编辑丨王多鱼 排版丨水成文 大脑中的神经元通过突触相互连接，形成复杂的神经网络。突触传递的强度和效率 持续 发生变化，这一现 象称为 突触可塑性 ，被认为是学习和记忆的细胞基础。 NMDA 受体 是一类离子型谷氨酸受体，在介导兴 奋性神经传递和调控突触可塑性方面发挥着核心作用。当 NMDA 受体功能异常时，可能导致癫痫、精神分 裂症、抑郁症以及阿尔茨海默病等多种神经系统疾病。 NMDA 受体是由不同亚基组成的异源四聚体 ， 通常包含两个必需的 GluN1 亚基和两个 GluN2 亚基 （ GluN2A-D ） 或 GluN3 亚基 （ GluN3A-B ） 。不同亚基的组合赋予受体不同的功能特性：含 GluN2A 的受体激活速度快，含 GluN2B 的受体则激活较慢但持续时间更长。这种亚基组成的差异也影响受体对药 物的反应，因此解析天然状态下受体的 亚基组成、组装方式和门控转换机制 ，对于开发靶向特定亚型的治 疗药物具有重要意义。 该研究发现，含 GluN2A 亚基的受体在 全脑 中占主导地位。 GluN2A 的氨基末端结构域 （ ATD ） 表现 出显著的构象柔性，这种动态变化可能 调节 从 ATD 到 L ...

来源丨医诺维 突触 是神经元之间传递信息的关键连接，其可塑性 （即连接强度增强或减弱） 是大脑适应环境、学习和 记忆的神经基础。 众所周知，夜间睡眠能调节突触连接强度，白天清醒时，大脑持续接收信息会导致突触连接强度升高，最 终达到饱和状态，阻碍接收新信息；而正常的夜间睡眠可降低整体突触连接强度，相当于"重置"了突触可 塑性，为新的学习和记忆腾出空间。 既往的人类研究表明，正常的夜间睡眠可 "重置" 突触可塑性，而一晚的睡眠剥夺则会削弱突触可塑性。然 而，尚不清楚午睡是否足以像夜间睡眠一样，"重置"大脑突触可塑性。 2026 年 1 月 14 日，瑞士 日内瓦大学的研究人员在 NeuroImage 期刊发表了题为： A nap can recalibrate homeostatic and associative synaptic plasticity in the human cortex 的研究论文。 这项研究 首次在人类中证实，短暂的午睡能够"重置"大脑突触可塑性，显著降低整体突触连接强度，并增 强大脑形成新突触连接的能力，为后续工作与学习提供最佳状态。 试验期间，通过经颅磁刺激 （TMS） 测量皮质兴奋 ...

Core Insights - Brain science is reshaping the understanding of emotional issues, indicating that anxiety and depression are not merely psychological problems but are linked to pathological changes in brain neural circuits [2][3] - The concept of "pain emotion" is introduced, suggesting that chronic psychological discomfort can activate specific neural circuits, leading to persistent anxiety or depression [3][4] - The need for precise identification and intervention in emotional issues is emphasized, distinguishing between short-term and chronic anxiety [5] Group 1: Understanding Emotional Issues - The development of brain science clarifies the neural mechanisms behind emotional problems, focusing on learned changes in brain circuits rather than just psychological states [3] - Chronic anxiety is linked to molecular mechanisms that become reinforced in the brain, making it difficult to resolve simply through cognitive understanding [4] - Modern lifestyle factors, such as constant exposure to information via smartphones and social media, contribute to heightened sensitivity in neural circuits, increasing the prevalence of emotional issues [4] Group 2: Identification and Intervention Strategies - Accurate identification of emotional problems is crucial for effective intervention, with a focus on differentiating between short-term and chronic anxiety [5] - A layered judgment approach is proposed for assessing chronic anxiety, involving self-awareness, professional evaluation, and AI-assisted monitoring tools [5] - Multi-dimensional intervention strategies are recommended, including environmental changes, psychological counseling, and memory restructuring techniques [5][6] Group 3: Future of the Emotional Health Industry - Emotional issues represent a global public health challenge, creating significant demand for industry solutions, but the translation of brain science findings into practical applications requires collaboration among academia, industry, and research [7] - Innovative drug development is identified as a key area for translating brain science into marketable solutions, with a focus on creating targeted therapies that selectively inhibit overactive neural circuits [7] - The research team is optimistic about the potential for precision-targeted medications to be clinically available within the next 5 to 10 years, aiming for effective treatments for anxiety and depression similar to those for other common diseases [7]

