Pharmacologically induced absence seizures versus kindling in Wistar rats

OpenAlex İngilizce

K indling is the classical model for temporal lobe epilepsy with a repeated focal application of the low-intensity electrical current to a particular forebrain structure that predictably triggers the initial partial seizure [1][2][3][4].The resistance to kindling induced secondary generalization from limbic seizures is a phe-nomenon observed in genetically determined genetic rat models of absence epilepsy; the Genetic Absence Epilepsy Rats from Strasbourg (GAERS) and Wistar Albino Glaxo rats from Rijswijk (WAG/Rij) [5,6].In these models, the presence of generalized spikeand-wave discharges (SWDs) is clearly associated ABSTRACT OBJECTIVE: This study aimed to investigate the effects of γ-butyrolactone (GBL), a prodrug of gamma-Hydroxybutyric acid -induced absence seizures on the development of kindling in Wistar rats. METHODS:Three groups of adult male Wistar rats under anesthesia were implanted with bilateral cortical recording electrodes for the GBL group (GBL) and/or bipolar stimulation electrodes into the right basolateral amygdala for the Kindling group (KI) alone and Kindling plus GBL group (GBL+KI).Rats in the KI and GBL+KI groups were stimulated twice daily at the afterdischarge threshold until they reached Racine's stage 5 seizure state.The animals in the GBL + group had an i.p injection of GBL 20 minutes before each electrical stimulation, and the effects of GBL-induced seizures on the development of kindling were investigated.The animals in the GBL group were injected GBL twice daily i.p. for 15 days without receiving any electrical stimulation. RESULTS:The KI animals reached stage 5 seizure stage at 12 th stimulations, whereas the GBL+KI rats reached at 27 th stimulations.The mean numbers of stimulations needed for the development of the first stage 3, 4, or 5 generalized seizures were significantly higher in the GBL+KI group than the KI group. CONCLUSION:The resistance to amygdala kindling in the GBL model can be modulated by the absence seizure mechanism alone, without the intervention of an abnormal genetic background.