Abstract
Involvement of some signalling pathways in response to photodynamic therapy (PDT) of sulfonated aluminium phthalocyanine Photosens has been studied in isolated nerve cell. Neurone photosensitisation with 10 −7 M Photosens gradually inhibited firing and irreversibly abolished neuronal activity. Activation of protein kinase C (PKC) by phorbol ester 12- O-tetradecanoylphorbol 13-acetate (TPA) precipitated PDT-induced abolition of neurone activity and caused nucleus swelling and impairment of the nucleus border. Elevation of cytosolic Ca 2+ concentration by ionomycin or thapsigargin also reduced neurone lifetime. In contrast, the PKC inhibitors staurosporine, hypericin or chelerythrine as well as the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitors wortmannin or LY294002 increased neurone lifetime. These results showed that PKC, PI 3-kinase and Ca 2+ are involved in PDT-induced neurone inactivation and following death.
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