预约演示

更新于：2025-05-07

GluN2B

更新于：2025-05-07

基本信息

别名

GluN2B、Glutamate [NMDA] receptor subunit epsilon-2、glutamate ionotropic receptor NMDA type subunit 2B

+ [9]

简介

Component of N-methyl-D-aspartate (NMDA) receptors (NMDARs) that function as heterotetrameric, ligand-gated cation channels with high calcium permeability and voltage-dependent block by Mg(2+) (PubMed:24272827, PubMed:24863970, PubMed:26875626, PubMed:26919761, PubMed:27839871, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). Participates in synaptic plasticity for learning and memory formation by contributing to the long-term depression (LTD) of hippocampus membrane currents (By similarity). Channel activation requires binding of the neurotransmitter L-glutamate to the GluN2 subunit, glycine or D-serine binding to the GluN1 subunit, plus membrane depolarization to eliminate channel inhibition by Mg(2+) (PubMed:24272827, PubMed:24863970, PubMed:26875626, PubMed:26919761, PubMed:27839871, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). NMDARs mediate simultaneously the potasium efflux and the influx of calcium and sodium (By similarity). Each GluN2 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators (PubMed:26875626, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). In concert with DAPK1 at extrasynaptic sites, acts as a central mediator for stroke damage. Its phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity inducing injurious Ca2+ influx through them, resulting in an irreversible neuronal death (By similarity).

关联

磺胺甲噁唑/甘草酸二钾/氨基己酸/牛磺酸

靶点

11β-HSD1 x GluN2B x Plasminogen activators x bacterial DHPS

作用机制

11β-HSD1抑制剂 [+4]

在研机构

OPTUS Pharmaceutical Co., Ltd.

原研机构

OPTUS Pharmaceutical Co., Ltd.

在研适应症

睑缘炎 [+2]

非在研适应症-

最高研发阶段批准上市

首次获批国家/地区

韩国

首次获批日期2024-10-17

Taurine

牛磺酸

靶点

GluN2B

作用机制

GluN2B拮抗剂 [+1]

在研机构-

原研机构-

在研适应症

膳食补充剂

非在研适应症-

最高研发阶段批准上市

首次获批国家/地区-

首次获批日期1800-01-20

Salfaprodil

索法地尔

靶点

GluN2B

作用机制

GluN2B拮抗剂

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段临床3期

首次获批国家/地区-

首次获批日期1800-01-20

104

项与 GluN2B 相关的临床试验

NCT06721949

/ Not yet recruiting临床2/3期IIT

Taurine Supplementation as a Novel Therapeutic Approach for Neurocognitive Symptoms in Long COVID

The COVID-19 pandemic has swept across the globe, affecting millions of individuals with varying degrees of severity. While many individuals recover from the acute phase of the infection, a significant proportion continue to experience persistent and debilitating symptoms long after the initial SARS-CoV-2 infection. This condition, known as Long COVID (LC) or sometimes referred to as Post-COVID Condition (PCC) or post-acute sequelae of COVID-19, has emerged as a complex multisystemic condition and challenging health issue, affecting approximately 10% of COVID-19 patients. Various symptoms characterize LC, including fatigue, sleep disturbances, cognitive impairment, and mood disturbances. Some of the symptoms are shared with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) - a condition marked by debilitating fatigue and a host of other symptoms without precise biomarkers or objective tests for diagnosis. Effective LC treatments remain elusive and LC patients continue to grapple with persistent symptoms that significantly impact their quality of life. Given the lack of effective treatments, it is imperative to explore novel therapeutic approaches that may alleviate the suffering of this patient population.

开始日期2025-06-01

申办/合作机构

University of Alberta

[+2]

CTRI/2025/04/084293

/ Not yet recruiting临床3期

Safety and Efficacy of a fixed dose combination of Taurine, N-Acetyl Cysteine and Coenzyme Q10 (Uralbu TM) on Microalbuminuria in Type II Diabetic Patients: A Randomized Controlled, Double-Blind Trial - NIL

开始日期2025-04-25

申办/合作机构

Mmc Pharmaceuticals Ltd.

