Poster (download) Pavel D. Lisachev1, Anna L. Proskura21Institute of Computational Technologies SB RAS, lisachev@ngs.ru2Institute of Computational Technologies SB RAS, annleop@mail.ru AbstractBcl-2 family protein Bax is involved in mechanisms of synaptic plasticity. The induction of long term potentiation in hippocampal slices leads to increased Bax expression, but the localization of these changes remains unclear. Bax immunoreactivity is visually detected mainly in the layer of pyramidal neurons and is rarely detected in S100B-positive glial cells. However, a quantitative assessment of Bax colocalization with glial and neuronal markers (S100B and NeuN, respectively) showed that although the Bax content in S100B-positive glial cells is really low, the Bax neuronal somatic pool is not the main source of Bax protein in the hippocampus.
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