Neuron and gliocyte death induced by photodynamic treatment: signal processes and neuron-glial interactions.

The mechanisms of photodynamic (PD) damage to neurons and gliocytes are discussed. The spike reactions of neurons are described, with stimulation at high concentrations of photosensitizer and inhibition at low concentrations, accompanying necrosis. Glial cells developed both necrosis and apoptosis. Local laser inactivation of neurons increased light-induced apoptosis of gliocytes, i.e., neurons maintained gliocyte survival. Inter-and intracellular signaling plays an important role in the photolesioning of these cells. Studies using inhibitors and activators of signal proteins demonstrated the involvement of the Ca(2+)-dependent, adenylate cyclase, and tyrosine kinase pathways in the responses of neurons and gliocytes to PD treatment. Pharmacological modulation may alter the selectivity of PD neuron and gliocyte damage and the efficacy of PD treatment.

[Death of neurons and glial cells, induced by a photodynamic injury: signaling processes and neurone-glial interactions].

The mechanisms of photodynamic (PD) injury of neurons and glial cells are reviewed. Neuron responses: firing stimulation at high photosensitizer concentrations and inhibition at low concentrations (< 10(-7) M) that were followed by necrosis, are described. Glial cells died from both necrosis and apoptosis. Local laser inactivation of a neuron enhanced PD-induced apoptosis of glial cells, thus indicating that neuron maintained the survival of glia. Inter- and intracellular signaling mediated photodamage of these cells. Using inhibitors or activators of signaling proteins, the involvement of Ca(2+)-, adenylate cyclase- and tyrosine kinase-mediated signaling pathways in responses of neurons and glial cells to photosensitization was shown. Their pharmacological modulation can change selectivity of PD injury of neuronal and glial cells and efficiency of PD therapy.