Previous research has suggested that neurons in multiple sclerosis (MS) exhibit metabolic exhaustion, believed to be caused by chronic hyperexcitability, which can lead to neurodegeneration. Researchers from Heidelberg University and affiliated organizations aimed to investigate the role of nodal Kv7 (outward rectifying) and perinodal oligodendroglial Kir4.1 (inward rectifying) channels as potential therapeutic targets for neuroprotection through balancing of neuronal excitability caused by inflammatory demyelination.