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Protection of Crayfish Glial Cells but not Neurons from Photodynamic Injury by Nerve Growth Factor

Authors
  • Lobanov, A. V.1
  • Uzdensky, A. B.1
  • 1 Southern Federal University, Institute for Neurocybernetics, 194/1 Stachky ave., NII NK, Rostov-on-Don, 344090, Russia , Rostov-on-Don (Russia)
Type
Published Article
Journal
Journal of Molecular Neuroscience
Publisher
Springer-Verlag
Publication Date
Apr 18, 2009
Volume
39
Issue
1-2
Pages
308–319
Identifiers
DOI: 10.1007/s12031-009-9199-2
Source
Springer Nature
Keywords
License
Yellow

Abstract

Photodynamic treatment that causes intense oxidative stress and cell death is currently used in neurooncology. However, along with tumor cells, it may damage healthy neurons and glia. In order to study photodynamic effect on normal nerve and glial cells, we used crayfish stretch receptor, a simple system consisting of only two identified sensory neurons surrounded by glial cells. Photodynamic treatment induced firing abolition and necrosis of neurons as well as necrosis and apoptosis of glial cells. Nerve growth factor but not brain-derived neurotrophic factor or epidermal growth factor protected glial cells but not neurons from photoinduced necrosis and apoptosis. Inhibitors of tyrosine kinases or protein kinase JNK eliminated anti-apoptotic effect of nerve growth factor in photosensitized glial cells but not neurons. Therefore, these signaling proteins were involved in the anti-apoptotic activity of nerve growth factor. These data indicate the possible presence of receptors capable of recognizing murine nerve growth factor in crayfish glial cells. Thus, intercellular signaling mediated by nerve-growth-factor-like neurotrophin, receptor tyrosine kinase, and JNK may be involved in crayfish glia protection from apoptosis induced by photodynamic treatment.

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