Intra-amygdaloid injection of kainic acid in rats with genetic absence epilepsy: The relationship of typical absence epilepsy and temporal lobe epilepsy

Gurbanova A. A. , GÜLHAN R., ŞİRVANCI S., DEMİRALP T., Onat F.

JOURNAL OF NEUROSCIENCE, vol.28, no.31, pp.7828-7836, 2008 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 28 Issue: 31
  • Publication Date: 2008
  • Doi Number: 10.1523/jneurosci.1097-08.2008
  • Title of Journal : JOURNAL OF NEUROSCIENCE
  • Page Numbers: pp.7828-7836


We showed previously that genetic absence epilepsy rats from Strasbourg (GAERS) resist secondary generalization of focal limbic seizures after electrical kindling. We now investigate the effect of intra-amygdaloid injection of kainic acid, as another model of temporal lobe epilepsy, focusing on epileptogenesis, spike-and-wave discharges (SWDs), and the transition from basal to SWD states in GAERS. The EEG was recorded from the hippocampus and cortex of adult GAERS and Wistar rats before kainic acid injections into the basolateral amygdala and for 3 months thereafter. EEG and video recordings monitored SWDs and convulsive seizures. We analyzed spectral changes of the EEG during kainic acid-induced status epilepticus, SWDs, for 10s before (silent period) and for 2s before (transition period) SWDs. After the injection of kainic acid, all animals experienced convulsive seizures for at least 3 h. The first convulsive seizure was significantly delayed in GAERS compared with Wistar rats. SWDs and increases in power of the delta, alpha, and beta frequency ranges during the transition period disappeared after the kainic acid injection for 1-3 d and gradually reappeared. Power increases in the delta and alpha ranges were significantly correlated with the number of SWDs, in the beta and alpha ranges with their mean duration. Neo-Timm's staining at the end of experiments demonstrated that mossy fiber sprouting in GAERSis less pronounced than in Wistar rats. Our findings show that mechanisms underlying absence epilepsy and temporal lobe epilepsy interact with each other, although a site of this interaction remains to be defined.