Effects of vigabatrin on spike and wave discharges in the eeg of rats
Nijmegen : NICI
InLuijtelaar, E.L.J.M. van; Kuznetsova, G.D.; Coenen, A.M.L. (ed.), The WAG/Rij model of absence epilepsy: the Nijmegen - Russian Federation papers, pp. 179-185
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Luijtelaar, E.L.J.M. van
SW OZ DCC SMN
SW OZ NICI BI
Luijtelaar, E.L.J.M. van; Kuznetsova, G.D.; Coenen, A.M.L. (ed.), The WAG/Rij model of absence epilepsy: the Nijmegen - Russian Federation papers
In the present study, the effects of vigabatrin on type I and type II SWDs in the EEG of rats were studied. Vigabatrin is an irreversible GABA transaminase inhibitor which increases, long lasting, GABA concentrations, thus affecting both GABAA and GABAB conductances. Type I SWDs occur abundantly in WAG/Rij rats, whereas this type is virtually absent in ACI rats. In ACI rats however, type II SWDs do occur. The type I SWDs were studied in WAG/Rij rats after inter-peritoneal injection of 15-500 mg/kg of vigabatrin, 6 hours after injection. The type II SWDs were studied in ACI rats after inter-peritoneal injection of 500 mg/kg of vigabatrin, 6 hours after injection. The incidence of both type I and type II SWDs was significantly increased after vigabatrin as compared to saline. The duration of type II SWDs was also increased after vigabatrin as compared to saline treatment, whereas the duration of type I SWDs was not affected. The peak-frequency of both type I and type II SWDs was decreased after vigabatrin. Thus, vigabatrin alters not only the incidence but also the morphology of both type I and type II SWDs. These results might fit well with predictions of a theoretical model, in which both GABAA and GABAB conductances are modulated, as proposed by Destexhe (1999).
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