title: Amygdala kindling in the WAG/Rij rat model of absence epilepsy.
abstract: OBJECTIVE
  The kindling model in rats with genetic absence epilepsy is suitable for studying mechanisms involved in the propagation and generalization of seizure activity in the convulsive and nonconvulsive components of epilepsy. In the present study, we compared the amygdala kindling rate and afterdischarge characteristics of the nonepileptic Wistar control rat with a well-validated model of absence epilepsy, the WAG/Rij rat, and demonstrated the effect of amygdala kindling on spike-and-wave discharges (SWDs) in the WAG/Rij group.
  
  
  METHODS
  Electrodes were stereotaxically implanted into the basolateral amygdala of rats for stimulation and recording and into the cortex for recording. After a recovery period, the animals were stimulated at their afterdischarge thresholds. EEG was recorded to analyze SWDs and afterdischarge durations. The seizure severity was evaluated by using Racine's 5-stage scale.
  
  
  RESULTS
  All nonepileptic control and four of seven WAG/Rij animals reached a stage 5 seizure state, whereas three animals failed to reach stage 3, 4, or 5 and stayed at stage 2 after application of 30 stimulations. Interestingly, WAG/Rij rats, resistant to kindling, demonstrated a significantly longer duration of SWDs on the first day of the experiment before kindling stimulation than did the kindled WAG/Rij animals. Additionally, the cumulative total duration and the number of SWDs after the kindling stimulation were statistically increased compared with SWDs before kindling stimulation.
  
  
  CONCLUSIONS
  The results of our study demonstrate that the progress of amygdala kindling is changed in rats with genetic absence epilepsy, perhaps as a consequence of the hundreds of daily SWDs.
authors.affiliation: Department of Pharmacology and Clinical Pharmacology, School of Medicine, Marmara University, Istanbul.
authors.forename: Rezzan Gülhan
authors.initials: RG
authors.lastname: Aker
authors.forename: Hasan Raci
authors.initials: HR
authors.lastname: Yananli
authors.forename: Ayten Azizova
authors.initials: AA
authors.lastname: Gurbanova
authors.forename: Aydan Ergün
authors.initials: AE
authors.lastname: Ozkaynakçi
authors.forename: Nurbay
authors.initials: N
authors.lastname: Ateş
authors.forename: Gilles
authors.initials: G
authors.lastname: van Luijtelaar
authors.forename: Filiz Yilmaz
authors.initials: FY
authors.lastname: Onat
mesh_terms: D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D004569:Electroencephalography / Q000379:methods / Q000706:statistics & numerical data*; D004832:Epilepsy, Absence / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology*; D007839:Functional Laterality / Q000502:physiology; D007696:Kindling, Neurologic / Q000502:physiology*; D008032:Limbic System / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013238:Stereotaxic Techniques