Voltage-gated sodium channels (VGSCs) in the presynaptic nerve terminal of the excitatory glutamate receptors are the molecular target for phenytoin, CBZ, and lamotrigine as well as some of the newer AEDs, such as OXC, felbamate (FBM), and zonisamide.18 These aromatic AEDs inhibit excessive neuronal firing by binding to a site near the inactiva-tion gate, thereby prolonging inactivation of VGSCs.20 Figure 14.1 illustrates how phenytoin interacts with the hypothetical inactivation gate receptor according to a pharmacophore model suggested by Unverferth et al.21 as a result of molecular simulations with these aromatic AEDs. This model includes an aromatic binding site and two separate hydrogen bonding sites for interacting with potent AEDs such as phenytoin and lamotrigine.
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