[+1]

ACTRN12624001440516

/ Recruiting临床1期

An Open-label, 2 Part, Study to Assess the Pharmacokinetics of a Spray Dried Dispersion Formulation of Radiprodil Under Fasted and Fed Conditions in Healthy Adult Subjects: Part B

开始日期2025-01-16

申办/合作机构

GRIN Therapeutics, Inc.

[+1]

100 项与 GluN2B 相关的临床结果

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100 项与 GluN2B 相关的转化医学

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0 项与 GluN2B 相关的专利（医药）

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5,473

项与 GluN2B 相关的文献（医药）

2025-12-31·Animal Cells and Systems

Loss of neuronal βPix isoforms impairs neuronal morphology in the hippocampus and causes behavioral defects

Article

作者: Park, Dongeun ; Choi, June-Seek ; Lee, Seung Joon ; Shin, Yoon Kyung ; Kwon, Younghee ; Shin, Jung Eun

βPix is a guanine nucleotide exchange factor for the Rac1 and Cdc42 small GTPases, which play important roles in dendritic spine morphogenesis by modulating actin cytoskeleton organization. The formation and plasticity of the dendritic spines are essential for normal brain function. Among the alternatively spliced βPix isoforms, βPix-b and βPix-d are expressed specifically in neurons. Our previous studies using cultured hippocampal neurons identified the roles of βPix-b and βPix-d in spine formation and neurite development, respectively. Here, we analyzed the in vivo role of the neuronal βPix isoforms in brain development and function by using βPix neuronal isoform knockout (βPix-NIKO) mice, in which the expression of the βPix-b and βPix-d isoforms is blocked, while the expression of the ubiquitous βPix-a isoform is maintained. Loss of the neuronal βPix isoforms leads to reduced activity of Rac1 and Cdc42, decreased dendritic complexity and spine density, and increased GluN2B and Ca²⁺/calmodulin-dependent protein kinase IIα expression in the hippocampus. The defects in neurite development, dendritic spine maturation, and synaptic density in cultured βPix-NIKO hippocampal neurons were rescued by the expression of βPix-b or βPix-d. In behavioral studies, βPix-NIKO mice exhibited robust deficits in novel object recognition and decreased anxiety levels. Our findings suggest that neuronal morphogenetic signaling by the neuronal βPix isoforms contributes to normal behaviors.

2025-12-31·OncoImmunology

Glutamate promotes CCL2 expression to recruit tumor-associated macrophages by restraining EZH2-mediated histone methylation in hepatocellular carcinoma

Article

作者: Zhuang, Hao ; Wang, Run-Zheng ; Zhang, Yun-Fei ; Chen, Jing ; Li, Wen-Jiao ; Jia, Miao-Miao ; Xue, Ning ; Sun, Hong-Wei ; Wang, Yong-Kui ; Xu, Qing-Xia ; Wang, Hao

Glutamate is well-known as metabolite for maintaining the energy and redox homeostasis in cancer, moreover it is also the primary excitatory neurotransmitter in the central nervous system. However, whether glutamatergic signaling can regulate hepatocellular carcinoma (HCC) progression and the specific regulatory mechanisms are unknown. In the present study, we found that glutamate and its receptor NMDAR2B were significantly elevated in HCC patients, which predicts poor prognosis. Glutamate could upregulate CCL2 expression on hepatoma cells and further enhance the capability of tumor cells to recruit tumor-associated macrophages (TAMs). Mechanistically, glutamate could facilitate CCL2 expression through NMDAR pathway by decreasing the expression of EZH2, which regulates the H3K27me3 levels on the CCL2 promoter, rather than affecting DNA methylation. Moreover, inhibiting glutamate pathway with MK801 could significantly delay tumor growth, with reduced TAMs in implanted Hepa1-6 mouse HCC models. Our work suggested that glutamate could induce CCL2 expression to promote TAM infiltration by negatively regulating EZH2 levels in hepatoma cells, which might serve as a potential prognostic marker and a therapeutic target for HCC patients.

