INOS expression in the pyramid layer of the rat hippocampus in the modeling of chronic cerebral discirculatory disorder

Abstract

AbstractBackgroundStudying of various forms of NO‐synthases is of great interest, since they are involved in many of the mechanisms of neuronal injury, aggravating the ischemic cascade and negatively affect the clinical status of cerebrovascular diseases. Impaired functioning of NO synthase plays an important role in the progressing of neurodegenerative diseases, since nitric oxide is a modulator of neuroplasticity.MethodChronic cerebrovascular disorder was modeled on rats by the method of overloading in the caudo‐cranial vector with a force 9 G for 5 minutes with an interval of 12 hours for 28 days. The level of iNOS expression was assessed by calculating the relative area of the immunoreactive material.ResultThe heterogeneity of the distribution of the immunoreactive material was expressed both in dust‐like cytoplasmic accumulation and in the presence of small‐lumpy deposits of iNOS‐positive material in the neurons of the pyramidal layer and in the neuropil, and in glial cells the intensity of expression was more pronounced, reaching a pronounced one. The relative area of iNOS‐positive material increased most significantly in CA3, by 8.3% (p<0.001), amounting to 12.1% [9.8;14.3]%. In CA1, the increase in the same indicator relative to the control was 3.9% (p<0.001), reaching 5.7 [4.5;6.1]%. In CA2 and CA4, respectively, the increase in the relative area of the IRM was 4.5% (p<0.05).ConclusionWe presume that the pronounced neuronal injury that is observed in the chronic cerebrovascular disorder modeling is a factor in the disruption of the hematoencephalic barrier, leading to edema, the subsequent acquisition of a pro‐inflammatory phenotype by astrocytic and microglia and the switch from the constitutive type of NO‐synthesis to the predominantly inducible type associated with activation of iNOS.