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

Carl E. Stafstrom, Avtar Roopra, Thomas P. Sutula

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)97-100
Number of pages4
JournalEpilepsia
Volume49
Issue numberSUPPL. 8
DOIs
StatePublished - Nov 1 2008

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Keywords

  • 2-deoxy-D-glucose
  • Epilepsy
  • Glycolysis
  • Ketogenic diet
  • Kindling

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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