2025-12-01·Cognitive Neurodynamics

Alterations of synaptic plasticity and brain oscillation are associated with autophagy induced synaptic pruning during adolescence

Article

作者: Wang, Hui ; Yang, Zhuo ; Xu, Xiaxia ; Zhang, Tao

Adolescent brain development is characterized by significant anatomical and physiological alterations, but little is known whether and how these alterations impact the neural network. Here we investigated the development of functional networks by measuring synaptic plasticity and neural synchrony of local filed potentials (LFPs), and further explored the underlying mechanisms. LFPs in the hippocampus were recorded in young (21 ~ 25 days), adolescent (1.5 months) and adult (3 months) rats. Long term potentiation (LTP) and neural synchrony were analyzed. The results showed that the LTP was the lowest in adolescent rats. During development, the theta coupling strength was increased progressively but there was no significant change of gamma coupling between young rats and adolescent rats. The density of dendrite spines was decreased progressively during development. The lowest levels of NR2A, NR2B and PSD95 were detected in adolescent rats. Importantly, it was found that the expression levels of autophagy markers were the highest during adolescent compared to that in other developmental stages. Moreover, there were more co-localization of autophagosome and PSD95 in adolescent rats. It suggests that autophagy is possibly involved in synaptic elimination during adolescence, and further impacts synaptic plasticity and neural synchrony.

项与 GluN2B 相关的新闻（医药）

2025-03-17

·PRNewswire

GRIN Therapeutics Receives FDA Orphan Drug Designation for Radiprodil for the Treatment of GRIN-Related Neurodevelopmental Disorder

