Morphologic Studies on Forebrain of Thiamine Deficient Rats Induced by Thiamine eficient Diet and Pyrithiamine.
- Author:
Seung Hyun KIM
1
;
Myung Ho KIM
;
Tai Kyoung BAIK
Author Information
1. Department of Neurology, College of Medicine, Hanyang University, Korea.
- Publication Type:Original Article
- MeSH:
Animals;
Ataxia;
Body Temperature;
Brain;
Diet*;
Hippocampus;
Models, Animal;
Muscle Hypotonia;
Necrosis;
Neurologic Manifestations;
Neurons;
Prosencephalon*;
Pyrithiamine*;
Rats*;
Rats, Sprague-Dawley;
Reflex, Righting;
Thalamus;
Thiamine Deficiency;
Thiamine*;
Viola;
Weight Loss;
Wernicke Encephalopathy
- From:Journal of the Korean Neurological Association
1995;13(4):725-735
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: This study was designed for developing a new experimental animal model of Wernicke's encephalopathy, and for investigating the timesequential morphological changes in the thiamine deficient rat brain by thiamine deficient diet with short term treatment of pyrithiamine. METHODS: A total of 40 healthy Sprague-Dawley strain rats, weighing about 2OOgm were used as experimental animals, divided into 10 control rats and 30 thiamine deficient experimental rats. Pyrithiamine (50mg/lOOgm/day) was injected intraperitonially for 9 days and thiamine deficient diet (20gm/rat/day) was continuously supplied until sacrifice. Then thiamine deficient experimental rats were subdivided into 3 groups according'to the exposure time of thiamine deficiency. For observing the morphological features in thalamus, medial mammillary nucleus and CA, sector in hippocampus, luxol-fast blue-cresy violet stain was performed. RESULTS: Treatment with pyrithiamine and thiamine deficient diet results in weight loss and decrement of body temperature on the 12th-14th day, followed by various neurologic manifestations, such as ataxia, hypotonia, circling movement, opisthotonus and loss of righting reflex, on the 16th-20th day, and then died on the 23th-25th, day. Chromatolysis and nuclear condensation of neurons in thalamus, medial mammillary nucleus and CA1 region of hippocampus are observed in group I. Mild edematous changes with neuronal necrosis in group II, and marked neuronal loss with severe edematous necrosis in group III are noted in same regions. CONCLUSION: These time sequential consistent morphological changes suggest that our experimental method could be used as a new animal model of Wernicke's encephalopathy in studying the sequential changes of thiamine deficient rat brain.
