| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4345413 | Neuroscience Letters | 2011 | 8 Pages |
Comorbidity in the affective domain seems rather typical for idiopathic epilepsy. Whether seizures are causative for the behavioral abnormalities or whether they are a common genetic cause remains to be established. Although the most proper control groups are not always available, there seems to be some consistency in the behavioral patterns seen in rats with absence epilepsy. Formal behavioral testing has shown that genetic absence models such as WAG/Rij's and GAERS, but also other rat lines endowed with spontaneous occurring spike-wave discharges (APO-SUS and Long-Evans rats), show all signs of depression-like behavior, while some lines show an even more complex affective comorbidity. The availability of a treatment that prevents both the neurodevelopment of the genetically programmed seizure and the comorbid symptomatology may help in answering whether seizures are causative for or epiphenomena of changes in affective behavior. If absence seizures and depressive-like behavior is indeed caused by the same underlying factors, then it is predicted that preventing environmental stress in absence epileptic rats will also prevent the affective disturbances.
► The depressive-like phenotype in rats with absence epilepsy seems well established. ► Pre- and post-weaning manipulations may oppositely affect absences. ► Early and chronic pharmacological interventions alter epileptogenesis in WAG/Rij rats. ► Absence prevention affects depressive-like symptoms in genetic absence epileptic rats.
