A metabolic link between the astrocytic α2-Na/K ATPase and episodic paralysis

Abstract

While loss-of-function mutations affecting the α2-Na/K ATPase are known to cause familial hemiplegic migraine, it is unclear how reduced protein activity could contribute toward migraine or paralysis observed in patients. A recent study from Sarah Smith and colleagues demonstrates that conditional deletion of the α2-Na/K ATPase in astrocytes can evoke episodic paralysis in mice, potentially due to altered metabolic processing of serine and glycine. By feeding juvenile α2-Na/K ATPase mutant mice a serine- and glycine-free diet, the authors are able to prevent the onset of episodic paralysis. This study suggests that loss of α2-Na/K ATPase in astrocytes may affect amino acid metabolism in the brain, ultimately leading to episodic paralysis.