Crayfish mechanoreceptor neuron prevents photoinduced apoptosis of satellite glial cells

Kolosov, M. S.; Uzdensky, Anatoly B.

doi:10.1016/j.brainresbull.2006.02.018

Cited by 31 publications

(18 citation statements)

References 29 publications

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“…Neurons and glial cells exchange metabolites and signaling molecules and maintain each other's survival. Nerve injury leads to the death of surrounding glial cells (Grinspan et al 1996;Kolosov and Uzdensky 2006;Kopp et al 1997), whereas glia destruction suppresses neuronal function and causes the death of neurons (Largo et al 1996). However, the mechanism of neuroglial exchange of metabolites, proteins, and other cellular components is not well understood.…”

Section: Introductionmentioning

confidence: 98%

Ultrastructure of neuroglial contacts in crayfish stretch receptor

Федоренко

Uzdensky

2009

Cell Tissue Res

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In order to explore neuroglial relationships in a simple nervous system, we have studied the ultrastructure of the crayfish stretch receptor, which consists of only two mechanoreceptor neurons enwrapped by glial cells. The glial envelope comprises 10-30 glial layers separated by collagen sheets. The intercellular space between the neuronal and glial membranes is generally less than 10-15 nm in width. This facilitates diffusion between neurons and glia but restricts neuron communication with the environment. Microtubule bundles passing from the dendrites to the axon through the neuron body limit vesicular transport between the perikaryon and the neuronal membrane. Numerous invaginations into the neuron cytoplasm strengthen glia binding to the neuron and shorten the diffusion pathway between them. Double-membrane vesicles containing fragments of glial, but not neuronal cytoplasm, represent the captured tips of invaginations. Specific triads, viz., "flat submembrane cisterns - vesicles - mitochondria", are presumably involved in the formation of the invaginations and double-membrane vesicles and in neuroglial exchange. The tubular lattice in the glial cytoplasm might transfer ions and metabolites between the glial layers. The integrity of the neuronal and glial membranes is impaired in some places. However, free neuroglial passage might be prevented or limited by the dense diffuse material accumulated in these regions. Thus, neuroglial exchange with cellular components might be mediated by transmembrane diffusion, especially in the invaginations and submembrane cisterns, by the formation of double-walled vesicles in which large glial masses are captured and by transfer through tubular lattices.

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Section: Introductionmentioning

confidence: 98%

Ultrastructure of neuroglial contacts in crayfish stretch receptor

Федоренко

Uzdensky

2009

Cell Tissue Res

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“…Neuron injury may induce death of surrounding glial cells (Kopp et al 1997;Kolosov and Uzdensky 2006). In turn, glia destruction may suppress neuronal functions and induce death of neurons.…”

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confidence: 99%

“…We have used the crayfish abdominal stretch receptor, a simple model preparation ( Fig. 1), which consists of only two identified sensory neurons (SN) enwrapped by satellite glial cells (SGC), for study of neuroglial interactions under photodynamic injury , Uzdensky 2008Kolosov and Uzdensky 2006). The glial envelope of sensory neurons looks like a multilayer Schwann cell envelope in vertebrates but glial layers are less dense than myelin and contain cytoplasm with organelles.…”

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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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“…At 6 hr after PDT, glial layers stuck together in some places and were extraordinarily dilated in others as a result of membrane disruption and edema. As shown earlier (Kolosov and Uzdensky, 2006), SN protects glial cells from PDTinduced apoptosis. According to the present ultrastructural data, the stretch receptor neuron supported survival of adjacent rather than remote glial cells, and this ability was lost after PDT.…”

Section: Discussionmentioning

confidence: 71%

Dynamics of ultrastructural alterations in photosensitized crayfish glial and neuronal cells: Structures involved in transport processes and neuroglial interactions

Федоренко

Fedorenko

et al. 2010

J. Neurosci. Res.

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Photodynamic therapy (PDT) is used for cancer treatment, including brain tumors. To explore the dynamics of photodynamic injury of glial cells and neurons and corresponding neuroglial interactions, we studied ultrastructure of the PDT-treated crayfish stretch receptor that consists of a single sensory neuron enwrapped by glial cells. Just after PDT, swelling of some mitochondria, dictyosomes, and endoplasmic reticulum cisterns occurred in neurons and glial cells. Tubular lattices involved in intraglial transport became swollen and disintegrated. At 1 hr postirradiation, these alterations were expanded to the whole cells. Segregation of the neuronal cytoplasm by Nissl bodies, which were involved in protein synthesis and transport along neurites, was lost. Swelling of submembrane cisterns prevented formation of glial protrusions and double-wall vesicles involved in the glia-to-neuron transport. Five hours later, glial layers lost organelles, stuck together, or dilated locally as a result of edema. In the neuronal cytoplasm, only demises of ER and swollen mitochondria were present, but few mitochondria retained normal structure. Thus, swelling of intracellular organelles, the first sign of photodynamic injury, occurred simultaneously in neurons and glia, but glial organelles were eliminated more quickly. Therefore, glial cells were less resistant to PDT than neurons. Adjacent glial layers were damaged less than remote ones, suggesting their protection by the neuron. The structures involved in glia-to-neuron (neuronal submembrane cisterns, glial protrusions, double-wall vesicles), intraglial (tubular lattices), and intraneuronal (Nissl bodies, Golgi apparatus, microtubular bundles) transport were impaired at the earlier stages of stretch receptor damage.

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Crayfish mechanoreceptor neuron prevents photoinduced apoptosis of satellite glial cells

Cited by 31 publications

References 29 publications

Ultrastructure of neuroglial contacts in crayfish stretch receptor

Ultrastructure of neuroglial contacts in crayfish stretch receptor

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

Dynamics of ultrastructural alterations in photosensitized crayfish glial and neuronal cells: Structures involved in transport processes and neuroglial interactions

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