Multielectrode array analysis of EEG biomarkers in a mouse model of Fragile X Syndrome.
Multielectrode array analysis of EEG biomarkers in a mouse model of Fragile X Syndrome.
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DOI：
10.1016/j.nbd.2020.104794
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发表时间：
2020-05
影响因子：
6.1
通讯作者：
Binder, Devin K.
中科院分区：
文献类型：
--
作者：
Jonak, Carrie R.;Lovelace, Jonathan W.;Ethell, Iryna M.;Razak, Khaleel A.;Binder, Devin K.
关键词：
脆性X综合征（FXS）是已知的导致智力残疾的主要遗传原因，其症状包括焦虑加剧、社交和感觉处理缺陷。最近对FXS患者的脑电图研究发现，神经振荡缺陷包括静息状态伽马功率增加，听觉诱发电位幅度增加，声诱发伽马振荡的试验间相一致性降低。在小鼠FXS模型中鉴定可比较的脑电图生物标志物可以促进临床前到临床的治疗管道。然而，虽然人类脑电图研究涉及128通道头皮脑电图采集，但尚未进行超过3个脑电图通道的小鼠研究。在本研究中，我们采用了最近开发的30通道小鼠多电极阵列（MEA）系统来记录和分析WT和Fmr1 KO小鼠的静息和刺激诱发的脑电信号。使用该系统，我们现在报告了强大的mea衍生表型，包括Fmr1 KO小鼠的静息脑电图功率更高，事件相关电位（ERPs）改变以及听觉啁啾刺激的试验间相一致性降低，这些与FXS患者的报告非常相似。我们提出MEA系统可用于：(1)推导更高层次的EEG参数；（ii）用于药物测试的脑电图生物标志物；（ii） FXS病理生理机制研究。
Fragile X Syndrome (FXS) is a leading known genetic cause of intellectual disability with symptoms that include increased anxiety and social and sensory processing deficits. Recent EEG studies in humans with FXS have identified neural oscillation deficits that include increased resting state gamma power, increased amplitude of auditory evoked potentials, and reduced inter-trial phase coherence of sound-evoked gamma oscillations. Identification of comparable EEG biomarkers in mouse models of FXS could facilitate the pre-clinical to clinical therapeutic pipeline. However, while human EEG studies have involved 128-channel scalp EEG acquisition, no mouse studies have been performed with more than three EEG channels. In the current study, we employed a recently developed 30-channel mouse multielectrode array (MEA) system to record and analyze resting and stimulus-evoked EEG signals in WT vs. Fmr1 KO mice. Using this system, we now report robust MEA-derived phenotypes including higher resting EEG power, altered event-related potentials (ERPs) and reduced inter-trial phase coherence to auditory chirp stimuli in Fmr1 KO mice that are remarkably similar to those reported in humans with FXS. We propose that the MEA system can be used for: (i) derivation of higher-level EEG parameters; (ii) EEG biomarkers for drug testing; and (ii) mechanistic studies of FXS pathophysiology.
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