Announcement follows FDA's February 2025 decision to grant radiprodil Breakthrough Therapy designation Company remains on track to initiate Phase 3 pivotal trial of radiprodil in mid-2025 NEW YORK, March 17, 2025 /PRNewswire/ -- GRIN Therapeutics, Inc., a leader in the development of therapies to treat serious neurodevelopmental disorders, today announced that the U.S. Food and Drug Administration (FDA) granted Orphan Drug designation for its investigational drug, radiprodil, for the treatment of GRIN-related neurodevelopmental disorder (NDD). Radiprodil is designed as a potent negative allosteric modulator selectively targeting the N-methyl-D-aspartate receptor subtype 2B (NR2B or GluN2B). The company is on track to initiate a pivotal Phase 3 trial for radiprodil in mid-2025 for the treatment of GRIN-related NDD with GoF mutations and has an ongoing global open-label clinical trial of radiprodil for the treatment of tuberous sclerosis complex (TSC) and focal cortical dysplasia (FCD) type II. "We are making rapid progress in our efforts to bring a first-ever treatment for GRIN-related neurodevelopmental disorder to patients. Supported by our promising clinical data, the FDA's decision to grant Orphan Drug designation to radiprodil is the latest milestone in that effort," said Michael A. Panzara, MD, MPH, Chief Medical Officer at Neurvati Neurosciences and GRIN Therapeutics. "As we plan to launch our pivotal Phase 3 clinical trial to evaluate the impact of radiprodil on seizures, behavioral abnormalities and functional outcomes associated with GRIN-related NDD in the coming months, we are very grateful to the patients and their families who continue to support this important research effort." Orphan Drug designation is designed to support innovation and research that can lead to more new treatments for diseases that affect fewer than 200,000 people in the United States. The designation grants drug developers the potential for seven years of market exclusivity for their drug after approval, during which time the FDA will generally not approve an application for the same drug targeting the same disease or condition. In February 2025, the FDA granted radiprodil Breakthrough Therapy designation for the treatment of seizures associated with GRIN-related NDD in patients with GoF mutations. "We look forward to continuing to engage with the FDA through the means offered by Breakthrough Therapy designation, as we advance our Phase 3 program with a goal of bringing radiprodil to patients," said Anne-Marie Li-Kwai-Cheung, MChem, MTOPRA, RAPS, Senior Vice President, Development, Regulatory, and Quality at Neurvati Neurosciences and GRIN Therapeutics. "We have heard from so many clinicians and patients about the urgent unmet need in the treatment of GRIN-related disorders and our entire team is dedicated to advancing this development program through late-stage clinical research and regulatory review as rapidly as possible." About GRIN-related neurodevelopmental disorder GRIN-related neurodevelopmental disorder is a family of rare, genetically defined pediatric neurodevelopmental disorders caused by mutations in GRIN genes. While symptoms of GRIN-related neurodevelopmental disorder can present as early as infancy, a diagnosis is often not confirmed until age two or later when a child fails to reach developmental milestones. Individuals may experience developmental delay, intellectual disabilities, epilepsy, muscular hypotonia, movement disorders, spasticity, feeding difficulties and behavioral problems. There are currently no approved therapies for GRIN-related neurodevelopmental disorder. About Radiprodil Radiprodil is an investigational, selective and potent negative allosteric modulator of the N-methyl-D-aspartate (NMDA) receptor subtype 2B (NR2B or GluN2B). In nonclinical