Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2008 Jul;1(1):13-24.
doi: 10.1177/1756285608094212.

Is levetiracetam different from other antiepileptic drugs? Levetiracetam and its cellular mechanism of action in epilepsy revisited

Rainer Surges  1 , Kirill E Volynski, Matthew C Walker
Affiliations

Is levetiracetam different from other antiepileptic drugs? Levetiracetam and its cellular mechanism of action in epilepsy revisited

Rainer Surges et al. Ther Adv Neurol Disord. 2008 Jul.

Erratum in

  • Ther Adv Neurol Disord. 2008 Sep;1(2):79

Abstract

Levetiracetam (LEV) is a new antiepileptic drug that is clinically effective in generalized and partial epilepsy syndromes as sole or add-on medication. Nevertheless, its underlying mechanism of action is poorly understood. It has a unique preclinical profile; unlike other antiepileptic drugs (AEDs), it modulates seizure-activity in animal models of chronic epilepsy with no effect in most animal models of acute seizures. Yet it is effective in acute in-vitro 'seizure' models. A possible explanation for these dichotomous findings is that LEV has different mechanisms of actions, whether given acutely or chronically and in 'epileptic' and control tissue. Here we review the general mechanism of action of AEDs, give an updated and critical overview about the experimental findings of LEV's cellular targets (in particular the synaptic vesicular protein SV2A) and ask whether LEV represents a new class of AED.

Keywords: SV2A; antiepileptic drugs; epilepsy; ion channels; levetiracetam; synaptic transmission.

PubMed Disclaimer

References

    1. Ambrosio A.F., Silva A.P., Malva J.O., Soares-da-Silva P., Carvalho A.P., Carvalho C.M.(1999) Carbamazepine inhibits L-type Ca2+ channels in cultured rat hippocampal neurons stimulated with glutamate receptor agonists. Neuropharmacology 38: 1349–1359 - PubMed
    1. Angehagen M., Margineanu D.G., Ben-Menachem E., Rönnbäck L., Hansson E., Klitgaard H.(2003) Levetiracetam reduces caffeine-induced Ca2+ transients and epileptiform potentials in hippocampal neurons. Neuroreport 14: 471–475 - PubMed
    1. Angehagen M., Ben-Menachem E., Shank R., Rönnbäck L., Hansson E.(2004) Topiramate modulation of kainate-induced calcium currents is inversely related to channel phosphorylation level. J Neurochem 88: 320–325 - PubMed
    1. Bardo S., Cavazzini M.G., Emptage N.(2006) The role of the endoplasmic reticulum Ca2+ store in the plasticity of central neurons. Trends Pharmacol Sci 27: 78–84 - PubMed
    1. Barton M.E., Klein B.D., Wolf H.H., White H.S.(2001) Pharmacological characterization of the 6 Hz psychomotor seizure model of partial epilepsy. Epilepsy Res 47: 217–227 - PubMed

LinkOut - more resources