Core Viewpoint - The study reveals that the oligomerization of Shank3 regulates the material properties of postsynaptic density (PSD) condensates, which are crucial for synaptic plasticity and neuronal functions related to learning and memory [3][5][7]. Summary by Sections - The research team from Southern University of Science and Technology published findings indicating that PSD condensates exhibit soft-glass-like properties, with Shank3 protein oligomerization playing a key role in governing these material characteristics [3][5]. - The study found that the reconstructed PSD condensates formed a soft-glass material without signs of irreversible amyloid-like structures. This glass-like formation relies on specific, multivalent interactions among scaffold proteins, which mediate the network flow of PSD proteins [4]. - Disruption of Shank3's SAM domain-mediated oligomerization, observed in patients with Phelan-McDermid syndrome, leads to a softening of PSD condensates, impairing synaptic transmission and plasticity, and resulting in autism-like behaviors in mice [4][5]. - Overall, the research emphasizes the importance of the material properties of PSD condensates in neuronal synaptic functions related to learning and memory [7].

Core Insights - The research reveals a convergent mechanism of echolocation in different mammalian species, providing new perspectives on the evolutionary origins of this complex behavior [1][2] - The study highlights the significance of non-coding regulatory regions in the convergent evolution of behaviors, challenging the traditional focus on protein-coding genes [2] Group 1: Research Findings - The study identifies 222 shared open chromatin regions in the hippocampal area of echolocating species, significantly higher than random expectations, indicating a complex gene regulatory network [1] - Traditional auditory-related genes are found to be abnormally active in the hippocampal regulatory networks of echolocating mammals, suggesting their role in spatial localization functions [2] Group 2: Methodology and Implications - The research employs innovative techniques such as chromatin accessibility sequencing, transcriptome sequencing, and transmission electron microscopy to compare the hippocampal gene regulatory features of various species [1] - The establishment of the Daluoshan pig-tailed mouse as a new model organism offers a valuable platform for further exploration of the neural mechanisms underlying echolocation [2]

Core Viewpoint - Researchers from the National University of Singapore (NUS) have demonstrated that a single standard silicon transistor can mimic the behavior of biological neurons and synapses, bringing hardware-based artificial neural networks (ANN) closer to reality [1][3]. Group 1: Research Findings - The NUS research team, led by Professor Mario Lanza, provides a scalable and energy-efficient solution for hardware-based ANN, making neuromorphic computing more feasible [1][3]. - The study published in Nature on March 26, 2025, shows that a single silicon transistor can replicate neural firing and synaptic weight changes, which are fundamental mechanisms of biological neurons and synapses [3][4]. Group 2: Technical Innovations - The research achieved this by adjusting the resistance of the transistor to specific values, controlling two physical phenomena: impact ionization and charge trapping [4]. - The team developed a dual-transistor unit called "neuro-synaptic random access memory" (NS-RAM), which operates in neuron or synapse states [4]. Group 3: Advantages of the New Approach - The method utilizes commercial CMOS technology, ensuring scalability, reliability, and compatibility with existing semiconductor manufacturing processes [4]. - Experimental results show that NS-RAM units exhibit low power consumption, stable performance over multiple operational cycles, and consistent behavior across different devices, essential for building reliable ANN hardware [4].