并伴有MBP表达下降和髓磷脂破坏。阿托伐他汀（10 mg/kg/天）可减轻机械超敏反应，改善学习能力，保留髓鞘结构，恢复MBP水平。炎症标志物CD95、CD95L、NF-κB和IL-1β在TNP大鼠中升高，阿托伐他汀则下调。这些发现表明海马髓磷脂损伤可能是与tnp相关的认知缺陷的基础，阿托伐他汀可能通过减轻神经炎症和髓磷脂损伤发挥神经保护作用。

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引用次数: 0

A novel brainstem-targeted G51D α-synuclein fibril-injected mouse model exhibits sequential emergence of sleep and motor dysfunction 一种新的脑干靶向G51D α-突触核蛋白原纤维注射小鼠模型显示连续出现睡眠和运动功能障碍。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2026-01-16 DOI: 10.1016/j.neures.2026.105023

Shinnosuke Yasugaki , Ami Kaneko , Hibiki Okamura , Hideki Hayakawa , Kensuke Ikenaka , Cesar Aguirre , Masashi Yanagisawa , Hideki Mochizuki , Kousuke Baba , Yu Hayashi

Abnormal accumulation of alpha-synuclein (α-syn) is a central pathologic hallmark of synucleinopathies such as Parkinson’s disease (PD), with rapid eye movement sleep behavior disorder (RBD) widely recognized as a prodromal manifestation of these disorders. Although several mouse models recapitulate the α-syn pathology, most fail to reproduce the brainstem-originating pathology propagation proposed by Braak and do not exhibit the RBD-like phenotypes expected in the prodromal phase. Here, we focused on the G51D mutation of α-syn, a familial PD-associated variant that leads to early disease onset and severe clinical symptoms. We microinjected G51D mutant α-syn fibrils into the pontine tegmental area of the brainstem in mice, a region critically involved in REM sleep regulation, and evaluated the effects on sleep architecture, pathologic progression, and motor function. Our results revealed that microinjection of G51D fibrils into the brainstem induces more extensive pathologic changes compared with wild-type fibrils and leads to the sequential emergence of RBD-like behaviors, motor deficits, and dopaminergic neuronal loss. These findings support the hypothesis that the G51D mutation worsens disease severity and establish this model as a valuable tool for investigating the mechanisms underlying synucleinopathies and their prodromal symptoms.

α-突触核蛋白（α-syn）的异常积累是突触核蛋白病（如帕金森病（PD））的中心病理标志，而快速眼动睡眠行为障碍（RBD）被广泛认为是这些疾病的前驱表现。尽管一些小鼠模型再现了α-syn病理，但大多数小鼠模型未能再现Braak提出的脑干起源的病理繁殖，也没有表现出前驱期预期的rbd样表型。在这里，我们重点研究了α-syn的G51D突变，这是一种家族性pd相关变异，可导致疾病早期发病和严重的临床症状。我们将G51D突变体α-syn原纤维微注射到小鼠脑干的脑桥被盖区，这一区域对REM睡眠的调节至关重要，并评估了其对睡眠结构、病理进展和运动功能的影响。我们的研究结果显示，与野生型原纤维相比，将G51D原纤维显微注射到脑干中可引起更广泛的病理改变，并导致rbd样行为、运动缺陷和多巴胺能神经元丢失的顺序出现。这些发现支持了G51D突变加重疾病严重程度的假设，并将该模型建立为研究突触核蛋白病及其前驱症状的潜在机制的有价值的工具。

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引用次数: 0

Gradual proactive regulation of body state by reinforcement learning of homeostasis 通过强化体内平衡学习对身体状态的逐步主动调节。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2026-01-07 DOI: 10.1016/j.neures.2026.105021

