Short-term extracellular glucose exposure alters neurite outgrowth and intracellular reactive oxygen species without altering viability in neuronal cells

Abstract

Hyperglycemia is the main trigger for diabetic neuropathic pain and can cause degeneration of the sensory neurons. Here, we explored the effects of high glucose on the cell viability, oxidative stress (intracellular reactive oxygen species (ROS) generation, glutathione (GSH) and neurite outgrowth of primary cultured sensory neurons. Dorsal root ganglion (DRG) neurons isolated from the neonatal rat and mouse neuroblastoma (neuro-2a) cells were exposed to high glucose concentrations. Short-term exposure of high glucose leads to a decrease in the neurite outgrowth as compared to the normal glucose level in the DRG neurons and the neuro-2a cells. However, exposure to high glucose levels did not alter the cell viability. Furthermore, exposure to high glucose levels leads to an increase in the ROS and a decrease in the GSH as compared to the normal glucose levels in the DRG neurons and the neuro-2a cells. These results suggest that short-term exposure of the DRG neurons and the neuro-2a cells to extracellular glucose damages the morphology, thus, hampers the extension of neurite outgrowth without altering the cell viability. The neuronal injury may be induced by high levels of glucose, mediated through the ROS and GSH.