Glucose induced IEG expression in the thiamin-deficient rat brain

Glucose loading of rats made thiamin deficient by dietary deprivation of th iamin and the administration of pyrithiamin (40 mug/100 g, i.p.) precipitat es an acute neuropathy, a model of Wernicke's encephalopathy in man (Zimita t and Nixon, Metab. Brain Dis. 1999;14:1-20). Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in t he thiamin-deficient rat brain affected by glucose loading. As thiamin defi ciency progressed, the extent and intensity of Fos-Like immunoreactivity (F LI) in brain structures typically affected by thiamin deficiency (the thala mus, mammillary bodies, inferior colliculus, vestibular nucleus and inferio r olives) were markedly increased when compared to thiamin-replete controls . Glucose loading for 1-3 days further increased the intensity of FLI in th ese same regions, consistent with a dependence of Fos expression on carbohy drate metabolism as well as on thiamin deficiency. The timed acute changes that follow a bolus glucose load administered to thiamin-deficient animals may provide a sequential account of events in the pathogenesis of brain dam age in this model of Wernicke's encephalopathy. (C) 2001 Elsevier Science B .V. All rights reserved.