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MeCP2 缺陷型小鼠大脑皮质和海马区脑电图活动的改变。

Alterations of cortical and hippocampal EEG activity in MeCP2-deficient mice.

机构信息

Division of Genetics and Development, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada M5T 2S8.

出版信息

Neurobiol Dis. 2010 Apr;38(1):8-16. doi: 10.1016/j.nbd.2009.12.018. Epub 2010 Jan 4.

Abstract

Rett syndrome is a pediatric neurological condition caused by mutations of the gene encoding the transcriptional regulator MECP2. In this study, we examined cortical and hippocampal electroencephalographic (EEG) activity in male and female MeCP2-deficient mice at symptomatic stages during different behavioral states. During acute sleep, MeCP2-deficient mice displayed normal delta-like activity in cortex and sharp-wave activity in hippocampus. However, when the mice were awake but immobile, abnormal spontaneous, rhythmic EEG discharges of 6-9 Hz were readily detected in the somatosensory cortex. During exploratory activity, MeCP2-deficient mice displayed clear theta rhythm activity in hippocampus, but its peak frequency was significantly attenuated compared to wild type. Collectively, these findings indicate that a deficiency in MeCP2 function in mice leads to alterations in EEG activity with similarities to what has been observed clinically in Rett syndrome patients.

摘要

雷特综合征是一种儿科神经疾病,由编码转录调节剂 MECP2 的基因突变引起。在这项研究中,我们在不同行为状态下的症状期检查了雄性和雌性 MeCP2 缺陷型小鼠的大脑皮质和海马区脑电图(EEG)活动。在急性睡眠期间,MeCP2 缺陷型小鼠的大脑皮质表现出正常的类似 delta 的活动,海马区表现出尖波活动。然而,当小鼠处于清醒但不动的状态时,在躯体感觉皮质中很容易检测到异常的自发、有节奏的 6-9 Hz 的 EEG 放电。在探索性活动期间,MeCP2 缺陷型小鼠的海马区表现出明显的 theta 节律活动,但与野生型相比,其峰值频率明显减弱。总的来说,这些发现表明,小鼠中 MeCP2 功能的缺失导致 EEG 活动发生改变,与雷特综合征患者临床观察到的情况相似。

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