Abstract
In 1966, Reynolds et al. proposed that the antiepileptic actions of the then available antiepileptic drugs might be partially mediated through their antifolate effects. This idea gained further credence when it was discovered that folate and its derivatives were proconvulsant when given in large doses systemically or applied directly onto the cortex (Fisher 1989). The hypothesis resulted in the development of a number of antifolate agents and their testing in animal models of epilepsy. These experiments revealed a poor correlation between antifolate properties and anticonvulsant effects, but a group of phenyltriazine compounds, which had weak antifolate properties, proved to be potent anticonvulsants. Lamotrigine was developed from these compounds, though neither short-term nor chronic lamotrigine therapy appears to be associated with significant changes in serum or red cell folate concentrations (Sander and Patsalos 1992).
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Walker, M.C., Sander, J.W.A.S. (1999). Lamotrigine. In: Eadie, M.J., Vajda, F.J.E. (eds) Antiepileptic Drugs. Handbook of Experimental Pharmacology, vol 138. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60072-2_12
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