Neural correlate of resting-state functional connectivity under α2 adrenergic receptor agonist, medetomidine
Neural correlate of resting-state functional connectivity under α2 adrenergic receptor agonist, medetomidine
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DOI：
10.1016/j.neuroimage.2013.08.004
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发表时间：
2014-01-01
期刊：
影响因子：
5.7
通讯作者：
Chuang, Kai-Hsiang
中科院分区：
文献类型：
--
作者：
Nasrallah, Fatima A.;Lew, Si Kang;Chuang, Kai-Hsiang
静息状态下大脑中功能性MRI（fMRI）信号的相关波动已被视为功能连接性的衡量标准，但这种静息状态MRI（rsMRI）信号的神经基础尚不清楚。先前，我们发现α 2肾上腺素能激动剂美托咪定剂量依赖性地抑制rsMRI相关性，但不抑制刺激诱发的激活。为了了解潜在的电生理学和神经血管耦合，这可能是由于美托咪定的血管收缩性质，体感诱发电位（SEP）和静息脑电图（EEG）的改变进行了测量，并与相应的BOLD信号在大鼠大脑中的三个剂量的美托咪定。无论美托咪定剂量如何，电刺激两个前爪引起的SEP均无变化，这与BOLD激活一致。不同剂量的美托咪定对SEP和BOLD信号的相关性一致，表明神经血管耦合不受影响。在静息状态下，EEG功率相同，但在较高的美托咪定剂量下观察到γ频带中半球间EEG相干性的抑制。与美托咪定不同的是，随着异氟醚浓度的增加，静息脑电功率和BOLD功率及相干性均受到显著抑制。这种减少可能是由于神经活动受到抑制，如异氟烷下SEP和BOLD激活减少所示，表明静息状态下失去同步性的不同机制。尽管如此，电生理学和刺激和静息状态下BOLD之间的相似性表明美托咪定和异氟烷中存在紧密的神经血管耦合。我们的研究结果证实，美托咪定不抑制神经活动，但在躯体感觉皮层的连接分离。美托咪定及其受体特异性作用的差异效应支持功能连接的神经元起源，并暗示其镇静作用的机制。(C)2013 Elsevier Inc. All rights reserved.
Correlative fluctuations in functional MRI (fMRI) signals across the brain at rest have been taken as a measure of functional connectivity, but the neural basis of this resting-state MRI (rsMRI) signal is not clear. Previously, we found that the alpha 2 adrenergic agonist, medetomidine, suppressed the rsMRI correlation dose-dependently but not the stimulus evoked activation. To understand the underlying electrophysiology and neurovascular coupling, which might be altered due to the vasoconstrictive nature of medetomidine, somatosensory evoked potential (SEP) and resting electroencephalography (EEG) were measured and correlated with corresponding BOLD signals in rat brains under three dosages of medetomidine. The SEP elicited by electrical stimulation to both forepaws was unchanged regardless of medetomidine dosage, which was consistent with the BOLD activation. Identical relationship between the SEP and BOLD signal under different medetomidine dosages indicates that the neurovascular coupling was not affected. Under resting state, EEG power was the same but a depression of inter-hemispheric EEG coherence in the gamma band was observed at higher medetomidine dosage. Different from medetomidine, both resting EEG power and BOLD power and coherence were significantly suppressed with increased isoflurane level. Such reduction was likely due to suppressed neural activity as shown by diminished SEP and BOLD activation under isoflurane, suggesting different mechanisms of losing synchrony at resting-state. Even though, similarity between electrophysiology and BOLD under stimulation and resting-state implicates a tight neurovascular coupling in both medetomidine and isoflurane. Our results confirm that medetomidine does not suppress neural activity but dissociates connectivity in the somatosensory cortex. The differential effect of medetomidine and its receptor specific action supports the neuronal origin of functional connectivity and implicates the mechanism of its sedative effect. (C) 2013 Elsevier Inc. All rights reserved.