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本文引用的文献

1
Acid-sensing ion channels in pain and disease.酸敏离子通道与疼痛和疾病。
Nat Rev Neurosci. 2013 Jul;14(7):461-71. doi: 10.1038/nrn3529.
2
A novel sea anemone peptide that inhibits acid-sensing ion channels.一种抑制酸敏感离子通道的新型海葵肽。
Peptides. 2014 Mar;53:3-12. doi: 10.1016/j.peptides.2013.06.003. Epub 2013 Jun 10.
3
Acid-sensing ion channel-1a is not required for normal hippocampal LTP and spatial memory.酸敏离子通道 1a 对于正常海马体 LTP 和空间记忆并非必需。
J Neurosci. 2013 Jan 30;33(5):1828-32. doi: 10.1523/JNEUROSCI.4132-12.2013.
4
Targeting ASIC1 in primary progressive multiple sclerosis: evidence of neuroprotection with amiloride.靶向原发性进行性多发性硬化症中的 ASIC1:阿米洛利具有神经保护作用的证据。
Brain. 2013 Jan;136(Pt 1):106-15. doi: 10.1093/brain/aws325.
5
Acid-sensing ion channels in pathological conditions.酸性敏感离子通道在病理条件下的作用。
Adv Exp Med Biol. 2013;961:419-31. doi: 10.1007/978-1-4614-4756-6_36.
6
Black mamba venom peptides target acid-sensing ion channels to abolish pain.黑曼巴蛇毒液肽靶向酸敏离子通道以消除疼痛。
Nature. 2012 Oct 25;490(7421):552-5. doi: 10.1038/nature11494. Epub 2012 Oct 3.
7
Asic3 is a neuronal mechanosensor for pressure-induced vasodilation that protects against pressure ulcers.ASIC3 是一种神经元机械压力感受器,可促进压力诱导的血管舒张,从而预防压疮。
Nat Med. 2012 Aug;18(8):1205-7. doi: 10.1038/nm.2844. Epub 2012 Jul 29.
8
N-glycosylation of acid-sensing ion channel 1a regulates its trafficking and acidosis-induced spine remodeling.酸敏感离子通道 1a 的 N-糖基化调节其转运和酸中毒诱导的脊柱重塑。
J Neurosci. 2012 Mar 21;32(12):4080-91. doi: 10.1523/JNEUROSCI.5021-11.2012.
9
Physiological and pathological functions of acid-sensing ion channels in the central nervous system.酸敏感离子通道在中枢神经系统中的生理和病理功能。
Curr Drug Targets. 2012 Feb;13(2):263-71. doi: 10.2174/138945012799201685.
10
Modulation of acid-sensing ion channels: molecular mechanisms and therapeutic potential.酸敏感离子通道的调节:分子机制与治疗潜力
Int J Physiol Pathophysiol Pharmacol. 2011;3(4):288-309. Epub 2011 Nov 18.

酸敏离子通道参与神经毒性。

Acid-sensing ion channels contribute to neurotoxicity.

机构信息

Departments of Basic Medical Science and Anesthesiology, School of Medicine, University of Missouri-Kansas City, 2411 Holmes Street, Room M3-417, Kansas City, MO, 64108-2792, USA,

出版信息

Transl Stroke Res. 2014 Feb;5(1):69-78. doi: 10.1007/s12975-013-0305-y. Epub 2013 Nov 16.

DOI:10.1007/s12975-013-0305-y
PMID:24323724
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5776693/
Abstract

Acidosis that occurs under pathological conditions not only affects intracellular signaling molecules, but also directly activates a unique family of ligand-gated ion channels: acid-sensing ion channels (ASICs). ASICs are widely expressed throughout the central and peripheral nervous systems and play roles in pain sensation, learning and memory, and fear conditioning. Overactivation of ASICs contributes to neurodegenerative diseases such as ischemic brain/spinal cord injury, multiple sclerosis, Parkinson's disease, and Huntington's disease. Thus, targeting ASICs might be a potential therapeutic strategy for these conditions. This mini-review focuses on the electrophysiology and pharmacology of ASICs and roles of ASICs in neuronal toxicity.

摘要

在病理条件下发生的酸中毒不仅会影响细胞内信号分子,还会直接激活一类独特的配体门控离子通道:酸敏感离子通道(ASICs)。ASICs 在中枢和外周神经系统中广泛表达,在痛觉、学习和记忆以及恐惧条件反射中发挥作用。ASICs 的过度激活与神经退行性疾病有关,如缺血性脑/脊髓损伤、多发性硬化症、帕金森病和亨廷顿病。因此,针对 ASICs 可能是这些疾病的一种潜在治疗策略。这篇迷你综述重点介绍了 ASICs 的电生理学和药理学以及 ASICs 在神经元毒性中的作用。