. Author manuscript; available in PMC: 2022 Sep 6.

Published in final edited form as: J Neurol Sci. 2021 May 29;427:117515. doi: 10.1016/j.jns.2021.117515

Table 4. Common genetic mechanisms for the development of epilepsy.

Category	Component	Mechanism
Voltage-gated channelopathies	Na⁺ channel	Inappropriate activation of current Prolonging activation Incomplete activation of channels Acceleration of recovery from inactivation
	K⁺ channel	Prolong neuronal depolarization through slow deactivation, loss of high-frequency bursting, or prolongation of membrane repolarization
	Ca²⁺ channel	Promote neuron synchrony by lowering thresholds for electrogenesis
Ligand-gated channelopathies	GABA channel	Reduction of GABA-activated Cl-current Increase in rate of desensitization
	Nicotinic ACh receptor	Slowed desensitization
	NMDA glutamate receptor	Increased duration of excitation
	AMPA glutamate receptor	Initiating excitation
	Metabotrobic glutamate receptor	Blockade of accommodation to a steady current Potentiation of effects of NMDA, AMPA, and depolarization
	Serotonin receptor	Loss of inhibitory current
Neurotransmitter release machinery	Synapsins 1 and 2	Decreased size of presynaptic vesicle pool particularly in inhibitory synapses
	Sv2A	Sustained release of neurotransmitters
	Vesicular zinc sequestration	Neuron hypersynchrony
	Reduced recycling	Prolonging activation
Structural	Cortical dysplasias	Inhibited postnatal granule cell proliferation in dentate gyrus Hypertrophy of neocortex Cell migration, segmentation, and patterning reduced Inhibitory neurons reduced or inhibited