Nerve cells or neurons are connected to each other in a network of structures called axons that transmit electrical impulses. Axons are often wrapped in a fatty substance called myelin, which protects the cells below like a sheath. Myelinated axons in the brain, for one, play pivotal roles in brain function – the loss of myelin can spell serious disability.

Recently, researchers from the Netherlands Institute for Neuroscience (NIN) discovered how myelin loss might underpin aberrant brain activity as observed in people with multiple sclerosis (MS), an autoimmune disease characterised by demyelination. Research findings suggest that myelination is required for neurons within the brain to successfully regulate important brain rhythms and cognitive processes in related gray matter areas.

This is the case for a fast firing connecting neuron in the brain known as the PV+ interneurons. PV+ interneurons have short, sparsely myelinated axons and exhibit inhibitory potential.

NIN researcher Mohit Dubey and colleagues found the inhibitory threshold of PV+ interneurons decreased in mice genetically engineered to lack myelin, leading to epileptic spikes. “As mice progressively lost myelin, the speed of inhibitory signals from PV+ interneuron did not change but their signal strength decreased,” said Dubey.

“As a result of being no longer inhibited by PV+ interneurons, the power of slow brain waves dramatically increased [and] triggered brief spikes resembling signals seen in epilepsy, only when the mice were inactive and quiet. Restoring the activity of PV+ interneurons helped to reverse the epileptic spikes.”

NIN researchers are yet to determine whether these brief epileptic spikes could be a biomarker of MS and/or a target for developing new therapeutic strategies to limit cognitive impairments.

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