Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bengaluru, India.
Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bengaluru, India.
Neuroscience. 2022 Jul 15;495:97-114. doi: 10.1016/j.neuroscience.2022.05.024. Epub 2022 May 25.
Sleep dysfunctions in epilepsy increase the burden of seizures and cognitive impairments. Seizures and certain anti-seizure drugs (ASDs) can affect sleep quality, leading to excessive daytime sleepiness and poor cognitive performance. Therefore, it is imperative to develop non-pharmacological strategies to curb epilepsy and related sleep dysfunction. Enriched environment (EE) has been demonstrated to ameliorate seizures and associated comorbidity in animal models of epilepsy. However, its effects on epilepsy-induced sleep dysfunctions and altered neural activity remain unexplored. To study the same, chronic epilepsy was induced in male Wistar rats and subjected to standard or enriched housing (6 h/day for 14 days), after which sleep/wake cycle, EEG spectral power and coherence during all vigilance states were analysed. Further, hippocampal parvalbumin-positive (PV) interneurons were quantified to correlate the functional implications with the electrophysiological changes. Epileptic rats showed decreased rapid eye movement (REM) sleep, prolonged REM latency, and extended wake after sleep onset (WASO). Power spectrum analysis indicated an increase in delta and theta activity with a concomitant decrease in gamma activity during wake, an increase in prefrontal cortex (PFC)- Cornu ammonis (CA1) coherence, and a significant loss of hippocampal PV interneuron density. Exposure to EE restored REM sleep duration and latency without altering WASO in epileptic rats. EE also restored delta power during non-rapid eye movement (NREM) and theta, gamma power during wake, PFC-CA1 coherence, and PV interneurons density. These results further strengthen the role of EE's positive effects on brain plasticity and aid in developing non-pharmacological strategies to mitigate epilepsy-associated comorbidities.
癫痫中的睡眠功能障碍会增加癫痫发作和认知障碍的负担。癫痫发作和某些抗癫痫药物（ASD）会影响睡眠质量，导致白天过度嗜睡和认知表现不佳。因此，开发非药物策略来控制癫痫和相关睡眠功能障碍迫在眉睫。丰富环境（EE）已被证明可改善癫痫动物模型中的癫痫发作和相关合并症。然而，其对癫痫引起的睡眠功能障碍和改变的神经活动的影响仍未得到探索。为了研究这一点，在雄性 Wistar 大鼠中诱导慢性癫痫，并使其接受标准或丰富的环境（每天 6 小时，持续 14 天），然后分析所有警觉状态下的睡眠/觉醒周期、脑电图频谱功率和相干性。此外，还定量了海马区钙结合蛋白阳性（PV）中间神经元，以将功能意义与电生理变化相关联。癫痫大鼠表现出快速眼动（REM）睡眠减少、REM 潜伏期延长和睡眠后觉醒时间延长（WASO）。功率谱分析表明，在觉醒期间，delta 和 theta 活动增加，同时 gamma 活动减少，前额叶皮层（PFC）-Cornu ammonis（CA1）相干性增加，海马区 PV 中间神经元密度显著降低。暴露于 EE 可恢复 REM 睡眠持续时间和潜伏期，而不改变癫痫大鼠的 WASO。EE 还恢复了非快速眼动（NREM）期间的 delta 功率、觉醒时的 theta 和 gamma 功率、PFC-CA1 相干性和 PV 中间神经元密度。这些结果进一步加强了 EE 对大脑可塑性的积极影响，并有助于开发非药物策略来减轻癫痫相关的合并症。