studies, radiprodil has been shown to potently and selectively modulate GluN2B. Radiprodil has also demonstrated an antiseizure effect in a number of in vitro and in vivo preclinical seizure and epilepsy models and specifically in models characterized by an enhanced GluN2B NMDA transmission, which can occur with gain-of-function (GoF) mutations in GRIN-related neurodevelopmental disorder. In vitro analysis of brain tissues extracted from both tuberous sclerosis complex (TSC) and focal cortical dysplasia (FCD) lesions has shown enhanced GluN2B NMDA expression supporting the potential ability of radiprodil to control seizures in these conditions. About GRIN Therapeutics GRIN Therapeutics is dedicated to the research and development of precision therapeutics for pediatric neurodevelopmental disorders with the goal of bringing hope to patients and caregivers. Late last year, GRIN Therapeutics reported promising topline data from a Phase 1b/2a clinical trial (the Honeycomb Trial) evaluating radiprodil in GRIN-related neurodevelopmental disorder in patients with GoF variants, leading to the decision to advance to a Phase 3 trial. The company has an additional ongoing clinical trial to evaluate radiprodil for the potential treatment of tuberous sclerosis complex (TSC) and focal cortical dysplasia (FCD) type II. GRIN Therapeutics is an affiliate of Neurvati Neurosciences, a portfolio company of Blackstone Life Sciences (BXLS). For more information, please visit About Neurvati Neurosciences Neurvati Neurosciences, a portfolio company of Blackstone Life Sciences, identifies and advances the development of high-potential drug candidates across the neuroscience landscape. Neurvati employs a collaborative model that establishes fit-for-purpose affiliate companies, aligning dedicated resources with long-term strategic capital to catalyze innovative treatment options in areas of unmet need. Neurvati's team of experienced operators and drug developers seeks opportunities to challenge current treatment paradigms and make a difference for patients suffering from a wide range of neurological and psychiatric disorders. For more information, please visit About Blackstone Life Sciences Blackstone Life Sciences is an industry-leading private investment platform with capabilities to invest across the life cycle of companies and products within key life science sectors. By combining scale investments and hands-on operational leadership, Blackstone Life Sciences helps bring to market promising new medicines and medical technologies that improve patients' lives and currently has more than $12 billion in assets under management. Corporate Contact Elliott Ruiz +1 201.674.5417 [email protected] SOURCE GRIN Therapeutics Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

临床3期孤儿药突破性疗法

2025-02-26

·药明康德

超70%患者获得缓解！别构小分子调节剂获FDA突破性疗法认定

GRIN Therapeutics今日宣布，美国FDA已授予其在研疗法radiprodil突破性疗法认定，用于治疗携带功能获得性突变的GRIN相关神经发育障碍患者的癫痫。Radiprodil是一款选择性靶向N-甲基-D-天冬氨酸（NMDA）受体亚型2B（GluN2B）的负向别构调节剂。该公司计划于2025年中启动针对GRIN相关神经发育障碍的关键性3期临床试验。这一突破性疗法认定的依据来自在携带GRIN基因功能获得性突变的小儿患者的1b期临床试验Honeycomb的积极数据。数据显示，radiprodil治疗的总体耐受性良好。符合条件的癫痫患者的中位可计数运动性癫痫发作（CMS）频率较基线减少了86%。在试验期间，71%的患者CMS减少超过50%，且7例患者中有6例在为期8周的维持期内至少80％的日子无癫痫发作。最常观察到的不良事件与感染或潜在疾病症状相关，3例患者出现了与感染相关的严重不良事件（SAE），均被评估为与radiprodil无关。 GRIN相关神经发育障碍是一组由GRIN基因突变引起的罕见小儿神经发育障碍。患者可能会出现发育迟缓、智力障碍、癫痫、肌张力低下、运动障碍、痉挛、进食困难和行为问题。目前尚无获批治疗GRIN相关神经发育障碍的疗法。 Radiprodil是一种在研GluN2B的选择性强效负向别构调剂。Radiprodil在多种体内外癫痫模型中均表现出抗癫痫作用，特别是在那些以增强GluN2B信号传导为特征的模型中。对GRIN相关神经发育障碍患者脑组织的分析显示，患者的GluN2B表达水平提高。这些发现支持radiprodil在控制这些疾病中癫痫发作方面的潜力。参考资料： [1] GRIN Therapeutics Receives FDA Breakthrough Therapy Designation for Radiprodil. Retrieved February 25, 2025, from https://www.prnewswire.com/news-releases/grin-therapeutics-receives-fda-breakthrough-therapy-designation-for-radiprodil-302384417.html 内容来源于网络，如有侵权，请联系删除。

