Glycolytic concomitant of brain inflammation produced by goldthioglucose

In order to determine the effect of inflammation on brain glycolysis in the absence of leukocyte infiltration, [14C]deoxyglucose autoradiography and hematoxylin-eosin (HE) counter-staining were applied to mice at various times after the induction of chemotoxic inflammatory brain lesions by the systemic administration of goldthioglucose. Glycolysis was intensely stimulated in affected circumventricular organs, without cellular infiltration. This result is consistent with the activation of anaerobic glycolysis by inflammatory sequelae that culminate in ischemic hypoxia in the lesion sites.