Abstract
The central nucleus of the amygdala complex is the integrative center and the main channel of communication with the rest of the brain. It has been shown that it is associated with the most important hypothalamic and visceral centers. Studying the morphology of its neurons and their response is necessary to understand how this structure regulates various aspects of behavior in normal conditions and in mental disorders. The purpose of this study was the morphological organization of astrocytes in the central nucleus of the amygdala complex in DAT-HET rats. DAT-HET rats are heterozygotes (HET) for knockout of the dopamine transporter (DAT) protein gene and have a number of behavioral characteristics, increased motor and exploratory activity, and at the same time increased behavioral anxiety. The study was carried out on male laboratory rats of two lines: Wistar line (n=8), DAT-HET line (n=7) with body weight from 200 g to 265 g at the age of 5-6 months. The central nucleus of the amygdala complex was studied in a series of frontal sections of the rat brain. In the structure of the central nucleus of the amygdala complex in the studied groups of animals, the medial and lateral sub-nuclei and the intermediate part that unites them are well differentiated. A study of morphometric indicators of the area of the sub-nuclei of the central nucleus of the amygdala complex showed that in Wistar rats the area of the lateral sub-nucleus is significantly higher when compared with the same indicator in DAT-HET rats, and this difference is 29%. Comparison of the degree of expression of immune-positive cells for the marker of glial fibrillary acidic protein - type III intermediate filament protein, which is expressed by numerous types of cells of the central nervous system, including astrocytes and ependymal cells, revealed that in DAT-HET rats the area occupied by immune-positive cells is also significantly larger. The results obtained indicate possible processes of remodeling the shape and size of astrocytes that occur in response to changes in dopaminergic transmission caused by knockout of the corresponding gene.
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