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本文引用的文献

1
Inhibition of the potassium channel K3.1 by senicapoc reverses tactile allodynia in rats with peripheral nerve injury.塞尼卡波对钾通道K3.1的抑制作用可逆转周围神经损伤大鼠的触觉异常性疼痛。
Eur J Pharmacol. 2017 Jan 15;795:1-7. doi: 10.1016/j.ejphar.2016.11.031. Epub 2016 Nov 19.
2
Differential Kv1.3, KCa3.1, and Kir2.1 expression in "classically" and "alternatively" activated microglia.“经典”激活和“替代”激活的小胶质细胞中Kv1.3、KCa3.1和Kir2.1的差异表达
Glia. 2017 Jan;65(1):106-121. doi: 10.1002/glia.23078. Epub 2016 Oct 3.
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Efficient derivation of microglia-like cells from human pluripotent stem cells.从人类多能干细胞高效衍生小胶质细胞样细胞。
Nat Med. 2016 Nov;22(11):1358-1367. doi: 10.1038/nm.4189. Epub 2016 Sep 26.
4
How neuroinflammation contributes to neurodegeneration.神经炎症如何导致神经退行性变。
Science. 2016 Aug 19;353(6301):777-83. doi: 10.1126/science.aag2590.
5
Myeloid cells - targets of medication in multiple sclerosis.髓样细胞——多发性硬化症治疗药物的靶点。
Nat Rev Neurol. 2016 Sep;12(9):539-51. doi: 10.1038/nrneurol.2016.110. Epub 2016 Aug 12.
6
Quantification of the functional expression of the Ca -activated K channel K 3.1 on microglia from adult human neocortical tissue.成人人类新皮质组织小胶质细胞上钙激活钾通道K 3.1功能表达的定量分析。
Glia. 2016 Dec;64(12):2065-2078. doi: 10.1002/glia.23040. Epub 2016 Jul 29.
7
Purinergic signaling in epilepsy.癫痫中的嘌呤能信号传导
J Neurosci Res. 2016 Sep;94(9):781-93. doi: 10.1002/jnr.23770. Epub 2016 Jun 14.
8
KCa 3.1-a microglial target ready for drug repurposing?KCa 3.1——一个可供药物重新利用的小胶质细胞靶点?
Glia. 2016 Oct;64(10):1733-41. doi: 10.1002/glia.22992. Epub 2016 Apr 28.
9
The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke.钾通道KCa3.1构成了与缺血/再灌注性中风相关的神经炎症的药理学靶点。
J Cereb Blood Flow Metab. 2016 Dec;36(12):2146-2161. doi: 10.1177/0271678X15611434. Epub 2015 Nov 2.
10
Microglia in Alzheimer's disease: the good, the bad and the ugly.阿尔茨海默病中的小胶质细胞:有益、有害与丑陋面
Curr Alzheimer Res. 2016;13(4):370-80. doi: 10.2174/1567205013666151116125012.

小胶质细胞中钾通道的表达和功能:可塑性及可能的物种差异。

Potassium channel expression and function in microglia: Plasticity and possible species variations.

机构信息

a Department of Pharmacology , University of California , Davis, Davis , CA , USA.

b Saniona A/S , Ballerup , Denmark.

出版信息

Channels (Austin). 2017 Jul 4;11(4):305-315. doi: 10.1080/19336950.2017.1300738. Epub 2017 Mar 1.

DOI:10.1080/19336950.2017.1300738
PMID:28277939
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5555259/
Abstract

Potassium channels play important roles in microglia functions and thus constitute potential targets for the treatment of neurodegenerative diseases like Alzheimer, Parkinson and stroke. However, uncertainty still prevails as to which potassium channels are expressed and at what levels in different species, how the expression pattern changes upon activation with M1 or M2 polarizing stimuli compared with more complex exposure paradigms, and - most importantly - how these findings relate to the in vivo situation. In this mini-review we discuss the functional potassium channel expression pattern in cultured neonatal mouse microglia in the light of data obtained previously from animal disease models and immunohistochemical studies and compare it with a recent study of adult human microglia isolated from epilepsy patients. Overall, microglial potassium channel expression is very plastic and possibly shows species differences and therefore should be studied carefully in each disease setting and respective animal models.

摘要

钾通道在小胶质细胞功能中发挥重要作用,因此成为治疗阿尔茨海默病、帕金森病和中风等神经退行性疾病的潜在靶点。然而,目前仍不确定在不同物种中表达哪些钾通道以及表达水平如何,在与更复杂的暴露范式相比,用 M1 或 M2 极化刺激激活时表达模式如何变化,以及 - 最重要的是 - 这些发现与体内情况有何关系。在这篇迷你综述中,我们根据先前从动物疾病模型和免疫组织化学研究中获得的数据,讨论了培养的新生小鼠小胶质细胞中的功能性钾通道表达模式,并将其与最近一项从癫痫患者中分离出的成人人类小胶质细胞的研究进行了比较。总体而言,小胶质细胞钾通道表达非常具有可塑性,并且可能表现出物种差异,因此应在每种疾病环境和相应的动物模型中仔细研究。