Changes in the Expression of Bcl-2 Protein in Neurons in the Hippocampal Fields after Use of Ischemic Postconditioning of the Brain

Abstract

The expression of Bcl-2 protein in pyramidal neurons in hippocampal fields CA1, CA2, CA3, and CA4 was studied in Mongolian gerbils (Meriones unguiculatus) in the early (two days) and late (seven days) reperfusion periods after 7-min ischemia of the forebrain, after use of ischemic postconditioning (IPostC) and in sham-operated animals (n = 60). The highest level of Bcl-2 expression in the latter group was seen in neurons in field CA4 and the lowest in neurons in field CA1 (p < 0.01). Reversible ischemic injury led to an increase in the deficit of morphologically unaltered neurons in the hippocampus at the later period of reperfusion and a significant decrease in neuronal Bcl-2 expression at the early reperfusion period, this decrease being significantly smaller in the late reperfusion period. IPostC consisting of three episodes of reperfusion-ischemia (15/15 sec) promoted a significant increase in the number of morphologically unaltered neurons in fields CA1 and CA3 in the early reperfusion period. An increase in the level of Bcl-2 expression was seen in the cytoplasm of morphologically unaltered neurons in all hippocampal fields. In the late reperfusion period after IPostC, the number of unaltered neurons was increased in fields CA1, CA3, and CA4 (p < 0.05); only hippocampal field CA1 neurons showed a significant increase in Bcl-2 expression (by 12.7%, p < 0.01). These results lead to the conclusion that the cytoporotective effect of IPostC for hippocampal field CA1 is mediated by a mechanism leading to an increase in Bcl-2 expression, i.e., via blockade of apoptosis.