The role of NO synthase isoforms in PDT-induced injury of neurons and glial cells

V. D. Kovaleva; E. V. Berezhnaya; A. B. Uzdensky

doi:10.1117/12.2179702

19 March 2015 The role of NO synthase isoforms in PDT-induced injury of neurons and glial cells

V. D. Kovaleva, E. V. Berezhnaya, A. B. Uzdensky

Proceedings Volume 9448, Saratov Fall Meeting 2014: Optical Technologies in Biophysics and Medicine XVI; Laser Physics and Photonics XVI; and Computational Biophysics; 94480M (2015) https://doi.org/10.1117/12.2179702
Event: Saratov Fall Meeting 2014, 2014, Saratov, Russian Federation

Abstract

Nitric oxide (NO) is an important second messenger, involved in the implementation of various cell functions. It regulates various physiological and pathological processes such as neurotransmission, cell responses to stress, and neurodegeneration. NO synthase is a family of enzymes that synthesize NO from L-arginine. The activity of different NOS isoforms depends both on endogenous and exogenous factors. In particular, it is modulated by oxidative stress, induced by photodynamic therapy (PDT). We have studied the possible role of NOS in the regulation of survival and death of neurons and surrounding glial cells under photo-oxidative stress induced by photodynamic treatment (PDT). The crayfish stretch receptor consisting of a single identified sensory neuron enveloped by glial cells is a simple but informative model object. It was photosensitized with alumophthalocyanine photosens (10 nM) and irradiated with a laser diode (670 nm, 0.4 W/cm2). Antinecrotic and proapoptotic effects of NO on the glial cells were found using inhibitory analysis. We have shown the role of inducible NO synthase in photoinduced apoptosis and involvement of neuronal NO synthase in photoinduced necrosis of glial cells in the isolated crayfish stretch receptor. The activation of NO synthase was evaluated using NADPH-diaphorase histochemistry, a marker of neurons expressing the enzyme. The activation of NO synthase in the isolated crayfish stretch receptor was evaluated as a function of time after PDT. Photodynamic treatment induced transient increase in NO synthase activity and then slowly inhibited this enzyme.

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V. D. Kovaleva, E. V. Berezhnaya, and A. B. Uzdensky "The role of NO synthase isoforms in PDT-induced injury of neurons and glial cells ", Proc. SPIE 9448, Saratov Fall Meeting 2014: Optical Technologies in Biophysics and Medicine XVI; Laser Physics and Photonics XVI; and Computational Biophysics, 94480M (19 March 2015); https://doi.org/10.1117/12.2179702

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KEYWORDS

Glia

Neurons

Photodynamic therapy

Receptors

Cell death

Indium oxide

Injuries

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