Glucose induced IEG expression in the thiamin-deficient rat brain

• Published in: Brain research Vol. 892; no. 1; pp. 218 - 227
• Main Authors: Zimitat, Craig, Nixon, Peter F
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 16.02.2001; Amsterdam Elsevier; New York, NY
• Subjects: Animals; Antimetabolites - pharmacology; Biological and medical sciences; Brain - drug effects; Brain - metabolism; Brain - pathology; Brain damage; Disease Models, Animal; Gene Expression Regulation - drug effects; Gene Expression Regulation - physiology; Genes, fos; Genes, Immediate-Early; Glucose - metabolism; Glucose - pharmacology; Humans; IEG expression; Medical sciences; Nervous system involvement in other diseases. Miscellaneous; Neurology; Organ Specificity; Pyrithiamine - pharmacology; Rats; Rats, Wistar; Thiamin deficiency; Thiamine Deficiency - genetics; Thiamine Deficiency - pathology; Thiamine Deficiency - physiopathology; Wernicke Encephalopathy - genetics; Wernicke Encephalopathy - pathology; Wernicke Encephalopathy - physiopathology; Wernicke's encephalopathy; Wernicke’s encephalography; Brain damage; IEG expression; Wernicke’s encephalography; Disorders of the neurons system; Thiamin deficiency; Animal model; Nervous system diseases; Rat; Pathogenesis; Rodentia; Central nervous system; Vitamin deficiency; B-Vitamins; Glucose; Gene expression; Cerebral disorder; Vertebrata; Mammalia; Central nervous system disease; Malnutrition; Wernicke encephalopathy; Nutritional status; Thiamine; Brain (vertebrata); Immediate early gene
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(00)03297-2

Glucose loading of rats made thiamin deficient by dietary deprivation of thiamin and the administration of pyrithiamin (40 μg/100 g, i.p.) precipitates an acute neuropathy, a model of Wernicke’s encephalopathy in man (Zimitat and Nixon, Metab. Brain Dis. 1999;14:1–20). Immunohistochemical detection of Fos proteins was used as a marker to identify neuronal populations in the thiamin-deficient rat brain affected by glucose loading. As thiamin deficiency progressed, the extent and intensity of Fos-like immunoreactivity (FLI) in brain structures typically affected by thiamin deficiency (the thalamus, mammillary bodies, inferior colliculus, vestibular nucleus and inferior olives) were markedly increased when compared to thiamin-replete controls. Glucose loading for 1–3 days further increased the intensity of FLI in these same regions, consistent with a dependence of Fos expression on carbohydrate 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 damage in this model of Wernicke’s encephalopathy.