Université de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.
Neurobiol Dis. 2012 Dec;48(3):409-17. doi: 10.1016/j.nbd.2012.07.015. Epub 2012 Jul 27.
The pathophysiology of Huntington's disease (HD) is primarily associated with striatal degeneration and a number of behavioral symptoms such as involuntary movements, cognitive decline, psychiatric disorders, and in the most juvenile-onset cases with epilepsy. In addition to several changes in cellular and synaptic properties previously reported in HD, attention was recently driven towards the potential relationships between cognitive deficits and sleep disturbances in patients and animal models of Huntington's disease. In the present study, we have investigated whether the population-activity patterns normally expressed by the hippocampal and neocortical circuits during active and slow-wave states are affected in R6/1 mice, a model of Huntington's disease. By performing electrophysiological recordings from the hippocampus and neocortex of R6/1 mice that were either freely moving, head restrained or anesthetized, we observed an altered segregation of active and slow wave brain states, in relation with an epileptic phenotype. Slow-wave state (SWS) in R6/1 was characterized by the intrusion of active-state features (increased 6-10 Hz theta power and depressed 2-3 Hz delta power) and transient, temporally misplaced ("ectopic") theta oscillations. The epileptic phenotype, in addition to previously reported occasional ictal seizures, was characterized by the systematic presence of interictal activity, confined to SWS. Ectopic theta episodes, which could be reversed by the cholinergic antagonist atropine, concentrated interictal spikes and phase-locked hippocampal sharp-wave-ripples. These results point to major alterations of neuronal activity during rest in R6/1 mice, potentially involving anomalous activation of the cholinergic system, which may contribute to the cognitive deficits observed in Huntington's disease.
亨廷顿病(HD)的病理生理学主要与纹状体变性和许多行为症状相关,如不自主运动、认知能力下降、精神障碍,以及在最年轻发病的病例中与癫痫相关。除了先前在 HD 中报道的几种细胞和突触特性的改变外,最近人们开始关注亨廷顿病患者和动物模型中认知缺陷与睡眠障碍之间的潜在关系。在本研究中,我们研究了在 R6/1 小鼠(亨廷顿病模型)中,海马和新皮层电路在活跃和慢波状态下正常表达的群体活动模式是否受到影响。通过对自由移动、头部固定或麻醉的 R6/1 小鼠的海马体和新皮层进行电生理记录,我们观察到与癫痫表型相关的活跃和慢波脑状态的分离发生改变。R6/1 的慢波状态(SWS)的特征是活跃状态特征(增加 6-10 Hz theta 功率和降低 2-3 Hz delta 功率)的入侵以及暂时的、时间错位的(“异位”)theta 振荡。除了先前报道的偶发性癫痫发作外,癫痫表型的特征还包括系统性存在局限于 SWS 的发作间期活动。异位 theta 发作可被胆碱能拮抗剂阿托品逆转,浓缩发作间期棘波和相位锁定的海马尖波涟漪。这些结果表明 R6/1 小鼠在休息时神经元活动发生重大改变,可能涉及胆碱能系统的异常激活,这可能导致亨廷顿病中观察到的认知缺陷。