On the role of protein kinase C in response of isolated neuron to photodynamic therapy

The role of protein kinase C (PKC) in response of neuronal and glial cells to photosensitization with low concentration (10(-7) M) of sulphonated aluminium phthalocianine Photosens was investigated. Changes in neuron firing and in the structure of chromatin morphology of neuron and glial nuclei were studied using PKC activator 12-0-Tetradecanoylphorbol 13-acetate (TPA) or PKC inhibitors staurosporine, hypericin or chelerythrine. Protein kinase C is shown to be involved in the neuronal and glial cell responses. Its activation by TPA decreased neuron lifetime, caused nucleus swelling characteristic for necrosis, strongly suppressed apoptotic death of glial cells, and induced gliosis. These effects were probably associated with PKC-induced Ca2+ entry into cytosol. The possible cell death mechanism in this case was necrosis. Inhibition of PKC, oppositely, increased neuron lifetime and caused a moderate nucleus swelling. Chelerythrine exerted pro-apoptotic effect on the glial cells surrounding the neuron, whereas other PKC inhibitors, staurosporine and hypericin, suppressed apoptosis.