Seizure-Convulsion Ion Channel Portfolio

Ion channels expressed in the central nervous system (CNS) are closely linked to hereditary epilepsy. Gain-of-function mutations in excitatory ion channels, including voltage-gated sodium channels Nav1.1, Nav1.2, Nav1.3 and Nav1.6, the voltage-gated calcium channel Cav3.2, and hyperpolarization-activated HCN1 and HCN2 channels, can generate sustained depolarizing currents and excessive neuronal excitability. This hyperexcitability is a key driver of epileptic seizures and convulsions.

Similarly, loss-of-function mutations in inhibitory channels, including the voltage-gated potassium channel KCNQ, calcium-activated potassium channel BK, and ligand-gated chloride channels such as GABAA, can also result in neuronal hyperexcitability. Drug-induced changes that mimic these mutation-related effects may further increase the risk of neurological complications.

Other relevant channels include CLC-2 chloride channels, which help maintain chloride homeostasis and neuronal stability, and ligand-gated NMDA receptors, which regulate excitatory neurotransmission and are frequently implicated in seizure activity.

Antiepileptic drugs often counteract these effects by inhibiting excitatory channels or activating inhibitory channels. Accordingly, the ion channels included in this seizure–convulsion panel represent relevant targets for evaluating hyperexcitability-related conditions, including seizures, pain, neurodegeneration, anxiety, migraines and psychosis, as well as for assessing the risk of adverse neurological events.

Seizure–Convulsion Ion Channel Portfolio

Our seizure–convulsion ion channel portfolio focuses on CNS ion channels involved in the neuronal hyperexcitability underlying seizures and convulsions. By integrating excitatory and inhibitory channel targets, the panel supports the evaluation of compounds intended to modulate neuronal activity and manage epilepsy-related mechanisms.