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Photodynamic treatment causes intense oxidative stress and kills cells. It is currently used in neurooncology. However,
along with tumor it damages surrounding healthy neuronal and glial cells. In order to study the possible role of the
phosphatidylinositol 3-kinase/protein kinase Akt/glycogen synthase kinase-3β signaling pathway in photodynamic
damage to normal neurons and glia, we used isolated crayfish stretch receptor that consists only of a single neuron
surrounded by glial cells. It was photosensitized with alumophthalocyanine Photosens (100 nM). The laser diode
(670nm, 0.4W/cm2) was used as a light source. Application of specific inhibitors of the enzymes involved in this
pathway showed that phosphatidylinositol 3-kinase did not participate in photoinduced death of neurons and glia.
Protein kinase Akt was involved in photoinduced necrosis but not in apoptosis of neurons and glia. Glycogen synthase
kinase-3β participated in photoinduced apoptosis of glial cells and in necrosis of neurons. Therefore, the
phosphatidylinositol 3-kinase/protein kinase Akt/glycogen synthase kinase-3β pathway was not involved as a whole in
photodynamic injury of crayfish neurons and glial cells but its components, protein kinase Akt and glycogen synthase
kinase-3β, independently and cell-specifically regulated photoinduced death of neurons and glial cells. These data
showed that in this system necrosis was not non-regulated and catastrophic mode of cell death. It was controlled by
some signaling proteins. The obtained results may be used for search of pharmacological agents that selectively
modulate injury of normal neurons and glial cells during photodynamic therapy of brain tumors.
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