Effect of in vitro Hyperglycemia on Excitability of the Rat Dorsal Root Ganglia (DRG) Neurons

초록

Diabetic neuropathy results from various changes in the environment of peripheral sensory neurons. Diabetic peripheral neuropathy exhibits various sensory symptoms such as loss of nociception or allodynia and hyperalgesia. Diabetic peripheral neuropathy sensory symptoms have been linked to functional, structural and biochemical abnormalities in sensory neurons. Studies using diabetic animal models and in vitro high glucose treatment have reported that activities of several ion channels as well as pain related molecules, including cytokines and growth factors, are modified in the sensory neurons. In this study, we investigated whether the excitability of sensory neurons changes when cultured under high glucose condition using a whole-cell patch clamp technique. In vitro high glucose (50 mM) did not change morphology and viability of the DRG neurons until the 7th day. Unlike studies using diabetic animal models, resting membrane potential, peak amplitude of action potential, as well as rheobase and threshold were not significantly changed in the high glucose treated DRG neurons. Half width (APD50) was significantly decreased in the high glucose treated DRG neurons. Parameters related to neuronal excitability were not changed by H2O2 (10 mM) or LPS (10 μg/ml) treatment. These results suggest that the hyperalgesia or loss of pain associated with diabetic peripheral neuropathy may be related to a complex changes in molecular level rather than simply a change in basal excitability of peripheral sensory neurons, even in vitro.