MORPHOLOGICAL AND FUNCTIONAL CHARACTERISTICS OF THE MICROVASCULATURE AND NEURONS IN NEOCORTEX AFTER ISCHEMIC POSTCONDITIONING

PECAM-1/CD31 (biomarker of endothelial function and neovascularization) was used to assess protein expression in microvessels of cortical layers II, III and V in Mongolian gerbils ( Meriones unguiculatus ) in the early (Day 2) and late (Day 7) reperfusion period after a 7-minute forebrain ischemia and subsequent ischemic postconditioning (IPostC), as well as in sham-operated animals (n=60). The latter demonstrated the lowest level of immunoreactivity to PECAM-1/CD31 in the structures in cortical layer III. Reversible ischemic brain damage manifested itself in the reduction of number of morphologically unchanged neocortical neurons and extension of the reperfusion period; in addition to that, an increase in the level of immunoreactivity to PECAM-1/CD31 was observed in layers II, III and V of the cortex and it was significantly augmented towards the late reperfusion period. IPostC, performed by three stimulating cycles of ischemia-reperfusion lasting 15/15 seconds, resulted in a significant increase in the number of morphologically unchanged neurons in cortical layers II and III in the early reperfusion period. In the late reperfusion period, after IPostC, the number of unchanged neurons in layers II, III and V of the cortex was increased, while the level of immunoreactivity for PECAM-1/CD31 in these structures was significantly decreased. These results allow to conclude that the cytoprotective effect of IPostC under ischemia was implemented through the physiological mechanism of adaptation, which enhanced immunoreactivity for PECAM-1/CD31 in microvessels of the cerebral cortex in the early reperfusion period, and inhibited it in the late reperfusion period.

neocortex, neurons, PECAM-1/CD31, ischemiareperfusion, ischemic postconditioning