Seizure suppression via glycolysis inhibition with 2-deoxy-D-glucose (2DG)

Epilepsia. 2008 Nov;49 Suppl 8:97-100. doi: 10.1111/j.1528-1167.2008.01848.x.


Metabolic regulation of neuronal excitability is increasingly recognized as a factor in seizure pathogenesis and control. Inhibiting or bypassing glycolysis may be one way through which the ketogenic diet provides an anticonvulsant effect. 2-deoxy-D-glucose (2DG), a nonmetabolizable glucose analog that partially inhibits glycolysis, was tested in several acute and chronic seizure models. Acutely, 2DG decreases the frequency of high-K(+)-, bicuculline- and 4-aminopyridine-induced interictal bursts in the CA3 region of hippocampal slices; 2DG also exerts anticonvulsant effects in vivo against perforant path kindling in rats. Chronically, 2DG has novel antiepileptic effects by retarding the progression of kindled seizures. Finally, 2DG has a favorable preliminary toxicity profile. These factors support the possibility that 2DG or other modifiers of glycolysis can be used as novel treatments for epilepsy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Anticonvulsants / pharmacology*
  • Deoxyglucose / pharmacology*
  • Glycolysis / drug effects*
  • Hippocampus / drug effects*
  • Humans
  • Kindling, Neurologic / drug effects
  • Neurons / drug effects*
  • Rats
  • Seizures / drug therapy*


  • Anticonvulsants
  • Deoxyglucose