Memory impairment is the most common cognitive deficit in patients with temporal lobe epilepsy (TLE). This type of epilepsy is currently regarded as a network disease because of its brain-wide alterations in functional connectivity between temporal and extra-temporal regions. In patients with TLE, network dysfunctions can be observed during ictal states, but are also described interictally during rest or sleep. Here, we examined the available literature supporting the hypothesis that hippocampal-cortical coupling during sleep is hijacked in TLE. First, we look at studies showing that the coordination between hippocampal sharp-wave ripples (100-200 Hz), corticothalamic spindles (9-16 Hz), and cortical delta waves (1-4 Hz) during nonrapid eye movement (NREM) sleep is critical for spatial memory consolidation. Then, we reviewed studies showing that animal models of TLE display precise coordination between hippocampal interictal epileptiform discharges (IEDs) and spindle oscillations in the prefrontal cortex. This aberrant oscillatory coupling seems to surpass the physiological ripple-delta-spindle coordination, which could underlie memory consolidation impairments. We also discuss the role of rapid eye movement (REM) sleep for local synaptic plasticity and memory. Sleep episodes of REM provide windows of opportunity for reactivation of expression of immediate early genes (i.e., zif-268 and Arc). Besides, hippocampal theta oscillations during REM sleep seem to be critical for memory consolidation of novel object place recognition task. However, it is still unclear which extend this particular phase of sleep is affected in TLE. In this context, we show some preliminary results from our group, suggesting that hippocampal theta-gamma phase-amplitude coupling is exacerbated during REM in a model of basolateral amygdala fast kindling. In conclusion, there is an increasing body of evidence suggesting that circuits responsible for memory consolidation during sleep seem to be gradually coopted and degraded in TLE.

中文翻译：

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颞叶癫痫睡眠期间海马-皮质振荡耦合的劫持

记忆障碍是颞叶癫痫 (TLE) 患者最常见的认知缺陷。这种类型的癫痫目前被认为是一种网络疾病，因为它的颞区和颞区之间的功能连接发生了全脑的改变。在 TLE 患者中，可以在发作状态期间观察到网络功能障碍，但也可以在休息或睡眠期间进行间歇性描述。在这里，我们检查了支持以下假设的现有文献，即睡眠期间的海马-皮质耦合在 TLE 中被劫持。首先，我们研究表明在非快速眼动 (NREM) 睡眠期间海马尖波涟漪 (100-200 Hz)、皮质丘脑纺锤体 (9-16 Hz) 和皮质 delta 波 (1-4 Hz) 之间的协调是空间记忆巩固的关键。然后，我们回顾了表明 TLE 动物模型显示海马发作间期癫痫样放电 (IED) 和前额叶皮层纺锤波振荡之间精确协调的研究。这种异常的振荡耦合似乎超过了生理涟漪-三角洲-主轴协调，这可能是记忆巩固障碍的基础。我们还讨论了快速眼动 (REM) 睡眠对局部突触可塑性和记忆的作用。REM 的睡眠发作为立即早期基因（即 zif-268 和 Arc）的表达重新激活提供了机会窗口。此外，REM 睡眠期间的海马 theta 振荡似乎对于新物体位置识别任务的记忆巩固至关重要。然而，目前尚不清楚在 TLE 中，这一特定睡眠阶段的哪个延长会受到影响。在这种情况下，我们展示了我们小组的一些初步结果，表明在基底外侧杏仁核快速点燃模型中，在 REM 期间海马 theta-gamma 相位-幅度耦合加剧。总之，越来越多的证据表明负责睡眠期间记忆巩固的回路似乎在 TLE 中逐渐被合并和退化。