Mana Fujiwara , Honda Naoki

Living systems maintain physiological variables such as temperature, blood pressure, and glucose within narrow ranges—a process known as homeostasis. Homeostasis involves not only reactive feedback but also anticipatory adjustments shaped by experience. Prior homeostatic reinforcement learning (HRL) models have provided a computational account of anticipatory regulation under homeostatic challenges. However, existing formulations lack mechanisms for gradual, trial-by-trial adjustment and for extinction learning. To address this issue, we developed a continuous HRL framework that enables trial-wise tuning of anticipatory regulation. The model incorporates biologically informed components: asymmetric reinforcement, weighting negative outcomes more than positive outcomes; and a dual-unit, context-gated inhibitory mechanism. We applied the framework to thermoregulatory conditioning with ethanol-induced hypothermia and successfully reproduced cue-triggered compensation, gradual tolerance, and rapid reacquisition after extinction. We then extended the framework to multiple physiological variables influenced by shared neural or hormonal control signals, where compensating one variable can necessarily incur costs in others (e.g., heating at the expense of a fuel-like resource). Under uneven regulatory priorities, deviations propagated through shared control, yielding cascading, system-wide failure to stabilize near the ideal state—a failure mode discussed in autonomic dysregulation (e.g., dysautonomia, myalgic encephalomyelitis/chronic fatigue syndrome). Overall, our framework provides a computational basis to advances a systems-level understanding of multi-organ homeostatic dysregulation in vivo.

生命系统将体温、血压和葡萄糖等生理变量维持在一个狭窄的范围内，这一过程被称为体内平衡。内稳态不仅包括反应性反馈，还包括由经验形成的预期调整。先前的稳态强化学习（HRL）模型提供了稳态挑战下预期调节的计算说明。然而，现有的配方缺乏渐进的、逐个试验的调整机制和灭绝学习机制。为了解决这个问题，我们开发了一个连续的HRL框架，可以在试验中对预期调节进行调整。该模型包含了生物学信息成分：不对称强化，负面结果的权重大于积极结果；以及一个双单元、情境控制的抑制机制。我们将该框架应用于乙醇诱导的低温热调节条件，并成功再现了线索触发的补偿、逐渐耐受和灭绝后的快速重新获取。然后，我们将该框架扩展到受共享神经或激素控制信号影响的多个生理变量，其中补偿一个变量必然会导致其他变量的成本（例如，以燃料类资源为代价的加热）。在不平衡的调控优先级下，偏差通过共享控制传播，产生级联的、系统范围的失败，无法稳定在理想状态附近——自主神经失调（例如，自主神经失调、肌痛性脑脊髓炎/慢性疲劳综合征）中讨论的失败模式。总的来说，我们的框架提供了一个计算基础，以推进对体内多器官稳态失调的系统级理解。

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引用次数: 0

A computational model of canonical cortical microcircuits for dynamic Bayesian inference and control as inference 典型皮质微电路的动态贝叶斯推理和控制计算模型。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2026-01-01 DOI: 10.1016/j.neures.2025.105002

Naohiro Yamauchi , Yoshimasa Tawatsuji , Yudai Suzuki , Hiroshi Yamakawa , Kenji Doya

Canonical cortical microcircuits (CCMs), a six-layer architecture conserved across the mammalian neocortex, play a crucial role in cognitive functions such as sensory inference, decision-making, and motor planning. However, the computational mechanisms underlying these functions remain unclear, and existing models often lack detailed representations of cell types and interlayer connectivity. In this study, we applied the structure-constrained interface decomposition (SCID) method (Yamakawa, 2021) to construct a biologically plausible computational model of CCMs for dynamic Bayesian inference (DBI) and control as inference (CAI). Our model explicitly assigns computational roles to all major excitatory neuronal populations and incorporates the contributions of inhibitory neurons via circuit motifs. Based on this framework, we constructed CCM models of the somatosensory cortex for DBI and motor cortex for CAI. Through simulations of a mouse lever-push/pull perceptual decision-making and control task, our model reproduced key behavioral features, including psychometric curves and “change of mind” behaviors. Furthermore, we conducted layer-specific perturbation simulations that produced experimentally testable predictions about the functional roles of different cortical layers. Based on the duality of inference and control, this study addresses the long-standing challenge of giving a unified account of CCMs’ functions in sensory and motor cortices.

