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

Uzdenskii, A. B.; Kolosov, M. S.; Lobanov, A. V.

doi:10.1007/s11055-008-9042-1

Cited by 11 publications

(6 citation statements)

References 48 publications

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“…Unlike neurons, apoptosis of glial cells was often induced by PDT. Apoptosis of photosensitized cells is controlled by diverse intracellular signaling pathways (Almeida et al 2004;Castano et al 2005;Uzdensky et al 2008). In the present work, inhibition of tyrosine kinases or JNK eliminated the anti-apoptotic but not anti-necrotic effect of NGF in photosensitized glial cells.…”

Section: Discussionmentioning

confidence: 99%

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

Lobanov¹,

Uzdensky²

2009

J Mol Neurosci

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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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Section: Discussionmentioning

confidence: 99%

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

Lobanov¹,

Uzdensky²

2009

J Mol Neurosci

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“…GP serve as a supporting and defense apparatus for neurons [12]. They supply neurons with energy by donating glycogen and other energy substrates for Na + /K + -ATPases, maintain the concentration of Ca 2+ ions and pH in the extracellular medium, regulate synapse formation and nerve pulse conduction, and protect neurons from oxidative stress [5]. GP metabolism is closely related to metabolism of The appearance of glial wrappings observed by us is comparable with the results of studies on crab axon [8,9] lacking myelin sheaths.…”

Section: Resultsmentioning

confidence: 99%

“…Neuroglial, in particular, neuron-astrocyte interactions are now intensively studied, because they are activated during critical periods of development and under conditions of damage to the nervous system [5,6,11]. Recent studies showed that neurons and astrocytes mutually support the functions and survival of each other via cell-cell contacts, exchange of energy substrates and various molecular mediators involved in signal transmission [6,7,10,14].…”

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confidence: 99%

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Role of Glycogen in Processes of Cerebellar Glial Cells under Conditions of Its Damage with Sodium Nitrite

2010

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Ultrastructure of processes of glial cell, astrocytes of the molecular layer of cerebellar cortex in Rana temporaria frog, under conditions of damage to the cerebellum caused by NO-generating compound sodium nitrite was studied under an electron microscope. It was found that astrocytes have at least two types of processes: the first (fibrillar) primarily contained numerous fibrils and few glycogen granules and the second (granular) primarily containing glycogen granules. In the presence of NO-generating compound in toxic doses, fibrillar processes are damaged or completely degrade more rapidly than granular ones. The processes containing glycogen can protect both damaged synapses and individual synaptic buttons by forming a compact structure, wrapping, around them. We analyzed the possible role of glycogen of cerebellar glial cell processes in neuroglial interactions in the presence of sodium nitrite.

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“…PDT effects on a single mechanoreceptor neuron and surrounding glial cells including PDT-mediated alterations of neuronal activity, bioenergetic and signaling processes, cell ultrastructure, necrosis and apoptosis have been carefully studied previously [7][8][9][10][11][12] . In present work we studied PDT effect on the ventral nerve cord of crayfish, which contains nerve and glial cells in their natural relationships.…”

Section: Introductionmentioning

confidence: 99%

Photodynamic damage of glial cells in crayfish ventral nerve cord

2010

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Photodynamic therapy (PDT) is a promising method for treatment of brain tumors, the most of which are of glial origin. In the present work we studied PDT-mediated injury of glial cells in nerve tissue, specifically, in abdominal connectives in the crayfish ventral nerve cord. The preparation was photosensitized with alumophthalocyanine Photosens and irradiated 30 min with the diode laser (670 nm, 0.1 or 0.15 W/cm 2 ). After following incubation in the darkness during 1-10 hours it was fluorochromed with Hoechst 33342 and propidium iodide to reveal nuclei of living, necrotic and apoptotic cells. The chain-like location of the glial nuclei allowed visualization of those enveloping giant axons and blood vessels. The level of glial necrosis in control preparations was about 2-5 %. Apoptosis was not observed in control preparations. PDT significantly increased necrosis of glial cells to 52 or 67 % just after irradiation with 0.1 or 0.15 W/cm 2 , respectively. Apoptosis of glial cells was observed only at 10 hours after light exposure. Upper layers of the glial envelope of the connectives were injured stronger comparing to deep ones: the level of glial necrosis decreased from 100 to 30 % upon moving from the connective surface to the plane of the giant axon inside the connective. Survival of glial cells was also high in the vicinity of blood vessels. One can suggest that giant axons and blood vessels protect neighboring glial cells from photodynamic damage. The mechanism of such protective action remains to be elucidated.

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

Cited by 11 publications

References 48 publications

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

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

Role of Glycogen in Processes of Cerebellar Glial Cells under Conditions of Its Damage with Sodium Nitrite

Photodynamic damage of glial cells in crayfish ventral nerve cord

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