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Additional info for Clinical and Genetic Aspects of Epilepsy
2005). , 2007). In addition to P-gp, data indicate that BCRP plays a significant role in drug efflux at the blood-brain barrier. , 2007). However, little information is available on the extent to which BCRP contributes to AED resistance and if Pgp and BCRP work in concert in AED efflux from the brain. , 2005). More studies are needed to unequivocally clarify the role of BCRP, especially in conjunction with P-gp, in AED-resistant epilepsy. Only little information is available on the multidrug resistance proteins (Mrps) in epilepsy.
Nemeroff and Crisley made a critical discovery in 1975 when they found that glutamate is involved in seizure induction and increases cerebrovascular permeability in rats (Nemeroff & Crisley, 1975). , 1977). In 1989, Clarke and Gabrielsen demonstrated seizure-induced bloodbrain barrier leakage in humans using computed tomography (Clarke & Gabrielsen, 1989). In 1995, Tishler et al. , 1995). , 2008). , 2005). Today, the role of some of these transporters in epilepsy is still unclear. , 2007). , 2007).
1995). The findings by Tishler et al. , 2002) and it was suggested that this phenomenon could prevent AEDs from entering the brain and cause AED resistance. , 2003). , 2007). They demonstrated that phenytoin permeation was 10-fold lower in endothelial cells from AED-resistant patients compared to purchased human endothelial cells. Although this comparison is flawed, inhibiting P-gp increased phenytoin permeation in the AED-resistant cells. , 2007). Using a drug-resistant epilepsy rat model, Potschka et al.