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P2X7 receptor blockade prevents ATP excitotoxicity in neurons and reduces brain damage after ischemia.P2X7 受体阻断可防止神经元中的 ATP 兴奋性毒性,并减少缺血后的脑损伤。
Neurobiol Dis. 2012 Mar;45(3):954-61. doi: 10.1016/j.nbd.2011.12.014. Epub 2011 Dec 11.
2
The GPR17 receptor in NG2 expressing cells: focus on in vivo cell maturation and participation in acute trauma and chronic damage.NG2 表达细胞中的 GPR17 受体:聚焦于体内细胞成熟及参与急性创伤和慢性损伤。
Glia. 2011 Dec;59(12):1958-73. doi: 10.1002/glia.21237. Epub 2011 Sep 28.
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Purinergic signalling: from normal behaviour to pathological brain function.嘌呤能信号转导:从正常行为到病理性脑功能。
Prog Neurobiol. 2011 Oct;95(2):229-74. doi: 10.1016/j.pneurobio.2011.08.006. Epub 2011 Sep 1.
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White matter lesions defined by diffusion tensor imaging in older adults.老年人的弥散张量成像定义的白质病变。
Ann Neurol. 2011 Sep;70(3):465-76. doi: 10.1002/ana.22484.
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Reduction in expression of the astrocyte glutamate transporter, GLT1, worsens functional and histological outcomes following traumatic spinal cord injury.星形胶质细胞谷氨酸转运体 GLT1 表达减少会加重创伤性脊髓损伤后的功能和组织学结果。
Glia. 2011 Dec;59(12):1996-2005. doi: 10.1002/glia.21241. Epub 2011 Aug 31.
6
Control of local protein synthesis and initial events in myelination by action potentials.动作电位对局部蛋白质合成和髓鞘形成初始事件的控制。
Science. 2011 Sep 16;333(6049):1647-51. doi: 10.1126/science.1206998. Epub 2011 Aug 4.
7
Axon-glia synapses are highly vulnerable to white matter injury in the developing brain.轴突-胶质突触在发育中的大脑的白质损伤中极易受到影响。
J Neurosci Res. 2012 Jan;90(1):105-21. doi: 10.1002/jnr.22722. Epub 2011 Aug 2.
8
The axo-myelinic synapse.轴突-髓鞘突触。
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Increased expression of cystine/glutamate antiporter in multiple sclerosis.胱氨酸/谷氨酸反向转运体在多发性硬化症中的表达增加。
J Neuroinflammation. 2011 Jun 3;8:63. doi: 10.1186/1742-2094-8-63.
10
Bax and calpain mediate excitotoxic oligodendrocyte death induced by activation of both AMPA and kainate receptors.Bax 和 calpain 介导了 AMPA 和 kainate 受体激活诱导的兴奋毒性少突胶质细胞死亡。
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脑白质在中枢神经系统病理生理学中的作用。

Roles of white matter in central nervous system pathophysiologies.

机构信息

Departamento de Neurociencias and CIBERNED, Universidad del Pas Vasco, Leioa, Spain.

出版信息

ASN Neuro. 2012 Mar 22;4(2):e00079. doi: 10.1042/AN20110060.

DOI:10.1042/AN20110060
PMID:22313331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3310305/
Abstract

The phylogenetic enlargement of cerebral cortex culminating in the human brain imposed greater communication needs that have been met by the massive expansion of WM (white matter). Damage to WM alters brain function, and numerous neurological diseases feature WM involvement. In the current review, we discuss the major features of WM, the contributions of WM compromise to brain pathophysiology, and some of the mechanisms mediating WM injury. We will emphasize the newly appreciated importance of neurotransmitter signalling in WM, particularly glutamate and ATP signalling, to understanding both normal and abnormal brain functions. A deeper understanding of the mechanisms leading to WM damage will generate much-needed insights for developing therapies for acute and chronic diseases with WM involvement.

摘要

大脑皮层的系统发生扩张最终导致了人类大脑的形成,这使得大脑产生了更高的沟通需求,而这一需求是通过大量的 WM(白质)扩张来满足的。WM 的损伤会改变大脑的功能,许多神经退行性疾病都涉及 WM 损伤。在当前的综述中,我们讨论了 WM 的主要特征、WM 损伤对大脑病理生理学的影响,以及介导 WM 损伤的一些机制。我们将强调神经递质信号在 WM 中的新作用,特别是谷氨酸和 ATP 信号,以了解正常和异常的大脑功能。对导致 WM 损伤的机制的深入了解将为开发针对 WM 损伤的急性和慢性疾病的治疗方法提供急需的见解。