Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition.
Dynamics of Circadian Thalamocortical Flow of Information during a Peripheral Neuropathic Pain Condition.
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DOI：
10.3389/fnint.2011.00043
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发表时间：
2011
影响因子：
3.5
通讯作者：
Galhardo V
中科院分区：
文献类型：
--
作者：
Cardoso-Cruz H;Sameshima K;Lima D;Galhardo V
据了解，丘脑皮层回路在编码疼痛刺激的感觉辨别特征中起着至关重要的作用。然而，只有少数研究已经解决了丘脑皮质动力学的变化，可能会发生慢性疼痛发作后。我们的目标是评估慢性神经性疼痛的诱导如何影响丘脑皮质环路内的信息流，贯穿睡眠-觉醒周期的大脑状态。为了解决这个问题，我们记录了局部场电位（LFPs）-在清醒的自由移动的成年大鼠长期植入多电极阵列在外侧丘脑和初级体感皮层神经病理性疼痛的建立之前和之后。我们的研究结果表明，神经病理性损伤引起的觉醒和慢波睡眠（SWS）状态发作的数量的变化，特别是在大脑状态之间的转换总数。此外，部分定向相干分析显示，在神经病动物中，皮层和丘脑之间的信息流量显著减少，表明总体丘脑活动比皮层活动具有更小的权重。然而，丘脑皮质LFPs显示较高的相位锁定在清醒和SWS发作后的神经损伤，这表明更快的传输相关信息沿着丘脑皮质环路。所观察到的变化与慢性疼痛发作后丘脑功能障碍的假设一致，并且可能是由于初级躯体感觉皮层对外侧丘脑的抑制作用减弱。
It is known that the thalamocortical loop plays a crucial role in the encoding of sensory–discriminative features of painful stimuli. However, only a few studies have addressed the changes in thalamocortical dynamics that may occur after the onset of chronic pain. Our goal was to evaluate how the induction of chronic neuropathic pain affected the flow of information within the thalamocortical loop throughout the brain states of the sleep–wake cycle. To address this issue we recorded local field potentials (LFPs) – both before and after the establishment of neuropathic pain in awake freely moving adult rats chronically implanted with arrays of multielectrodes in the lateral thalamus and primary somatosensory cortex. Our results show that the neuropathic injury induced changes in the number of wake and slow-wave-sleep (SWS) state episodes, and especially in the total number of transitions between brain states. Moreover, partial directed coherence – analysis revealed that the amount of information flow between cortex and thalamus in neuropathic animals decreased significantly, indicating that the overall thalamic activity had less weight over the cortical activity. However, thalamocortical LFPs displayed higher phase-locking during awake and SWS episodes after the nerve lesion, suggesting faster transmission of relevant information along the thalamocortical loop. The observed changes are in agreement with the hypothesis of thalamic dysfunction after the onset of chronic pain, and may result from diminished inhibitory effect of the primary somatosensory cortex over the lateral thalamus.