Increased synaptic GluR1 subunits in the anterior cingulate cortex of rats with peripheral inflammation
Increased synaptic GluR1 subunits in the anterior cingulate cortex of rats with peripheral inflammation
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DOI：
10.1016/j.ejphar.2010.11.027
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发表时间：
2011-02-25
影响因子：
5
通讯作者：
Naguib, Mohamed
中科院分区：
文献类型：
--
作者：
Bie, Bihua;Brown, David L.;Naguib, Mohamed
适应的AMPA受体亚单位的运输，包括AMPA能传输，作为一个重要的机制，长期的神经元可塑性在几个病理生理条件下，包括疼痛。同时，前扣带皮层（anterior cingulate cortex，ACC）也参与了伤害性刺激的中枢处理和调制，但在慢性疼痛中的神经适应性研究还不十分清楚。为了解决这些问题，本工作进行了探索ACC神经元的AMPA受体亚单位的适应在左后爪的完全弗氏佐剂（CFA）诱导的炎症大鼠。结果表明，ACC神经元AMPA受体介导的兴奋性突触后电流增加，表明基础兴奋性突触传递增强。此外，在ACC神经元中观察到突触GluR1亚基的分布增加。我们的结论是，慢性外周炎症显着增强突触插入的GluR1亚基在ACC神经元，从而增加了慢性疼痛过程中的中枢兴奋性传递。这项调查可能会澄清，至少部分地，潜在的脊髓上的机制，适应性神经递质传输在慢性疼痛引起的外周炎症。(C)2010 Elsevier B.V.保留所有权利。
Adaptation of glutamatergic transmission, including the trafficking of AMPA receptor subunits, serves as an important mechanism underlying long-term neuronal plasticity under several pathophysiological conditions, including pain. Meanwhile, the anterior cingulate cortex (ACC) is found to be critically involved in the central processing and modulation of noxious stimulus, although the neuroadaptation in the ACC has not yet been well established in the setting of chronic pain. To address these issues, the present work was undertaken to explore the adaptation of glutamatergic AMPA receptor subunits in ACC neurons in rats with inflammation in the left hindpaw induced with Complete Freund's Adjuvant (CFA). The results showed an increased AMPA receptor-mediated glutamatergic evoked EPSC in the ACC neurons, indicating an enhanced basal glutamatergic transmission. Furthermore, an increased distribution of the synaptic GluR1 subunit was observed in the ACC neurons. We conclude that chronic peripheral inflammation significantly enhances the synaptic insertion of GluR1 subunits in the ACC neurons, which consequently increases the central excitatory transmission during chronic pain. This investigation may clarify, at least partially, the underlying supraspinal mechanism for adaptation of glutamatergic transmission during chronic pain induced by peripheral inflammation. (C) 2010 Elsevier B.V. All rights reserved.