典型皮层微回路（CCMs）是一种分布于哺乳动物新皮层的六层结构，在感觉推断、决策和运动计划等认知功能中起着至关重要的作用。然而，这些功能背后的计算机制尚不清楚，现有模型往往缺乏细胞类型和层间连接的详细表示。在本研究中，我们应用结构约束界面分解（SCID）方法（Yamakawa, 2021）构建了一个生物学上合理的ccm计算模型，用于动态贝叶斯推理（DBI）和控制推理（CAI）。我们的模型明确地为所有主要的兴奋性神经元群体分配计算角色，并通过电路基元纳入抑制性神经元的贡献。在此框架下，我们分别构建了DBI的体感皮层和CAI的运动皮层的CCM模型。通过模拟小鼠杠杆推/拉感知决策和控制任务，我们的模型再现了关键的行为特征，包括心理测量曲线和“改变想法”行为。此外，我们进行了特定层的扰动模拟，产生了关于不同皮质层的功能作用的实验可测试的预测。基于推理和控制的二元性，本研究解决了长期存在的挑战，即对CCMs在感觉和运动皮层中的功能给出统一的解释。

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引用次数: 0

Antidote administration in mice exposed to sarin resulted in brainwave stabilization without cognitive protection 在暴露于沙林的小鼠中给予解毒剂导致脑波稳定，但没有认知保护。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-12-30 DOI: 10.1016/j.neures.2025.105013

Mélanie Lagadec , Pauline Thiebot , Isabelle Malissin , Alexandre Champault , Julie Somkhit , Julie Knoertzer , Assia Belkebir , Bruno Megarbane , Karine Thibault , Gregory Dal Bo

Resurgence of sarin use in the Syrian conflict demonstrates that chemical weapons are a vivid threat. Like other organophosphate compounds, sarin inhibits acetylcholinesterase resulting in cholinergic crisis. The current antidote therapy includes atropine (a muscarinic cholinergic antagonist) + an oxime (e.g., pralidoxime) to reactivate the inhibited cholinesterases. Long-term sequelae reported in victims of the 1995 Tokyo subway sarin attack emphasize the need to improve neuroprotection and to delineate more precise biomarkers of intoxication severity. Previously, we proposed that brain oscillations could indicate exposure severity to a sublethal dose of a neurotoxic agent. In the present study, we evaluated the effects of atropine + pralidoxime in mice exposed to a sublethal dose of sarin (0.9 LD₅₀) on changes in short-term recovery, brainwaves and behavioral patterns. We demonstrated the benefits of the antidotes on alleviation of the sarin-induced encephalopathy, stabilization of brain oscillations, and attenuation of anhedonia behavior. Nevertheless, mice exhibited work memory impairments associated with the disruption of theta oscillations during the task, the disruption of sleep architecture and the anxiety-like behavior when exposed to the non-convulsive sarin dose. These outcomes were not mitigated by atropine + pralidoxime administration. Our findings suggest that the currently recommended antidote for sarin poisoning provides only partial neuroprotection. Despite stabilizing brain waves in resting state, current antidote is not effective in preventing long-term neurobehavioral complications.

在叙利亚冲突中再次使用沙林表明，化学武器是一个活生生的威胁。与其他有机磷化合物一样，沙林抑制乙酰胆碱酯酶，导致胆碱能危机。目前的解毒剂治疗包括阿托品（一种毒蕈碱类胆碱能拮抗剂）+肟（如普拉西肟）来重新激活被抑制的胆碱酯酶。1995年东京地铁沙林毒气袭击受害者报告的长期后遗症强调了改善神经保护和更精确描述中毒严重程度的生物标志物的必要性。以前，我们提出大脑振荡可以表明暴露于亚致死剂量的神经毒性物质的严重程度。在本研究中，我们评估了暴露于亚致死剂量沙林（0.9 LD50）的小鼠阿托品+普拉多肟对短期恢复、脑电波和行为模式变化的影响。我们证明了解毒剂在缓解沙林诱导的脑病、稳定脑振荡和减轻快感缺乏行为方面的益处。然而，当暴露于非惊厥性沙林剂量时，小鼠表现出与任务中θ波振荡中断、睡眠结构中断和焦虑样行为相关的工作记忆障碍。阿托品+普拉多肟并没有减轻这些结果。我们的研究结果表明，目前推荐的沙林中毒解毒剂只能提供部分神经保护。目前的解毒剂虽然能稳定静息状态下的脑电波，但对预防长期的神经行为并发症没有效果。

