Levetiracetam
Anticonvulsant / Levetiracetam is a clinically useful non-classical anticonvulsant.1 It has no effect on voltage-dependent Na+ channels, GABAergic transmission, or affinity for either GABAergic or glutaminergic receptors.2,3 Levetiracetam is believed to act via binding to the synaptic vesicle protein SV2A.4 Levetiracetam reduced intra-neuronal Ca2+ levels by inhibition of ryanodine and IP3 receptor-dependent Ca2+ release from the endoplasmic reticulum.5 It was also observed to lower the pH of neocortical pyramidal cells via weakening of the transmembrane HCO3(-)-mediated acid-extrusion.6
Biochemicals & reagents
102767-28-2
1) Wright et al. (2013) Clinical Pharmacology and Pharmacokinetics of Levetiracetam; Front. Neurol. 4 192 2) De Smedt et al. (2007) Levetiracetam: the profile of a novel anticonvulsant drug - part I: preclinical data; CNS Drug Rev. 13 43 3) Klitgaard and Verdru (2007) Levetiracetam: the first SV2A ligand for the treatment of epilepsy; Drug Discov. 2 1537 4) Lynch et al. (2004) The synaptic vesicle protein SV2A is the binding site for the antiepileptic drug levetiracetam; Proc. Natl. Acad. Sci. USA 101 9861 5) Nagarkatti et al. (2008) Levetiracetam inhibits both ryanodine and IP3 receptor activated calcium induced calcium release in hippocampal neurons in culture; Neurosci. Lett. 436 289 6) Bonnet et al. (2019) Levetiracetam mediates subtle pH-shifts in adult human pyramidal cells via an inhibition of the bicarbonate-driven neuronal pH-regulation - Implications for excitability and plasticity modulation; Brain Res. 1710 146
-20°C
PATHWAY: Intracellular transport; Calcium signaling -- RESEARCH AREA: Vesicles