突破性疗法临床结果免疫疗法

2025-02-26

·学术经纬

Neuron | 竺淑佳团队揭示镁离子对NMDA受体的多重调控机制

▎药明康德内容团队编辑 N-甲基-ᴅ-天冬氨酸（NMDA）受体是一类存在于突触上的离子型谷氨酸门控通道家族，广泛参与神经发育、突触可塑性、学习记忆、认知及情绪等高级脑功能调控，被视为学习和记忆的关键“分子开关”。作为突触可塑性的关键分子，NMDA受体的功能受镁离子（Mg2+）的电压依赖性阻断与电压非依赖的变构调控，但具体分子机制长期未明。 2025年2月25日，在一篇发表于《神经元》（Neuron）的研究论文中，中国科学院脑科学与智能技术卓越创新中心（神经科学研究所）竺淑佳团队系统揭示了Mg2+在NMDA受体中的多重作用机制，发现存在3个独立的Mg2+结合位点：其中，位点Ⅰ通过配位键与Mg2+结合，负责经典的电压依赖性阻断功能；位点Ⅱ和Ⅲ分别介导Mg2+的变构增强与抑制作用。该工作揭示了Mg2+在NMDA受体中的多重调控机制，诠释了Mg2+阻断和Ca2+通透的差异性分子机制，为理解NMDA受体在兴奋性突触传递中的功能，以及其在突触可塑性中的作用提供了新的视角。 Mg2+是神经系统中一种重要的二价阳离子，广泛参与神经发育、突触可塑性以及体内稳态的维持。Mg2+最为人熟知的功能之一是作为NMDA受体的电压依赖性阻断剂。具体而言，在静息膜电位下，Mg2+会结合NMDA受体并阻断其电流；当膜电位去极化时，这种阻断作用会被解除。这种双信号协同调控机制，使NMDA受体在突触前神经递质释放与突触后去极化同步发生时才被激活，进而触发Ca2+依赖的胞内信号级联反应。这一特性奠定了NMDA受体在学习记忆、长时程增强及神经发育中的核心地位。然而，由于Mg2+离子半径小，冷冻电镜的分辨率不足以清晰捕捉其结合位点。Mg2+在NMDA受体中的具体结合位点及其调控机制，以及Mg2+阻断而Ca2+通透的结构基础，一直未得到全面解析。在最新研究中，竺淑佳团队首先利用双电极电压钳技术，记录了在爪蟾卵母细胞上表达的NMDA受体，并记录电流-电压特性曲线。在负电压下，Mg2+对GluN1-N2A和GluN1-N2B两种NMDA受体亚型的阻断作用具有相似的亲和力；然而在正电压下，Mg2+仅对GluN1-N2B受体的外向电流表现出显著性的增强作用。这一结果与90年代中期在培养的神经元和脑片电生理记录中观察到的现象一致，即在去极化膜电位下，Mg2+显著增强了NMDA受体介导的外向电流。 ▲NMDA受体在突触传递中的功能与镁离子作用机制。A) 谷氨酸能突触传递的示意图。B) AMPA和NMDA受体介导的EPSC成分（摘自Hansen et al., 2018）。C) 谷氨酸激活受体的I-V curve（摘自Nowak et al., 1984）。D) 电压依赖性Mg2+对GluN1-N2A和GluN1-N2B亚型的不同作用。（图片来源：研究团队提供）为了进一步明确Mg2+调控GluN1-N2B的结构机制，研究团队纯化了人源的GluN1-N2B受体蛋白，并分别解析了在Mg2+或在二价离子螯合剂EDTA存在下的高分辨率三维结构。通过结构比较、点突变和电生理功能验证，研究团队鉴定出3个不同的Mg2+结合位点。具体而言，位点Ⅰ位于GluN1-N2B受体的选择性过滤器处，在天冬酰胺环的侧链与Mg2+形成配位键，介导了电压依赖性阻断效应。位点Ⅱ和位点Ⅲ位于GluN2B亚基的N端结构域上的不同口袋。其中，位点Ⅱ由三个酸性残基组成，当这些残基同时突变时，GluN2B特异性Mg2+增强作用完全消失；而位点Ⅲ与Zn2+结合口袋重叠，该位点的突变进一步提高了Mg2+的增强作用，证明该位点参与了变构抑制作用。 ▲Mg2+调控NMDA受体门控的分子机制。A）Mg2+结合的人源GluN1-GluN2B受体三维结构。B) Mg2+不同作用位点的功能验证。在负电压下，位点Ⅰ点突变显著减弱Mg2+的电压依赖性阻断效应。在正电压下，位点Ⅱ位点突变消除了GluN2B特异性的Mg2+增强效应；位点Ⅲ位点突变进一步提高Mg2+增强作用。（图片来源：研究团队提供）此外，研究团队通过分子动力学模拟揭示了Mg2+和Ca2+与NMDA受体残基相互作用的差异。在3次独立的模拟中，Mg2+始终与天冬酰胺残基形成稳定的相互作用，而Ca2+由于范德华力半径更大，主要与水分子形成配位键。这种差异导致Ca2+无法像Mg2+一样在天冬酰胺环形成的空间内紧密结合，从而为NMDA受体中对Mg2+阻断和Ca2+通透的选择性差异提供了新的认识。综上所述，研究团队通过整合单颗粒冷冻电镜、电压钳记录和分子动力学模拟等技术，揭示了Mg2+在NMDA受体中的多样化调控机制，阐明了GluN1-N2B受体通道对胞外Mg2+浓度的复杂响应特性。这一研究不仅深化了对Mg2+在NMDA受体中作用的理解，还为揭示其在突触可塑性中的关键调控机制提供了全方位的见解。 ▲Mg2+作用于GluN1-N2B受体的示意图。位点Ⅰ位于TMD区域内选择性滤器的顶端，在静息膜电位下通道被Mg2+阻断。这种阻断在膜去极化时得到解除，从而允许Ca2+流入神经元。位点Ⅱ和位点Ⅲ分别位于GluN2B-NTD的两侧，位点Ⅱ参与GluN2B-NTD驱动的变构增强，而位点Ⅲ参与变构抑制作用。（图片来源：研究团队提供）中国科学院脑智卓越中心和福建医科大学陈万金教授联合培养的博士生黄雪晶、中国科学院脑智卓越中心博士生孙小乐和深势科技王沁蕊为该论文共同第一作者。脑智卓越中心的张继林博士参与课题的初期设计，深势科技的温翰博士参与了分子动力学模拟工作。该工作获得了国家科技创新2030计划、国家自然科学基金、上海分院青攀人才计划和中国科学院青年交叉团队等项目资助。封面图来源：123RF 参考资料： [1] X.J. Huang, X.L. Sun, Q.R. Wang, et al., Structural insights into the diverse actions of magnesium on NMDA receptors. Neuron (2025). DOI: 10.1016/j.neuron.2025.01.021 本文来自药明康德内容微信团队，欢迎转发到朋友圈，谢绝转载到其他平台。如有开设白名单需求，请在“学术经纬”公众号主页回复“转载”获取转载须知。其他合作需求，请联系wuxi_media@wuxiapptec.com。免责声明：药明康德内容团队专注介绍全球生物医药健康研究进展。本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。更多推荐点个“在看”再走吧~

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