Abstract

Wistar Albino Glaxo Rijswijk (WAG/Rij) rats are widely used in basic and pre-clinical studies as a valid genetic model of absence epilepsy. Adult WAG/Rij rats exhibit generalized 8–10-Hz spike-wave discharges (SWDs) in the electroencephalogram. SWDs are known to result from thalamocortical circuit dysfunction, and this implies an intimate relationship between slow-wave EEG activity, sleep spindles, and SWDs. The present mini review summarizes relevant research on sleep-related disturbances associated with spike-wave epilepsy in WAG/Rij rats in the domain of slow-wave sleep EEG and microarousals. It also discusses enhancement of the intermediate stage of sleep. In general, sleep EEG studies provide important information about epileptogenic processes related to spike-wave epilepsy.

Highlights

  • Generalized spike-wave activity is a paroxysmal electroencephalographic (EEG) pattern occurring in various types of seizures, such as absence, myoclonic, atonic, tonic, and tonic–clonic seizures [1]

  • Wistar Albino Glaxo Rijswijk (WAG/Rij) and Genetic Absence Epilepsy rats from Strasburg (GAERS), are considered valid genetic models of absence epilepsy [7]

  • Inasmuch as here I refer to EEG seizure activity in the WAG/Rij rat model, I use the term “spike-wave epilepsy” instead of “absence epilepsy.”

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Summary

Introduction

Generalized spike-wave activity is a paroxysmal electroencephalographic (EEG) pattern occurring in various types of seizures, such as absence, myoclonic, atonic, tonic, and tonic–clonic seizures [1]. In 2011, we detected a relatively late debut age of spike-wave epilepsy in Moscow’s population of WAG/Rij rats (7–8 months) as compared to the original population [11]. Thalamocortical circuitry is known to produce physiological sleep oscillations such as slow-wave delta and spindles and epileptic SWDs [6, 16,17,18,19, 21,22,23,24].

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