Current Opinion in Neurobiology最新文献

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Emerging roles for tubulin PTMs in neuronal function and neurodegenerative disease

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2025.102971

JiaJie Teoh, Francesca Bartolini

Neurons are equipped with microtubules of different stability with stable and dynamic domains often coexisting on the same microtubule. While dynamic microtubules undergo random transitions between disassembly and assembly, stable ones persist long enough to serve as platforms for tubulin-modifying enzymes (known as writers) that attach molecular components to the α- or β-tubulin subunits. The combination of these posttranslational modifications (PTMs) results in a “tubulin code,” dictating the behavior of selected proteins (known as readers), some of which were shown to be crucial for neuronal function. Recent research has further highlighted that disturbances in tubulin PTMs can lead to neurodegeneration, sparking an emerging field of investigation with numerous questions such as whether and how tubulin PTMs can affect neurotransmission and synaptic plasticity and whether restoring balanced tubulin PTM levels could effectively prevent or mitigate neurodegenerative disease.

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Astrocyte regulation of critical period plasticity across neural circuits 星形胶质细胞对神经回路关键期可塑性的调节。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2024.102948

Jacob P. Brandt , Sarah D. Ackerman

Critical periods are brief windows of heightened neural circuit plasticity that allow circuits to permanently reset their structure and function to facilitate robust organismal behavior. Understanding the cellular and molecular mechanisms that instruct critical period timing is of broad clinical interest, as altered developmental plasticity is linked to multiple neurodevelopmental disorders. While intrinsic, neuronal mechanisms shape both neural circuit remodeling and critical period timing, recent data indicate that signaling from astrocytes and surrounding glia can both promote and limit critical period plasticity. In this short review, we discuss recent breakthroughs in our understanding of astrocytes in critical period plasticity and highlight pioneering work in Drosophila.

关键时期是神经回路可塑性增强的短暂窗口期，它允许回路永久地重置其结构和功能，以促进强健的机体行为。了解指导关键时期时间的细胞和分子机制具有广泛的临床意义，因为发育可塑性的改变与多种神经发育障碍有关。虽然内在的神经元机制塑造了神经回路重塑和关键时期的时间，但最近的数据表明，星形胶质细胞和周围胶质细胞的信号传导既可以促进也可以限制关键时期的可塑性。在这篇简短的综述中，我们讨论了最近在星形胶质细胞关键期可塑性理解方面的突破，并重点介绍了在果蝇方面的开创性工作。

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Roles of ANK2/ankyrin-B in neurodevelopmental disorders: Isoform functions and implications for autism spectrum disorder and epilepsy ANK2/锚蛋白b在神经发育障碍中的作用：自闭症谱系障碍和癫痫的异构体功能和意义。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2024.102938

Sehyoun Yoon , Peter Penzes

The ANK2 gene, encoding ankyrin-B, is a high-confidence risk factor for neurodevelopmental disorders (NDDs). Evidence from exome sequencing studies have repeatedly implicated rare variants in ANK2 in autism spectrum disorder. Recently, the functions of ankyrin-B isoforms on neuronal phenotypes have been investigated using a number of techniques including electrophysiology, proteomic screens and behavioral analysis using animal models with loss of distinct Ank2 isoforms or with targeted loss of Ank2 in different cell types and time points during brain development. ANK2 variants and their pathophysiology could provide valuable insights into the molecular mechanisms underlying NDDs. In this review, we focus on recently reported studies to help understand the pathological mechanisms of ANK2 loss and how it may facilitate the development of treatments for NDDs in the future.

编码锚蛋白b的ANK2基因是神经发育障碍（ndd）的高可信度危险因素。来自外显子组测序研究的证据一再暗示自闭症谱系障碍中ANK2的罕见变异。最近，研究人员利用电生理学、蛋白质组学筛选和行为分析等多种技术，研究了锚蛋白- b亚型对神经元表型的作用，这些技术使用的动物模型具有不同的Ank2亚型缺失或在大脑发育过程中不同细胞类型和时间点的Ank2靶向缺失。ANK2变异及其病理生理可以为ndd的分子机制提供有价值的见解。在这篇综述中，我们关注最近报道的研究，以帮助理解ANK2丢失的病理机制，以及它如何促进未来ndd治疗的发展。

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Spinal sensory innervation of the intestine

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2025.102973

Rachel L. Wolfson

Sensing our internal environment, or interoception, is essential under physiologic circumstances, such as controlling food intake, and under pathophysiologic circumstances, often triggering abdominal pain. The sensory neurons that innervate the gastrointestinal (GI) tract to mediate interoception originate in two separate parts of the peripheral nervous system: the spinal sensory neurons, whose cell bodies reside in the dorsal root ganglia (DRG), and the vagal sensory neurons, whose cell bodies reside in the nodose ganglia. While the vagal sensory neurons have been extensively studied for their roles in interoception, the roles of the DRG sensory neurons in internal gut sensing are only beginning to be uncovered. Here, we review the recent advances in understanding the diverse properties and functions of gut-innervating DRG sensory neurons and highlight the many unknowns with regards to this understudied population in regulating interoception.