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引用次数: 0

A novel probe for precise and symmetric bilateral in utero electroporation in the mouse 一种用于小鼠子宫内精确对称双侧电穿孔的新型探针。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-12-23 DOI: 10.1016/j.neures.2025.105009

Eichi Toyoizumi , Arthur J.Y. Huang , Dai Yanagihara , Tomomi Shimogori , Thomas J. McHugh

In utero electroporation (IUE) has been an invaluable tool for the efficient expression of genes in the developing brain and widely employed in characterizing the molecular mechanisms of circuit formation. However, its application to other fields of neurobiology, including cognitive development, has been hampered by several limitations, including sparse expression, high hemispheric lateralization, and difficulty in targeting specific cortical or hippocampal regions. To address these issues, here we describe a novel IUE approach, specifically designed for use in the mouse, that combines up to four paddle and needle-type electrodes and permits precise, robust, and symmetrical bilateral transfection in a safe and efficient manner. The ability to achieve reproducible symmetric transfection patterns in brain regions involved in cognition will allow more intricate investigations into the molecular and circuit mechanisms of early cognitive development.

子宫内电穿孔（IUE）是研究大脑发育过程中基因高效表达的宝贵工具，并被广泛用于表征神经回路形成的分子机制。然而，它在包括认知发展在内的其他神经生物学领域的应用受到了一些限制，包括稀疏表达、半球高度偏侧化以及难以靶向特定的皮层或海马区域。为了解决这些问题，我们在这里描述了一种新的IUE方法，专门设计用于小鼠，它结合了多达四个桨形和针状电极，并允许以安全有效的方式进行精确，稳健和对称的双侧转染。在涉及认知的大脑区域中实现可重复的对称转染模式的能力，将允许对早期认知发展的分子和电路机制进行更复杂的研究。

引用次数: 0

High-resolution optogenetics generates distinguishable neocortical activity patterns in awake mice 高分辨率光遗传学在清醒小鼠中产生可区分的新皮层活动模式。

IF 2.3 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-12-23 DOI: 10.1016/j.neures.2025.105012

Ryosuke Yoshida , Yamato Ishii , Kotaro Yamashiro , Kei Furuya , Tianben Ding , Keisuke Goda , Nobuyoshi Matsumoto , Yuji Ikegaya

The neural basis of cognition is rooted in precisely coordinated population activity unfolding on the millisecond timescale. To causally probe these spatiotemporally intricate network dynamics, we developed a digital micromirror device (DMD)-based photostimulation platform featuring grid patterns with up to 2-μm spatial and 0.2-ms temporal resolution across a 2-mm-diameter area. Spatiotemporally patterned photostimulation to the primary somatosensory cortex of channelrhodopsin-2-expressing mice reliably evoked distinct electrophysiological population responses that deep learning algorithms accurately classified. Notably, rapidly changing illumination patterns evoked cortical activity with greater trial-to-trial consistency than conventional constant photostimulation. Thus, DMD-based spatiotemporal optogenetics enables precise and reproducible control of in vivo neuronal population activity.

认知的神经基础植根于精确协调的群体活动，在毫秒的时间尺度上展开。为了探索这些时空复杂的网络动态，我们开发了一个基于数字微镜设备（DMD）的光刺激平台，该平台具有在2 mm直径区域内高达2 μm空间分辨率和0.2 ms时间分辨率的网格模式。对表达通道视紫红质-2的小鼠的初级体感觉皮层进行时空模式的光刺激，可以可靠地引起不同的电生理群体反应，深度学习算法可以准确分类。值得注意的是，与传统的恒定光刺激相比，快速变化的光照模式诱发的皮层活动具有更大的一致性。因此，基于dmd的时空光遗传学能够精确和可重复地控制体内神经元群的活动。

引用次数: 0