Photodynamic therapy (PDT) is used for treatment of cancer, including brain tumors. To explore the mechanism of photodynamic injury of neurons, we studied the PDT effect of 10(-7) M Photosens on ultrastructure of isolated crayfish stretch receptor neuron that was used as a model object. After a 5-min treatment that only slightly changed neuron activity, the initial injury (alteration of some mitochondria, vacuolization of the cytoplasm) was observed in parallel with compensatory changes (chromatin decondensation, elongation and aggregation of mitochondria, formation of lysosomes and autophagosomes). Longer photosensitization (30 min) abolished firing, destroyed mitochondria and Golgi apparatus, depleted energy sources (glycogen granules), and impaired granular endoplasmic reticulum and polysomes involved in protein synthesis. Therefore, mitochondria and Golgi apparatus were the primary targets for Photosens-mediated PDT in a single neuron. Their alteration might underlie functional shifts. These structural changes continued to develop after abolishment of neuronal activity and led to necrosis.
2007 Wiley-Liss, Inc.