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Endocytosis in the axon initial segment: Roles in neuronal polarity and plasticity 轴突初始段的内吞作用：在神经元极性和可塑性中的作用。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2024.102949

Kelsie Eichel

The axon initial segment (AIS) is a specialized domain that maintains neuronal polarity and is the site of action potential generation, both of which underlie the neuron's ability to send and receive signals. Disruption of the AIS leads to a loss of neuronal polarity, altered neuronal signaling, and an array of neurological disorders. Therefore, understanding how the AIS forms and functions is a central question in cellular neuroscience that is essential to understanding neuronal physiology. Decades of study have identified many molecular components and mechanisms at the AIS. Recently, endocytosis at the AIS has been identified to function in both maintaining neuronal polarity and in mediating AIS plasticity through its ability to dynamically remodel the plasma membrane composition. This review discusses the emerging evidence for the roles of endocytosis in regulating AIS function and structural insights into how endocytosis can occur at the AIS.

轴突初始段（AIS）是维持神经元极性的特殊区域，也是动作电位产生的场所，两者都是神经元发送和接收信号能力的基础。AIS的破坏会导致神经元极性的丧失、神经元信号的改变和一系列神经系统疾病。因此，理解AIS的形成和功能是细胞神经科学的一个核心问题，对理解神经元生理学至关重要。几十年的研究已经确定了AIS的许多分子成分和机制。最近，AIS的内吞作用已被确定为通过其动态重塑质膜组成的能力来维持神经元极性和介导AIS可塑性。这篇综述讨论了关于内吞作用在调节AIS功能中的作用的新证据，以及内吞作用如何在AIS中发生的结构见解。

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Zebrafish as a model to understand extraocular motor neuron diversity 斑马鱼作为了解眼外运动神经元多样性的模型。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2024.102964

Celine Bellegarda, Franziska Auer, David Schoppik

Motor neurons have highly diverse anatomical, functional and molecular features, and differ significantly in their susceptibility in disease. Extraocular motor neurons, residing in the oculomotor, trochlear and abducens cranial nuclei (nIII, nIV and nVI), control eye movements. Recent work has begun to clarify the developmental mechanisms by which functional diversity among extraocular motor neurons arises. However, we know little about the role and consequences of extraocular motor neuron diversity in eye movement control. Here, we highlight recent work investigating the anatomical, functional and molecular features of extraocular motor neurons. Further, we frame hypotheses where studying ocular motor circuits in the larval zebrafish is poised to illuminate the consequences of motor neuron diversity for behavior.

运动神经元具有高度多样化的解剖、功能和分子特征，在疾病的易感性上存在显著差异。眼外运动神经元位于动眼核、滑车核和外展颅核（nIII、nIV和nVI）中，控制眼球运动。最近的工作已经开始阐明眼外运动神经元功能多样性产生的发育机制。然而，我们对眼外运动神经元多样性在眼动控制中的作用和后果知之甚少。在这里，我们重点介绍了最近研究眼外运动神经元的解剖、功能和分子特征的工作。此外，我们提出假设，研究幼体斑马鱼的眼运动回路将阐明运动神经元多样性对行为的影响。

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Neural pathways of nausea and roles in energy balance 恶心的神经通路及其在能量平衡中的作用。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2024.102963

Chuchu Zhang

Our internal sensory systems encode various gut-related sensations, such as hunger, feelings of fullness, and nausea. These internal feelings influence our eating behaviors and play a vital role in regulating energy balance. Among them, the neurological basis for nausea has been the least well characterized, which has hindered comprehension of the connection between these sensations. Single-cell sequencing, along with functional mapping, has brought clarity to the neural pathways of nausea involving the brainstem area postrema. In addition, the newly discovered nausea sensory signals have deepened our understanding of the area postrema in regulating feeding behaviors. Nausea has significant clinical implications, especially in developing drugs for weight loss and metabolism. This review summarizes recent research on the neural pathways of nausea, particularly highlighting their contribution to energy balance.

