The dual effect of seletracetam is an overall decrease in the amount of action potential due to binding at N-type channels, which prevents over-excitation of the neuron, as well as a decrease in neurotransmitter release as a product of cellular excitation due to the interaction of the drug with SV2A, which reduces the spread of excitation to nearby cells.
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A correlation has been drawn between the binding affinity of seletracetam (and its analogues) to SV2A and the degree of seizure prevention in animal models.
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Other than SV2A and the high-voltage-activated Ca2+ channels, seletracetam does not significantly bind to other CNS receptors, ion channels, or uptake mechanisms.
SV2A |