Altered activity of ATP-sensitive K⁺ channels underlies the metabolic seizure resistance produced by genetic manipulation of the BAD protein in mice.

Oligodendrocytes in white matter use Kir4.1 inwardly rectifying potassium channels to prevent extracellular potassium accumulation, enabling neurons to sustain repetitive firing and limiting the initiation of seizures.

Sodium selenate is the first treatment with persistent disease-modifying effects reducing seizures and improving cognitive deficits, in chronically epileptic and drug-resistant TLE animals.

Glutamatergic neurons lacking the mitochondrial pyruvate carrier show reduced M-type potassium channel activity and hyperexcitability upon intense firing.

A single amino acid change in a neuronal ion channel called KCNQ2 blocks ion flow, prevents protein localization on axons, and results in severe epilepsy and slowed neurological development.

Purine recycling deficiency triggers metabolic and neurological defects reminiscent of Lesch–Nyhan disease in Drosophila, paving the way for studying this disorder and carrying out drug screening in an invertebrate organism.

Excitatory signaling impairment contributes to neurological deficits shared by Rett syndrome and a number of postnatal neuropsychiatric disorders.

Two genetic mouse models for HCN1-linked developmental epileptic encephalopathy display distinct biophysical changes in HCN1 ion channel properties but similar worsening of seizures in response to antiepileptic drugs, thereby recapitulating key features of the human disease.

Repurposing of a drug designed for pain relief can quickly and reversibly slow biochemical and metabolic activities in cells and organs and could facilitate organ transplantation and prevent tissue injury.