C-FOS AND CALBINDIN IN CINGULATE CORTEX NEURONS OF THE RAT BRAIN IN CHOLESTASIS
Abstract
Background. Cholestasis (bile stagnation) is known as a severe complication of many diseases of the liver and biliary tract. It occurs when the flow of bile from the liver into the duodenum is impaired resulting in digestive disorders
(especially those of lipid metabolism) and accumulation of bile components (bilirubin, bile acids, cholesterol) in blood and then in the brain, the latter inducing the disturbances in the brain structure and functions. It was of interest to
clarify the molecular mechanisms of the disorders, in particular the roles of c-fos protein and calbindin in the adaptation mechanisms of cingulate cortex neurons to cholestasis. Objective. To evaluate the effect of cholestasis on the content of c-fos protein and calbindin in neurons of the rat cingulate cortex. Material and methods. The object of the study were neurons of the small-cell and large-cell layers of the anterior cingulate cortex of the rat brain on days 2, 5, 10, 20, 45 and 90 after ligation/transection of the common bile duct (CBD) or sham surgery (a control group). Histological, immunohistochemical, morphometric and statistical methods were used. Results. An increase in the number of neurons with high c-fos immunoreactivity is observed even at early stages of cholestasis, reaching its maximum by the 5th day and remaining significantly elevated on the 10th-20th days (the peak of cholestasis), the number gradually decreasing with the elimination of cholestasis. The content of calbindin in neurons of both cingulate cortex layers of the rat brain increases significantly on the 10th and 20th days, then decreases on the 45th day. On the 90th day, the contents of c-fos and calbindin in neurons of the cingulate cortex normalize (do not differ from that of control). Conclusion. Cholestasis is marked by the growth in the number of neurons with increased immunoreactivity of c-fos protein and calbindin in the small-cell and large-cell layers of the rat cingulate cortex.
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