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Fig. 3.

Model synapse illustrating interaction of Na+ channel blocking anticonvulsants with voltage-activated Na+ channels and putative sites of action of newer anticonvulsants (gabapentin, pregabalin, and levetiracetam) that may more directly interact with release machinery. Gabapentin and pregabalin bind to α2-δ, which may inhibit voltage-activated Ca2+ entry through high voltage-activated Ca2+ channels or affect the way in which Ca2+ channels interact with vesicular release. Levetiracetam may also affect release by binding to synaptic vesicles protein SV2A. In contrast, action potentials are mediated by voltage-activated Na+ and K+ channels; Na+ channel blocking anticonvulsants suppress epileptiform action potential firing, which leads to inhibited release. Smaller yellow circles represent glutamate within synaptic vesicles (larger blue circles) and free in the synaptic cleft. Glutamate acts on ionotropic receptors of the NMDA, AMPA and kainate types to generate an excitatory postsynaptic potential (EPSP) in the postsynaptic neuron. Nefopam (NFP) shows an activity of the inhibition of long-term potentiation mediated by NMDA from the inhibition of calcium influx like gabapentinoid anticonvulsants or blockade of voltage-sensitive sodium channels like carbamazepine (Modified by Löscher W, Schmidt D. New Horizons in the development of antiepileptic drugs: Innovative strategies. Epilepsy Res 2006; 69: 183-272.).

Korean J Pain 2014;27:103~111
© Korean J Pain