Kril J J, Homewood J
Department of Pathology, University of Sydney, Australia.
J Neuropathol Exp Neurol. 1993 Nov;52(6):586-93. doi: 10.1097/00005072-199311000-00005.
The contribution of thiamin deficiency to the pathology of alcohol-related brain damage is still unclear. This study used a model of prolonged alcohol abuse in which animals were subjected to a brief period of mild thiamin deficiency. The episode of thiamin deficiency was early (after 4 weeks), in the middle (after 15 weeks) or late (after 26 weeks) in their 28 week alcohol treatment period. A control group of animals fed no alcohol and maintained on a thiamin-replete diet was used for comparison. The brains were removed and sectioned in the coronal plane at 50 microns intervals. Successive serial sections were stained with cresyl violet for Niss1 substance and immunohistochemically with antibodies to the calcium-binding proteins parvalbumin and calbindin. These calcium-binding proteins identify the majority of GABA-containing neurons in the cerebral cortex. The number of cells in the Fr1 region of the cerebral cortex was quantitated. A significant loss of Niss1-stained neurons was identified from the early group, while a loss of parvalbumin-immunoreactive neurons was seen in the early and middle groups. No loss of neurons was identified from the late group. In addition, no loss of calbindin-immunoreactive neurons was seen. This study represents the first report of cortical neuronal loss in an animal model of alcohol abuse and thiamin deficiency. Moreover, the results imply that thiamin deficiency is integrally involved in the pathogenesis of alcohol-related cortical neuronal loss.