我们的内部感觉系统编码各种与肠道相关的感觉，如饥饿、饱腹感和恶心。这些内在的感觉影响着我们的饮食行为，在调节能量平衡方面起着至关重要的作用。其中，恶心的神经学基础是最不清楚的，这阻碍了对这些感觉之间联系的理解。单细胞测序和功能图谱已经清晰地揭示了涉及脑干后期区域的恶心的神经通路。此外，新发现的恶心感觉信号加深了我们对后期区域调节摄食行为的理解。恶心具有重要的临床意义，特别是在开发减肥和代谢药物方面。本文综述了最近关于恶心的神经通路的研究，特别强调了它们对能量平衡的贡献。

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The multifunctionality of the brainstem breathing control circuit

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2025.102974

Kevin Yackle , Jeehaeh Do

Subconscious breathing is generated by a network of brainstem nodes with varying purposes, like pacing breathing or patterning a certain breath phase. Decades of anatomy, pharmacology, and physiology studies have identified and characterized the system’s fundamental properties that produce robust breathing, and we now have well-conceived computational models of breathing that are based on the detailed descriptions of neuronal connectivity, biophysical properties, and functions in breathing. In total, we have a considerable understanding of the brainstem breathing control circuit. But, in the last five years, the utilization of molecular and genetic approaches to study the neural subtypes within each node has led to a new era of breathing control circuit research that explains how breathing is integrated with more complex behaviors like speaking and running and how breathing is connected with other physiological systems and our state-of-mind. This review will describe the basic role of the key components of the brainstem breathing control circuit and then will highlight the new transformative discoveries that broaden our understanding of these breathing control brain areas. These new studies serve to illustrate the creativity and exciting future of breathing control research.

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CAMK2; four genes, one syndrome? Delineation of genotype–phenotype correlations CAMK2;四种基因，一种综合症？描述基因型-表型相关性。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2024.102935

Joshua S. Cheung , Geeske M. van Woerden , Danielle C.M. Veenma

Neurodevelopmental disorders are a heterogenous group of brain disorders impacting cognitive, adaptive, motor, and speech language development. With advancements in diagnostics an increasing number of causative genes are discovered, including synaptic genes. The calcium calmodulin dependent protein kinase type 2 (CAMK2) family is the most abundant kinase family in the synapse and has recently been established to cause NDD, with a growing number of unrelated NDD-individuals who carry pathogenic variations in one of the four CAMK2 genes. However, there is still much to learn about the specific phenotypic manifestations per CAMK2 paralog and per variant type, including the mechanism of how variants in these genes impact CAMK2 protein and synaptic functioning, and result in neurodevelopmental disorders. This review provides an overview of all CAMK2 cases published to date and reveals first genotype–phenotype correlations that can serve as a starting point to explain CAMK2 related symptoms, offering direction for future research.

神经发育障碍是一组影响认知、适应性、运动和言语语言发展的异质脑障碍。随着诊断技术的进步，越来越多的致病基因被发现，包括突触基因。钙钙调素依赖性蛋白激酶2型（CAMK2）家族是突触中最丰富的激酶家族，最近已被确定可引起NDD，越来越多不相关的NDD个体携带四个CAMK2基因之一的致病性变异。然而，关于每个CAMK2平行体和每个变异类型的具体表型表现，包括这些基因的变异如何影响CAMK2蛋白和突触功能，并导致神经发育障碍的机制，还有很多需要了解的。这篇综述概述了迄今为止发表的所有CAMK2病例，并揭示了基因型-表型相关性，可以作为解释CAMK2相关症状的起点，为未来的研究提供方向。

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Calcium signaling at the interface between astrocytes and brain inflammation 星形胶质细胞与脑炎症界面的钙信号。

IF 4.8 2区医学 Q1 NEUROSCIENCES

Current Opinion in Neurobiology

Pub Date : 2025-02-01 DOI: 10.1016/j.conb.2024.102940

Michaela M. Novakovic, Murali Prakriya

Astrocytes are the most prevalent glial cells of the brain and mediate vital roles in the development and function of the nervous system. Astrocytes, along with microglia, also play key roles in initiating inflammatory immune responses following brain injury, stress, or disease-related triggers. While these glial immune responses help contain and resolve cellular damage to the brain, dysregulation of astrocyte activity can in some cases amplify inflammation and worsen impact on neural tissue. As nonexcitable cells, astrocytes excitability is regulated primarily by Ca²⁺ signals that control key functions such as gene expression, release of inflammatory mediators, and cell metabolism. In this review, we examine the molecular and functional architecture of Ca²⁺ signaling networks in astrocytes and their impact on astrocyte effector functions involved in inflammation and immunity.

星形胶质细胞是大脑中最常见的胶质细胞，在神经系统的发育和功能中起着至关重要的作用。星形胶质细胞和小胶质细胞在脑损伤、压力或疾病相关触发因素引发的炎症免疫反应中也起着关键作用。虽然这些神经胶质免疫反应有助于抑制和解决大脑细胞损伤，但星形胶质细胞活动失调在某些情况下会放大炎症，加重对神经组织的影响。作为不可兴奋的细胞，星形胶质细胞的兴奋性主要由Ca2+信号调节，Ca2+信号控制关键功能，如基因表达、炎症介质的释放和细胞代谢。在这篇综述中，我们研究了星形胶质细胞中Ca2+信号网络的分子和功能结构及其对星形胶质细胞效应功能的影响，包括炎症和免疫。

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