Protein p53 Expression and Dark Neurons in Rat Hippocampus after Experimental Septoplasty Simulation

This study evaluated the dependence of p53 protein expression on the occurrence of dark neurons (DNs) in the hippocampus of rats during experimental modeling of septoplasty. Septoplasty simulation was carried out on 15 sexually mature male Wistar rats. We studied histological sections of the hippocampus stained with Nissl toluidine blue and antibodies to p53 protein. In the CA1 subfield, the number of p53-positive neurons significantly increased on the second, fourth ( p < 0.001), and sixth days ( p < 0.05). Dynamic assessment detected the peak of p53 protein expression in the cytoplasm of CA1 and CA2 neurons from the second to fourth days after surgery, while the number of these neurons decreased on the sixth day ( p < 0.001). In the cytoplasm of CA3 neurons at all periods after surgery, the expression of p53 protein increased compared to the control group. In the CA1 pyramidal layer, the number of DNs decreased on the sixth day ( p < 0.001). After 2 days, the minimal number of DNs was noted in CA2 compared with the fourth day ( p < 0.001). In CA3, there was a peak in number of DNs on the fourth day compared with the other days ( p < 0.001). A strong positive correlation was found at all periods of assessment and in all subfields of the hippocampus between the increase in the number of dark and p53-positive neurons. The occurrence of dark and p53-positive neurons in the hippocampal formation of rats after septoplasty modeling is a typical response of nervous tissue to stress. It is obvious that the expression of p53 protein is associated with basophilia of neural cytoplasm and the morphofunctional state of neurons. Presumably, the p53 protein can trigger not only the activation of damaged neurons in the hippocampus, but can also play a neuroprotective role. Upcoming studies should determine the role of p53 protein in further fate of damaged neurons in the pyramidal layer and differentiate the mechanisms of its expression.