Update on the mechanism of action of antiepileptic drugs.

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Meldrum BS

Update on the mechanism of action of antiepileptic drugs.

Epilepsia. 1996;37 Suppl 6:S4-11. doi: 10.1111/j.1528-1157.1996.tb06038.x.

PubMed ID

8941036 [ View in PubMed

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Abstract

Novel antiepileptic drugs (AEDs) are thought to act on voltage-sensitive ion channels, on inhibitory neurotransmission or on excitatory neurotransmission. Two successful examples of rational AED design that potentiate GABA-mediated inhibition are vigabatrin (VGB) by irreversible inhibition of GABA-transaminase, and tiagabine (TGB) by blocking GABA uptake. Lamotrigine (LTG) prolongs inactivation of voltage-dependent sodium channels. The anticonvulsant action of remacemide (RCM) is probably largely due to blockade of NMDA receptors and prolonged inactivation of sodium channels induced by its desglycinated metabolite. Felbamate (FBM) apparently blocks NMDA receptors, potentiates GABA-mediated responses, blocks L-type calcium channels, and possibly also prolongs sodium channel inactivation. Similarly, topiramate (TPM) has multiple probable sites of action, including sodium channels, GABA receptors, and glutamate (AMPA) receptors. Gabapentin (GBP) apparently has a completely novel type of action, probably involving potentiation of GABA-mediated inhibition and possibly also inactivation of sodium channels. The therapeutic advantages of the novel AEDs are as yet only partially explained by our present understanding of their mechanisms of action.

DrugBank Data that Cites this Article

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Lamotrigine	GABA(A) Receptor (Protein Group)	Protein group	Humans	Unknown	Antagonist Inducer	Details
Lamotrigine	GABA(A) Receptor Benzodiazepine Binding Site (Protein Group)	Protein group	Humans	Unknown	Inhibitor	Details