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Photodynamic treatment that causes intense oxidative stress and kills cells is currently used in neurooncology. However,
along with tumor it damages surrounding healthy neurons and glial cells. In order to study the possible role of
glutamate-related signaling pathways in photodynamic injury of neurons and glia, we investigated photodynamic effect
of alumophthalocyanine Photosens on isolated crayfish stretch receptor that consists of a single neuron surrounded by
glial cells. The laser diode (670 nm, 0.4 W/cm2) was used for dye photoexcitation. Application of glutamate increased
photodynamically induced necrosis of neurons and glial cells but significantly decreased glial apoptosis. The natural
neuroglial mediator N-acetylaspartylglutamate, which releases glutamate after cleavage in the extracellular space by
glutamate carboxypeptidase II, also inhibited photoinduced apoptosis. Inhibition of glutamate carboxypeptidase II,
oppositely, enhanced apoptosis of glial cells. These data confirm the anti-apoptotic activity of glutamate. Application of
NMDA or inhibition of NMDA receptors by MK801 did not influence photodynamic death of neurons and glial cells
that indicated nonparticipation of NMDA receptors in these processes. Inhibition of metabotropic glutamate receptors
by AP-3 decreased PDT-induced apoptosis. One can suggest that crayfish neurons naturally secrete NAAG, which being
cleaved by GCOP produces glutamate. Glutamate prevents photoinduced apoptosis of glial cells possibly through
metabotropic but not ionotropic glutamate receptors.
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