[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.
Uzdenskiĭ
A B
AB
Kolosov
M S
MS
Lobanov
A V
AV
D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D020013:Calcium Signaling; D016923:Cell Death; D006801:Humans; D008027:Light; D009457:Neuroglia / Q000187:drug effects* / Q000502:physiology / Q000528:radiation effects*; D009474:Neurons / Q000187:drug effects* / Q000502:physiology / Q000528:radiation effects*; D010778:Photochemotherapy; D017319:Photosensitizing Agents / Q000494:pharmacology*; D011505:Protein-Tyrosine Kinases / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000528:radiation effects
D017319:Photosensitizing Agents; D011505:Protein-Tyrosine Kinases; D000262:Adenylyl Cyclases