In vivo microdialysis in an animal model of neurological disease: thiamine deficiency (Wernicke) encephalopathy.
In vivo microdialysis allows for the constant monitoring of brain neurotransmitters in the extracellular fluid of awake and freely moving animals. Considerations including factors affecting probe recoveries, the blood-brain barrier, and tissue reactions to probe implantation are discussed in this paper. Details of the application of in vivo microdialysis to an animal model of encephalopathy are then presented. Thiamine deficiency encephalopathy is an animal model of Wernicke encephalopathy, a neurological disorder observed in alcoholics and in patients with severely compromised nutrition. Regionally selective neuronal cell death is observed in both patients and animals with thiamine deficiency (TD). Various thalamic nuclei suffer significant TD-induced cell death, and NMDA receptor-mediated glutamate excitotoxicity has been proposed as an underlying causative factor. A detailed methodology for the examination of the role of glutamate excitotoxicity using in vivo microdialysis in the neuronal cell death due to thiamine deficiency is presented.
Todd
K G
KG
Neurochemical Research Unit, Department of Psychiatry, 1E7.44 WMHSC, University of Alberta, Edmonton, Alberta, T6G 2R7, Canada. kgtodd@ualberta.ca
Butterworth
R F
RF
D000818:Animals; D001923:Brain Chemistry; D004195:Disease Models, Animal; D017551:Microdialysis / Q000379:methods*; D013832:Thiamine Deficiency / Q000503:physiopathology*; D014899:Wernicke Encephalopathy / Q000503:physiopathology*