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Photodynamic therapy (PDT), a potent inducer of oxidative stress, is a prospective method for destruction of brain tumors. PDT induced functional inactivation and necrosis of neurons, necrosis, apoptosis, and proliferation of glial cells. The roles of calmodulin, calmodulin\u2010dependent kinase II, phospholipase C, protein kinases A and C, and phosphodiesterase in these processes were studied by using their inhibitors: fluphenazine, KN\u201093, D\u2010609, H89, staurosporine, and papaverine, respectively. PDT\u2010induced firing abolishment was enhanced by H89 or papaverine, whereas staurosporine acted oppositely. Fluphenazine or KN\u201093 reduced necrosis of neurons and glial cells. H89 enhanced necrosis of neurons, whereas staurosporine enhanced necrosis of glial cells. Inhibition of protein kinases A and C enhanced PDT\u2010induced glial apoptosis. Photodynamic gliosis was prevented by KN\u201093 or staurosporine. These data indicate possible involvement of calmodulin and calmodulin\u2010dependent kinase II in photoinduced necrosis of neurons and glia. Protein kinase C could protect glial cells from necrosis and apoptosis and participate in photoinduced gliosis and loss of neuronal activity. Protein kinase A maintained neuronal firing and protected neurons from photoinduced necrosis and glial cells from apoptosis. Phosphodiesterase reduced necrosis of photosensitized neurons and glia. Thus, Ca<jats:sup>2+<\/jats:sup>\u2010 and cAMP\u2010mediated signaling pathways were involved in photooxidative injury of neurons and glia. Their pharmacological modulation may differently change the efficacy of photodynamic injury of neurons and glial cells. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21190","type":"journal-article","created":{"date-parts":[[2007,2,2]],"date-time":"2007-02-02T23:22:01Z","timestamp":1170458521000},"page":"860-870","source":"Crossref","is-referenced-by-count":21,"title":["Involvement of Ca<sup>2+<\/sup>\u2010 and cyclic adenosine monophosphate\u2010mediated signaling pathways in photodynamic injury of isolated crayfish neuron and satellite glial 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