Antiepileptic Drug Mechanisms

Despite considerable research, the precise mechanism(s) of action of the majority of AEDs is essentially unknown, with the exception of the GABA transaminase inhibitor, vigabatrin, and the selective GABA GAT1 uptake inhibitor, tiagabine, both of which were designed as AEDs based on a defined mechanism of action (Figure 2). While a multiplicity of targets for AEDs have been identified, primarily ion channels, including voltage-gated sodium and calcium channels, GABAa receptors, and, more recently, N-methyl-D-aspartate (NMDA)- and a-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-type glutamate receptors3'4 as well as HCN (hyperpolarization-activated, cyclic nucleotide-gated cation) or pacemaker channels,16 many of these represent only a part of a broader spectrum of the activity of different AEDs with the majority of these interactions occurring in the micromolar concentration range. For instance, while sodium valproate can block ion channels and increase GABA levels in brain, its use in the treatment of both epilepsy and bipolar disorder is predicated on its polypharmic role as a modulator of ion channel function and phosphatdiyl inositol signaling pathways, as an inhibitor of histone deacetylase (HDAC) and an activator of mitogen-activated protein kinases (MAPKs).17

Understanding And Treating Bipolar Disorders

Understanding And Treating Bipolar Disorders

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