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本文引用的文献

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Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury.补体因子 C1q 介导轻度脑损伤后睡眠纺锤波缺失和癫痫棘波。
Science. 2021 Sep 10;373(6560):eabj2685. doi: 10.1126/science.abj2685.
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Acute thalamic damage as a prognostic biomarker for post-traumatic epileptogenesis.急性丘脑损伤作为创伤后癫痫发生的预后生物标志物。
Epilepsia. 2021 Aug;62(8):1852-1864. doi: 10.1111/epi.16986. Epub 2021 Jul 9.
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Gamma rhythms and visual information in mouse V1 specifically modulated by somatostatin neurons in reticular thalamus.丘脑中的生长抑素神经元特异性调制小鼠 V1 中的伽马节律和视觉信息。
Elife. 2021 Apr 12;10:e61437. doi: 10.7554/eLife.61437.
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TLR4 pathway impairs synaptic number and cerebrovascular functions through astrocyte activation following traumatic brain injury.TLR4 通路通过创伤性脑损伤后星形胶质细胞的激活损害突触数量和脑血管功能。
Br J Pharmacol. 2021 Sep;178(17):3395-3413. doi: 10.1111/bph.15488. Epub 2021 Jun 1.
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Reactive astrocyte nomenclature, definitions, and future directions.反应性星形胶质细胞命名、定义和未来方向。
Nat Neurosci. 2021 Mar;24(3):312-325. doi: 10.1038/s41593-020-00783-4. Epub 2021 Feb 15.
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An epilepsy-associated ACTL6B variant captures neuronal hyperexcitability in a human induced pluripotent stem cell model.一种与癫痫相关的ACTL6B变体在人类诱导多能干细胞模型中体现出神经元的过度兴奋性。
J Neurosci Res. 2021 Jan;99(1):110-123. doi: 10.1002/jnr.24747. Epub 2020 Nov 3.
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The subcortical basis of outcome and cognitive impairment in TBI: A longitudinal cohort study.脑外伤结局和认知障碍的皮质下基础:一项纵向队列研究。
Neurology. 2020 Oct 27;95(17):e2398-e2408. doi: 10.1212/WNL.0000000000010825. Epub 2020 Sep 9.
8
Location, Location, Location: Transcriptional Control of Astrocyte Heterogeneity.位置,位置,位置:星形胶质细胞异质性的转录控制。
Trends Immunol. 2020 Sep;41(9):753-755. doi: 10.1016/j.it.2020.07.011. Epub 2020 Aug 12.
9
Glial Activation in the Thalamus Contributes to Vestibulomotor Deficits Following Blast-Induced Neurotrauma.丘脑胶质细胞激活导致爆炸诱导的神经创伤后前庭运动功能障碍。
Front Neurol. 2020 Jul 15;11:618. doi: 10.3389/fneur.2020.00618. eCollection 2020.
10
Synaptic properties of the feedback connections from the thalamic reticular nucleus to the dorsal lateral geniculate nucleus.从丘脑网状核到背外侧膝状体核的反馈连接的突触特性。
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局灶性皮质卒中与创伤性损伤后的丘脑二级神经炎症与皮质丘脑功能连接相吻合。

Secondary thalamic neuroinflammation after focal cortical stroke and traumatic injury mirrors corticothalamic functional connectivity.

机构信息

Gladstone Institute of Neurological Disease, San Francisco, California, USA.

Neuroscience Graduate Program, University of California, San Francisco, California, USA.

出版信息

J Comp Neurol. 2022 May;530(7):998-1019. doi: 10.1002/cne.25259. Epub 2021 Nov 1.

DOI:10.1002/cne.25259
PMID:34633669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8957545/
Abstract

While cortical injuries, such as traumatic brain injury (TBI) and neocortical stroke, acutely disrupt the neocortex, most of their consequent disabilities reflect secondary injuries that develop over time. Thalamic neuroinflammation has been proposed to be a biomarker of cortical injury and of the long-term cognitive and neurological deficits that follow. However, the extent to which thalamic neuroinflammation depends on the type of cortical injury or its location remains unknown. Using two mouse models of focal neocortical injury that do not directly damage subcortical structures-controlled cortical impact and photothrombotic ischemic stroke-we found that chronic neuroinflammation in the thalamic region mirrors the functional connections with the injured cortex, and that sensory corticothalamic regions may be more likely to sustain long-term damage than nonsensory circuits. Currently, heterogeneous clinical outcomes complicate treatment. Understanding how thalamic inflammation depends on the injury site can aid in predicting features of subsequent deficits and lead to more effective, customized therapies.

摘要

虽然皮质损伤,如创伤性脑损伤 (TBI) 和皮质卒中,会急性破坏皮质,但它们随后的大多数残疾都反映了随着时间的推移而发展的继发性损伤。丘脑神经炎症已被提议作为皮质损伤以及随之而来的长期认知和神经功能缺陷的生物标志物。然而,丘脑神经炎症在多大程度上取决于皮质损伤的类型或其位置尚不清楚。使用两种不直接损伤皮质下结构的局灶性皮质损伤小鼠模型——控制性皮质撞击和光血栓性缺血性卒中——我们发现,丘脑区域的慢性神经炎症反映了与损伤皮质的功能连接,并且感觉皮质丘脑区域可能比非感觉回路更有可能持续存在长期损伤。目前,混杂的临床结果使治疗变得复杂。了解丘脑炎症如何取决于损伤部位,可以帮助预测随后的缺陷特征,并导致更有效、定制化的治疗。