The use of rodent models to better characterize the relationship among epilepsy, sleep, and memory

Epilepsy, a neurological disorder characterized by recurrent seizures, is known to be associated with impaired sleep and memory. Although the specific mechanisms underlying these impairments are uncertain, the known role of sleep in memory consolidation suggests a potential relationship may exist between seizure activity, disrupted sleep, and memory impairment. A possible mediator in this relationship is the sleep spindle, the characteristic electroencephalographic (EEG) feature of non-rapid-eye-movement (NREM) sleep in humans and other mammals. Growing evidence supports the idea that sleep spindles, having thalamic origin, may mediate the process of long-term memory storage and plasticity by generating neuronal conditions that favor these processes. To study this potential relationship, a single model in which memory, sleep, and epilepsy can be simultaneously observed is of necessity. Rodent models of epilepsy appear to fulfill this requirement. Not only do rodents express both sleep spindles and seizure-induced sleep disruptions, but they also allow researchers to invasively study neurobiological processes both pre- and post- epileptic onset via the artificial induction of epilepsy (a practice that cannot be carried out in human subjects). However, the degree to which sleep architecture differs between rodents and humans makes direct comparisons between the two challenging. This review addresses these challenges and concludes that rodent sleep studies are useful in observing the functional roles of sleep and how they are affected by epilepsy.

Automated summary

This review explores the potential relationship between epilepsy, sleep, and memory. Sleep spindles may mediate the relationship between seizure activity, disrupted sleep, and memory impairment. Rodent models of epilepsy provide a unique opportunity to observe these factors simultaneously and study neurobiological processes through the induction of epilepsy, which is not possible in human subjects. However, the differences in sleep architecture between rodents and humans present challenges for direct comparisons.