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The brain in chronic CRPS pain: abnormal gray-white matter interactions in emotional and autonomic regions.慢性复杂性区域疼痛综合征(CRPS)疼痛中的大脑:情感和自主神经区域的灰白质异常相互作用。
Neuron. 2008 Nov 26;60(4):570-81. doi: 10.1016/j.neuron.2008.08.022.
2
The left amygdala knows fear: laterality in the amygdala response to fearful eyes.左侧杏仁核感知恐惧:杏仁核对恐惧眼神反应的偏侧化
Soc Cogn Affect Neurosci. 2008 Mar;3(1):47-54. doi: 10.1093/scan/nsn001. Epub 2008 Jan 31.
3
Amygdala-frontal connectivity during emotion regulation.杏仁核-前额叶连接在情绪调节中的作用。
Soc Cogn Affect Neurosci. 2007 Dec;2(4):303-12. doi: 10.1093/scan/nsm029.
4
Chapter 11 Subcortical processing of nociceptive information: basal ganglia and amygdala.第11章 伤害性信息的皮质下处理:基底神经节与杏仁核
Handb Clin Neurol. 2006;81:141-58. doi: 10.1016/S0072-9752(06)80015-1.
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Self-referential processing of negative stimuli within the ventral anterior cingulate gyrus and right amygdala.腹侧前扣带回和右侧杏仁核内负面刺激的自我参照加工。
Brain Cogn. 2009 Feb;69(1):218-25. doi: 10.1016/j.bandc.2008.07.010. Epub 2008 Aug 23.
6
PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior.杏仁核中的蛋白激酶A和细胞外信号调节激酶而非蛋白激酶C,参与疼痛相关的突触可塑性和行为。
Mol Pain. 2008 Jul 16;4:26. doi: 10.1186/1744-8069-4-26.
7
Hemispheric lateralization of a molecular signal for pain modulation in the amygdala.杏仁核中疼痛调节分子信号的半球侧化。
Mol Pain. 2008 Jun 23;4:24. doi: 10.1186/1744-8069-4-24.
8
Differential mechanisms of CRF1 and CRF2 receptor functions in the amygdala in pain-related synaptic facilitation and behavior.促肾上腺皮质激素释放因子1(CRF1)和促肾上腺皮质激素释放因子2(CRF2)受体在杏仁核中与疼痛相关的突触易化及行为中的不同作用机制
J Neurosci. 2008 Apr 9;28(15):3861-76. doi: 10.1523/JNEUROSCI.0227-08.2008.
9
The role of the amygdala in emotional processing: a quantitative meta-analysis of functional neuroimaging studies.杏仁核在情绪加工中的作用:功能神经影像学研究的定量荟萃分析
Neurosci Biobehav Rev. 2008;32(4):811-30. doi: 10.1016/j.neubiorev.2007.12.002. Epub 2008 Jan 17.
10
Pro- and anti-nociceptive effects of corticotropin-releasing factor (CRF) in central amygdala neurons are mediated through different receptors.促肾上腺皮质激素释放因子(CRF)在中央杏仁核神经元中的促伤害感受和抗伤害感受作用是通过不同受体介导的。
J Neurophysiol. 2008 Mar;99(3):1201-12. doi: 10.1152/jn.01148.2007. Epub 2008 Jan 2.

杏仁核神经元对疼痛处理的大脑两半球偏侧化。

Hemispheric lateralization of pain processing by amygdala neurons.

机构信息

Department of Neuroscience and Cell Biology, The University of Texas Medical Branch, Galveston, Texas 77555-1069, USA.

出版信息

J Neurophysiol. 2009 Oct;102(4):2253-64. doi: 10.1152/jn.00166.2009. Epub 2009 Jul 22.

DOI:10.1152/jn.00166.2009
PMID:19625541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2776996/
Abstract

Recent biochemical and behavioral data suggest right-hemispheric lateralization of amygdala functions in pain. Our previous electrophysiological studies showed pain-related neuroplasticity in the latero-capsular division of the central nucleus of the amygdala (CeLC) in the right brain hemisphere. Here we determined differences in the processing of pain-related signals in right versus left CeLC neurons. Individual CeLC neurons were recorded extracellularly before and after induction of an arthritis pain state in anesthetized rats. Brief innocuous and noxious test stimuli were applied to peripheral tissues ipsi- and contralateral to the recording site. A monoarthritis was induced in the ipsi- or contralateral knee by intraarticular injections of kaolin and carrageenan. Under normal conditions, CeLC neurons in the left amygdala had smaller receptive fields than those in the right, but the magnitude of background and evoked activity was not significantly different. After arthritis induction, neurons in the right, but not left, CeLC developed increased background activity and evoked responses, irrespective of the location of the arthritis (ipsi- or contralateral to the recording site). A protein kinase A (PKA) inhibitor decreased the activity of right CeLC neurons after arthritis induction but had no effect in the left amygdala. Forskolin, however, increased the activity of left and right CeLC neurons under normal conditions. The results show for the first time laterality of pain-related electrophysiological activity changes in individual amygdala neurons. Whereas both left and right amygdala neurons receive nociceptive inputs and can become sensitized in principle, a yet unknown mechanism prevents PKA activation and pain-related changes in the left amygdala.

摘要

最近的生化和行为数据表明,杏仁核功能在疼痛中存在右半球偏侧化。我们之前的电生理研究表明,右脑中杏仁核中央核的外侧区(CeLC)存在与疼痛相关的神经可塑性。在这里,我们确定了右 CeLC 神经元与左 CeLC 神经元在处理疼痛相关信号方面的差异。在麻醉大鼠中诱导关节炎疼痛状态之前和之后,通过细胞外记录单个 CeLC 神经元。将短暂的无害和有害测试刺激施加到记录部位同侧和对侧的外周组织。通过向关节内注射高岭土和角叉菜胶在同侧或对侧膝关节中诱导单关节炎。在正常情况下,左杏仁核中的 CeLC 神经元的感受野比右杏仁核中的小,但背景和诱发活动的幅度没有显著差异。关节炎诱导后,右 CeLC 神经元(而不是左 CeLC 神经元)的背景活动和诱发反应增加,无论关节炎的位置(同侧或对侧记录部位)如何。蛋白激酶 A(PKA)抑制剂可降低关节炎诱导后右 CeLC 神经元的活性,但对左杏仁核无影响。然而,福司可林在正常情况下会增加左 CeLC 和右 CeLC 神经元的活性。结果首次表明,个体杏仁核神经元的疼痛相关电生理活动变化存在偏侧化。虽然左和右杏仁核神经元都接收伤害性输入并且在原则上可以致敏,但一个未知的机制阻止了 PKA 的激活和左杏仁核的疼痛相关变化。