Introduction: Brain hypoperfusion leads to discirculatory changes in the cerebral cortex, which is accompanied by a reaction from the glia and changes in the expression of specific markers, including glial fibrillary acidic protein (GFAP) in astrocytes.

Aim: To study the expression level of glial fibrillary acidic protein in the sensorimotor cortex of rats under hypoperfusion conditions in the left carotid artery basin against the background of previous sensitization with brain antigen.

Materials and methods: The studies were carried out on 115 male white sexually mature Wistar rats weighing 260-290 g, which simulated hypoperfusion of the brain against the background of previous sensitization. The brain for research was taken 13, 15, 22, 42 and 102 days after sensitization with brain antigen, after excessive administration of sodium thiopental (200 mg / kg) to animals. We used histological, іmmunohistochemistry, densitometric and statistical research methods. An іmmunohistochemistry reaction for detecting GFAP was performed according to the manufacturer’s protocol with a primary antibody to GFAP (Dako, Denmark). An EnVisionTM FLEX detection system (Dako, Denmark) was used to visualize the IHC reaction products. Every second section was additionally stained with Gill hematoxylin. As a positive control, we used rat brain samples with a certain positive reactivity, and for a negative control, the procedure was performed without the use of primary antibodies.

Results: Observations have shown that sensitization with a brain antigen causes neurodegenerative changes in the sensorimotor cortex and a moderate increase in the amount of GFAP + – gliocytes gradually increases. Against the background of sensitization with a brain antigen, hypoperfusion of the brain leads to an increase in the number of a glial cell, which are marked by GFAP. In the affected hemisphere, their number increases during the first three days, after which it decreases. But even 3 months after hypoperfusion, there is almost twice as much as in conventionally intact rats. This may be a factor that will significantly affect the function of brain regions after a vascular accident. A slight increase in the amount of GFAP + – gliocytes in the contralateral hemisphere suggests a certain systemic nature of the reactions of astrocytic glia to hypoperfusion. An early response to an increase in the number of marked astrocytes already a day after hypoperfusion suggests that some of this type of a glial cell do not express GFAP under normal conditions.

Conclusions: Sensitization with a brain antigen causes neurodegenerative changes in the sensorimotor cortex and an increase in the amount of GFAP+ astrocytes. Sensitization with a brain antigen leads to a potentiated increase in the amount of GFAP+ astrocytes in response to hyporerfusion in the cerebral cortex.