Photodynamic inactivation of isolated crayfish neuron requires protein kinase C, PI 3-kinase and Ca2+

J Photochem Photobiol B. 2003 May-Jun;70(2):99-105. doi: 10.1016/s1011-1344(03)00071-x.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astacoidea
  • Calcium / metabolism*
  • In Vitro Techniques
  • Indoles / pharmacology*
  • Microscopy, Fluorescence
  • Neurons / drug effects*
  • Neurons / metabolism
  • Organometallic Compounds / pharmacology*
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Photochemotherapy*
  • Protein Kinase C / metabolism*

Substances

  • Indoles
  • Organometallic Compounds
  • aluminum phthalocyanine
  • Phosphatidylinositol 3-Kinases
  • Protein Kinase C
  • Calcium