NMDA receptor-independent synaptic plasticity in the central amygdala in the rat model of neuropathic pain
NMDA receptor-independent synaptic plasticity in the central amygdala in the rat model of neuropathic pain
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DOI：
10.1016/j.pain.2006.09.003
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发表时间：
2007-01-01
期刊：
影响因子：
7.4
通讯作者：
Kato, Fusao
中科院分区：
文献类型：
--
作者：
Ikeda, Ryo;Takahashi, Yukari;Kato, Fusao
杏仁核中央核（CeA）后囊部分的神经元，现在被称为“伤害性杏仁核”，主要通过臂旁核（PB）传递的传入通路接收来自背角的伤害性信息。据报道，PB传入神经和这些神经元之间的兴奋性突触传递在关节炎或内脏疼痛发生后的几个小时内就会增强，这可能是一种将慢性疼痛和不愉快的负面情绪体验联系起来的机制。然而，这种突触增强在慢性疼痛（如神经性疼痛，一种严重和常见的重要临床关注的疼痛类型）的长期持续形式中是否得到巩固或适应性消失，仍然是未知的。为了解决这个问题，我们记录了在1周前单侧脊髓神经结扎后，在患有神经性疼痛的年轻大鼠急性脑切片中，PB束刺激引起的CeA神经元突触后电流，并通过触觉异动反应进行评估。神经结扎对侧CeA神经元的突触后电流显著高于同侧CeA组和假手术组和未手术组。两侧突触增强程度与触觉异常性疼痛反应呈正相关。此外，阻断NMDA受体不影响这种增强。我们得出结论，PB-CeA突触的增强在长期神经性疼痛中得到巩固，但这种增强是由不同于关节炎和内脏疼痛的分子机制引起的。(c) 2006国际疼痛研究协会。Elsevier B.V.版权所有。
Neurons in the latero-capsular part of the central nucleus of the amygdala (CeA), a region now called the "nociceptive amygdala", receive predominantly nociceptive information from the dorsal horn through afferent pathways relayed at the nucleus parabrachialis (PB). Excitatory synaptic transmission between the PB afferents and these neurons is reported to become potentiated within a few hours of the establishment of arthritic or visceral pain, making it a possible mechanism linking chronic pain and unpleasant negative emotional experiences. However, it remains unknown whether such synaptic potentiation is consolidated or becomes adaptively extinct in the longer-lasting form of chronic pain, such as neuropathic pain, an as yet serious and frequent type of pain of important clinical concern. To address this issue, we recorded postsynaptic currents in CeA neurons evoked by PB tract stimulation in acute brain slices from young rats with neuropathic pain, as evaluated by tactile allodynic responses, following unilateral spinal nerve ligature made I week earlier. CeA neurons contralateral to the nerve ligation showed significantly larger-amplitude postsynaptic currents than those in the ipsilateral CeA and sham- and non-operated groups. The degree of synaptic potentiation, as compared between two sides, was positively correlated to that of tactile allodynia responses. In addition, blockade of NMDA receptors did not affect this potentiation. We conclude that potentiation of the PB-CeA synapse is consolidated in long-lasting neuropathic pain but that this potentiation results from a molecular mechanism distinct from that in arthritic and visceral pain. (c) 2006 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.