Protection effect of GDNF and neurturin on photosensitized crayfish neurons and glial cells.

Neurons and glial cells can protect each other from stress and following death by mutual exchange with neurotrophins. In order to examine involvement of different neurotrophic factors in neuroglial interactions in a photosensitized crayfish stretch receptor, a simple model object consisting of only two sensory neurons enveloped by glial cells, we studied the influence of glial cell line-derived neurotrophic factor (GDNF), neurturin, and ciliary neurotrophic factor (CNTF) on its photodynamic injury. Photodynamic treatment, which causes strong oxidative stress, induced firing abolition and necrosis of neurons, necrosis, and apoptosis of glial cells.

Elevated activity of the crayfish stretch receptor neuron increases resistance of surrounding glial cells to apoptosis induced by photodynamic treatment.

Neuroglial interaction is very important for functioning and survival of nerve and glial cells. In the present work, we studied the influence of the intense neuronal activity on survival of the isolated crayfish stretch receptor neuron and surrounding glial cells subjected to photodynamic treatment, which induces intense oxidative stress. In the experimental group, neurons were stimulated by multiple extensions of the receptor muscle for 1h so that the firing rate did not fall below 10-15 Hz, whereas in the control group, the receptor muscles were relaxed and neurons were silent.

Involvement of Ca2+- and cyclic adenosine monophosphate-mediated signaling pathways in photodynamic injury of isolated crayfish neuron and satellite glial cells.

To investigate the mechanisms of oxidative injury of neurons and glia, we studied the photodynamic effect on isolated stretch receptor that consists of only two sensory neurons enwrapped by satellite glial cells. Photodynamic therapy (PDT), a potent inducer of oxidative stress, is a prospective method for destruction of brain tumors. PDT induced functional inactivation and necrosis of neurons, necrosis, apoptosis, and proliferation of glial cells.