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- W350071479 abstract "Despite a considerable increase in the number of available antiepileptic drugs (AEDs) since about 1990, the percentage of pharmacoresistant patients (nearly 30%) has remained unaltered. The cellular and molecular mechanisms underlying the failure of AEDs are unknown. Two concepts explaining pharmacoresistance have been proposed: the target and the transporter hypotheses. The former is experimentally supported by molecular alterations of voltage- or ligand-gated ion channels, which reduce responsiveness to AEDs. The latter posits that the presence of multiple drug transporters result in a reduction of available AEDs in the CNS. We investigated the effects of lamotrigine and tiagabine on human cortical neurons in epilepsy surgery tissues from patients with drug-resistant epilepsy. The data obtained suggest that, in addition to these mechanisms, pharmacoresistance could be due to small net drug effects on excitability, with potentially beneficial effects counterbalanced by unexpected side effects or heterogeneity of neuronal properties." @default.
- W350071479 created "2016-06-24" @default.
- W350071479 creator A5013358412 @default.
- W350071479 date "2009-01-01" @default.
- W350071479 modified "2023-09-30" @default.
- W350071479 title "PHARMACORESISTANCE | Cellular and Molecular Mechanisms Contributing to Pharmacoresistance in Human Neocortical Tissue" @default.
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- W350071479 doi "https://doi.org/10.1016/b978-012373961-2.00061-8" @default.
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